Intelligent Design

Antibody affinity maturation as an engineering process (and other things)

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In Kairosfocus’ very good thread about functional complexity, I posted about antibody affinity maturation as an example of a very complex engineering process embedded in biological beings. Both Kairosfocus and Dionisio suggested that I could open a new thread to discuss the issue. When such good friends ask, I can only comply.  🙂

For lack of time, I will try to be very simple.

First of all, I paste here my original post (#6 in the original thread):

KF:

Thank you for the very good summary. Among many other certainly interesting discussions, we may tend to forget sometimes that functionally specified complex information is the central point in ID theory. You are very good at reminding that to all here.

I would like to suggest a very good example of multilevel functional complexity in biology, which is often overlooked. It is an old favourite of mine, the maturation of antibody affinity after the initial immunological response.

Dionisio has recently linked an article about a very recent paper. The paper is not free, but I invite all those interested to look at the figures and legends, which can be viewed here:

http://www.nature.com/nri/jour…..28_ft.html

The interesting point is that the whole process has been defined as “darwinian”, while it is the best known example of functional protein engineering embedded in a complex biological system.

In brief, the specific B cells which respond to the epitope (antigen) at the beginning of the process undergo a sequence of targeted mutations and specific selection, so that new cells with more efficient antibody DNA sequences can be selected and become memory cells or plasma cells.

The whole process takes place in the Germinative Center of lymph nodes, and involves (at least):

1) Specific B cells with a BCR (B cell receptor) which reacts to the external epitope.

2) Specific T helper cells

3) Antigen presenting cells (Follicular dendritic cell) which retain the original epitope (the external information) during the whole process, for specific intelligent selection of the results

4) Specific, controlled somatic hypermutation of the Variable region of the Ig genes, implemented by the following molecules (at least):

a) Activation-Induced (Cytidine) Deaminase (AID): a cytosine:guanine pair is directly mutated to a uracil:guanine mismatch.

b) DNA mismatch repair proteins: the uracil bases are removed by the repair enzyme, uracil-DNA glycosylase.

c) Error-prone DNA polymerases: they fill in the gap and create mutations.

5) The mutated clones are then “measured” by interaction with the epitope presented by the Follicular DC. The process is probably repeated in multiple steps, although it could also happen in one step.

6) New clones with reduced or lost affinity are directed to apoptosis.

7) New clones with higher affinity are selected and sustained by specific T helper cells.

In a few weeks, the process yields high affinity antibody producing B cells, in the form of plasma cells and memory cells.

You have it all here: molecular complexity, high control, multiple cellular interactions, irreducible complexity in tons, spacial and temporal organization, extremely efficient engineering. The process is so delicate that errors in it are probably the cause of many human lymphomas.

Now, that’s absolute evidence for Intelligent Design, if ever I saw it. :)

The most interesting answers came from Aurelio Smith and sparc. I have already answered AS’s comment in the original thread. Spark’s comments were more specific, so I paste them here  (#58 and 59):

You haven’t looked up evolution of AID, did you?

and

BTW, you let out the part of the B-cell development that occurs without any antigen. Lots of mutations, rearragements and selection. Where and how does ID interfere in these processes. Especially, in cases of man made synthetic artificial antigens that were not present 50 years ago?

OK, I will make just a couple of comments on these two points here, and let the rest to the discussion:

a) My point was not specifically about the evolution of the individual proteins in the system, but about the amazing complexity of the whole system. So, I have not done any detailed analysis of the individual proteins I quote. However, I will look at that aspect. As sparc seems aware of specific information about the evolution of AID, I invite him ot provide some references, and we can certainly go on from there.

b) I did not “let out” the part of the B-cell development. I simply focused on affinity maturation. However, the part sparc alludes to is extremely interesting too, so I will mention here in very general lines how it works, and why it is another wonderful example of intelligent engineering. And we can obviously discuss this second aspect too.

In brief, the adaptive immune system must solve the problem of reacting t a great number of potential antigens/epitope, which are not known in advance (I will use “epitope” from now on, because that is the immulogically active part of an antigen).

So, the two branches of the adaptive immune system (B system and T system) must be “prepared” to recognized possible epitopes coming from the outer world. They do that by a “sensor” which is the B cel receptor (BCR) in the B system, and the T cell receptor (TCR) in the T system.

Let’s focus the discussion on the B system.

To recognize the greatest number of possible epitopes (IOWs, of possible small biochemical configurations, mainly of proteins but also of other molecules), the B immune system builds what is usually known as the “basic repertoire”.Very simply, B cells underso a process of somatic genetic differentiation, essentially based on the recombination of VDJ genes, which generates a basic repertoire of different B clones with specific variable genes for the heavy and light chain, IOWs a specific BCR. In that sense, immune cells are different from other somatic cells, because they have a specific genetic recombination of the variable chains of the BCR (and therefore of the antibody that they will produce.

No one knows exactly how big that repertoire is in each individual, but new techniques are helping much in studying it quantitatively. From what I have read, I would say that the size is probably somewhere between 10^6 and 10^9 (more or less the total number of B cells in an organism).

Now, what is the purpose of this basic BCR (antibody) repertoire? We can consider it as a “network” of lower affinity antibodies covering in a loose way the space of possible epitope configurations. That repertoire is generated blindly (IOWs, without any information about specific antigens) by a process of sophisticated genetic engineering (VDJ recombination and other factors), which again uses random variation in a controlled way to generate diversity.

So, to sum up. two different complex algorithms act to ensure efficient immune responses.

1) The first one generates a “blind” repertoire of lower affinity antibodies covering as well as possible the whole space of configurations of possible epitopes.

2) The second one (affinity maturation) refines the affinity of the B cells selected in the primary response (from the basic repertoire) so that they become high affinity, specialized memory cells. This is the process I described in the beginning, in my post.

Both processes are wonderful examples of sophisticated engineering and irreducibly complex systems, and they are completely different one from the other. Both processes work together in sequence in a sophisticated and irreducibly complex meta-system.

Both use controlled random variation to generate diversity. The second process also uses intelligent selection based on existing information from the environment (the epitope conserved in the Follicular GC cell).

All that is very brief, and in no way covers the whole complexity of what is known. So, let’s open the discussion.

521 Replies to “Antibody affinity maturation as an engineering process (and other things)

  1. 1
    Dionisio says:

    Eccellente mio caro Dottore!
    Mile grazie!

    Now let the discussion start. Apparently some interlocutors have serious arguments to present here.
    Let’s hear them.

    PS. Perhaps this recent paper somehow relates to this discussed subject?
    http://journal.frontiersin.org.....00534/full

    In Kairosfocus’ very good thread about functional complexity, I wrote the following comment in post #61:

    Let’s keep in mind that there’s a substantial amount of detailed information to dissect further for this discussion.

    The enzymes involved in the processes could be reviewed, as well as their variations involved within different scenarios.

    But most importantly we should look carefully at the actual choreographies where the referred enzymes and their variations play any role. How did they get orchestrated? Special attention to timing, location, quantity? Other issues to consider too?

  2. 2
    Dionisio says:

    a) My point was not specifically about the evolution of the individual proteins in the system, but about the amazing complexity of the whole system.

    Yes, that’s a very important point to keep in mind during this discussion.

  3. 3
    Dionisio says:

    As in a chess match, grandmaster GP has made the first move and now the game clock is ticking for the opponent to respond. 🙂

  4. 4
    Dionisio says:

    #2 follow-up

    How did that amazingly complex system get setup to being with?
    What preceded it?
    How did it turn from the previous version to the current version?
    What was version 1.0?

  5. 5
    Dionisio says:

    Hey, the game clock is ticking…

    sparc are you still there?

    anybody else out there?

    🙂

    PS. Let’s hope the other players won’t start complaining about the curtains in the room or the distracting presence of the accredited media reporters. 🙂
    In this case the invisible onlookers/lurkers are quietly watching what’s going on from the sidelines. 🙂

  6. 6
    Dionisio says:

    This could be an interesting sneak preview of what could happen when we get an OP on the cell fate specification/determination interwoven mechanisms for multicellular development. 🙂
    That must be quite a thrilling rollercoaster ride to try here someday. 🙂
    Fasten your seatbelts… 🙂

  7. 7
    DNA_Jock says:

    Both use controlled random variation to generate diversity. The second process also uses intelligent selection based on existing information from the environment (the hapten conserved in the Folliculart GC cell).

    How is this selection “intelligent”?

  8. 8
    bornagain77 says:

    a few related notes on immunology:

    Falk’s fallacy – Feb. 2010
    Excerpt: This (the immune system) is one of the most amazing processes ever described.,,, Whatever may be said about it, it is a highly regulated, specified, directed and choreographed process. It is obviously the product of overwhelmingly brilliant design,,,
    http://www.uncommondescent.com.....ks-falacy/

    Response to Kathryn Applegate – Caroline Crocker PhD.- cell biologist and immunologist – October 2010
    Excerpt: Diversity of antibodies generated by B cells is due to deliberate, cell-engineered changes in the DNA sequence, not random mutations. In fact, I have never before heard the process whereby functional antibodies are formed (before they encounter antigen) described as mutation. And it is well-known that the appearance of functionality as a result of a mistake-mutation is extremely rare. Of course, after encountering antigen the hypervariable regions of the antibody DNA do undergo somatic hypermutation, but again this is in particular places and is controlled by enzymes.,,,
    http://www.uncommondescent.com.....more-15176

    Generation of Antibody Diversity is Unlike Darwinian Evolution – microbiologist Don Ewert – November 2010
    Excerpt: The evidence from decades of research reveals a complex network of highly regulated processes of gene expression that leave very little to chance, but permit the generation of receptor diversity without damaging the function of the immunoglobulin protein or doing damage to other sites in the genome.
    http://www.evolutionnews.org/2.....40661.html

    “A Masterful Feat of Courtroom Deception”: Immunologist Donald Ewert on Dover Trial – audio
    http://intelligentdesign.podom.....1_03-08_00

    In this following podcast, Casey Luskin interviews microbiologist and immunologist Donald Ewert about his previous work as associate editor for the journal Development and Comparitive Immunology, where he realized that the papers being published were comparative studies that had nothing at all to do with the evolution of such systems.

    What Does Evolution Have to Do With Immunology? Not Much – April 2011
    http://intelligentdesign.podom.....9_03-07_00

    How the Burgeoning Field of Systems Biology Supports Intelligent Design – July 2014
    Excerpt: “Adaptation,” where organisms are pre-engineered to be able to undergo small-scale adaptations to their environments. As Snoke explains, “These systems use randomization controlled by supersystems, just as the immune system uses randomization in a very controlled way,” and “Only part of the system is allowed to vary randomly, while the rest is highly conserved.”,,,
    per Evolution News and Views

    Evolutionists Are Now Saying That Evolution Created an Optimized Evolutionary Process (For Immunity System) – Cornelius Hunter – July 2012
    Excerpt: This type of problem, known as the calculus of variations, is important in many engineering problems.
    It also applies to our immune system. About ten years ago researchers used Pontryagin’s maximum principle—an important concept in engineering control theory involving the calculus of variations—to predict how our immune system works.
    http://darwins-god.blogspot.co.....-that.html

    The Cell Secret Immune System – BBC video
    http://www.youtube.com/watch?v=v1MnNO4I9aU

    Irreducible complexity meets multifunctionality:
    Immune system molecule with hidden talents – January 22, 2013
    Excerpt: The human immune system is made up of some half a dozen different cell types that are all working in tandem. Team work is key since each cell type has a single unique job to perform, which is central to its ability to help defend the body against invaders and ward off disease. If one of these players is taken out of commission, the entire system is thrown out of whack.,,,
    “We had no idea that B cells and dendritic cells use immunoglobulins to communicate with each other. It just goes to show you how complex the immune system really is and how we are a long way from truly grasping the full scope of its complexity,”
    http://medicalxpress.com/news/.....lents.html

    Of related note: Immunity bacteria are shown to be species specific (Regardless of the surprising result, Darwinists still insist evolution did it.)

    Our Microbes, Ourselves: Billions of Bacteria Within, Essential for Immune Function, Are Ours Alone – ScienceDaily (June 21, 2012)
    Excerpt: Chung repeated the experiment, only this time populating a third group of mice with microbes common to rats. This new group showed the same immune system deficiency as the humanized mice. “I was very surprised to see that,” Chung said. “Naturally, I would have expected more of a half-way response.”
    http://www.sciencedaily.com/re.....130643.htm

  9. 9
    Dionisio says:

    how do B cells adapt to their targets?

    Over the weeks following an invasion by a disease-causing microbe, the human immune system fine tunes its defenses, producing proteins called antibodies that are ever more precisely targeted at the invader.

    New research in Michel Nussenzweig’s Laboratory of Molecular Immunology helps explain how the immune system accomplishes this, suggesting new ways by which the body could be trained to fight disease.

    “We have understood this process, called affinity maturation, in broad strokes for decades; however, the mechanistic details have remained more elusive,” says Alex Gitlin, a graduate student in the lab and the first author of a study that delves into these mechanisms. “Our research helps explain how the immune system selects B cells that produce antibodies with a high affinity for a pathogen.”

    “These cycles of mutation, proliferation and selection happen over and over again. Over time, a few lines of high affinity B cells come to dominate the germinal centers,” Gitlin says. Their current findings shed light on how the higher affinity B cells out-compete lower affinity cells.

    The repeated process of hypermutation and selection creates a feed-forward loop, says Gitlin. “When a B cell is selected as being higher affinity, it is instructed by the T cell to divide a greater number of times, and through more cell divisions, they accumulate more mutations.”

    http://newswire.rockefeller.ed.....r-targets/

  10. 10
    Dionisio says:

    Clonal selection in the germinal centre by regulated proliferation and hypermutation

    doi:10.1038/nature13300

    During immune responses, B lymphocytes clonally expand and undergo secondary diversification of their immunoglobulin genes in germinal centres (GCs).

    High-affinity B cells are expanded through iterative interzonal cycles of division and hypermutation in the GC dark zone followed by migration to the GC light zone, where they are selected on the basis of affinity to return to the dark zone5, 6, 7, 8, 9, 10.

    Here we combine a transgenic strategy to measure cell division and a photoactivatable fluorescent reporter to examine whether the extent of clonal expansion and hypermutation are regulated during interzonal GC cycles.

    We find that both cell division and hypermutation are directly proportional to the amount of antigen captured and presented by GC B cells to follicular helper T cells in the light zone.

    Our data explain how GC B cells with the highest affinity for antigen are selectively expanded and diversified.

    http://www.nature.com/nature/j.....13300.html

  11. 11
    Dionisio says:

    Simulation of B Cell Affinity Maturation Explains Enhanced Antibody Cross-Reactivity Induced by the Polyvalent Malaria Vaccine AMA1

    doi: 10.4049/?jimmunol.1401054

    Polyvalent vaccines use a mixture of Ags representing distinct pathogen strains to induce an immune response that is cross-reactive and protective.

    However, such approaches often have mixed results, and it is unclear how polyvalency alters the fine specificity of the Ab response and what those consequences might be for protection.

    In this article, we present a coarse-grain theoretical model of B cell affinity maturation during monovalent and polyvalent vaccinations that predicts the fine specificity and cross-reactivity of the Ab response.

    RnWe stochastically simulate affinity maturation using a population dynamics approach in which the host B cell repertoire is represented explicitly, and individual B cell subpopulations undergo rounds of stimulation, mutation, and differentiation.

    Ags contain multiple epitopes and are present in subpopulations of distinct pathogen strains, each with varying degrees of cross-reactivity at the epitope level.

    This epitope- and strain-specific model of affinity maturation enables us to study the composition of the polyclonal response in granular detail and identify the mechanisms driving serum specificity and cross-reactivity.

    We applied this approach to predict the Ab response to a polyvalent vaccine based on the highly polymorphic malaria Ag apical membrane antigen-1.

    Our simulations show how polyvalent apical membrane Ag-1 vaccination alters the selection pressure during affinity maturation to favor cross-reactive B cells to both conserved and strain-specific epitopes and demonstrate how a polyvalent vaccine with a small number of strains and only moderate allelic coverage may be broadly neutralizing.

    Our findings suggest that altered fine specificity and enhanced cross-reactivity may be a universal feature of polyvalent vaccines.

    http://www.jimmunol.org/content/193/5/2073

  12. 12
    Dionisio says:

    Immunology: To affinity and beyond

    doi:10.1038/509573a

    Tracking B cells in germinal centres — hotspots of B-cell proliferation and mutation during an immune response — reveals that those cells presenting the most antigen on their surface are programmed to dominate.

    http://www.nature.com/nature/j.....9573a.html

  13. 13
    Dionisio says:

    What surrogate markers on B lymphocytes correlate with the state of affinity maturation?

    The early immune response tends to produce polyspecific antibodies, i.e. antibodies that recognize various epitopes and IgM antibodies are a classical example.

    However, during affinity maturation lymphocytes are progressively antigen-educated and the specificity of mutated antibodies to a foreign protein dramatically improves.

    I would be interested to understand what we know about the expression of proteins or surrogate markers on B lymphocytes that would tell us something about the state of maturity.

    http://www.researchgate.net/po.....maturation

  14. 14
    gpuccio says:

    DNA_Jock:

    “How is this selection “intelligent”?”

    I use the term “intelligent selection” to differentiate it from “natural selection”.

    In “NS”, the variation confers a reproductive advantage, and therefore it is “selected” (the term selection here is not completely proper), in the sense that it expands in the population and is more or less fixed (positive and negative selection).

    The key point here is that the variation itself confers an advantage to the organism in terms of fitness and reproduction. There is no special organized system in the environment that “measures” any property of the variation. In a sense, the new organism “selects itself” because it can use better the resources of the environment.

    IS is any situation in which the system actively measures some property of the mutated object and reacts to that measure in a specific way. In this case, only the measured property can trigger the active response of the environment which “selects” (this time in a completely correct sense) the result, and expands and supports it.

    In affinity maturation, the process is an intelligent selection in all senses. The variations in sequence due to random (but controlled) mutagenesis generate different affinity for the hapten which was originally used to select the responsive clones. The hapten is retained in the Follicular GC cell, and then is used again to measure the variation of affinity. Two different active responses of the system are triggered by the measure (indeed, we still don’t know, as far as I can say, how that part works).

    In the case of a reduction of affinity, apoptosis in initiated. That is in no way a direct consequence of the higher affinity of lower affinity of the new molecule, because the B cell at present is in no way engaged in defending the organism from any attack. It is the programmed response to a specific signal, to the result of a measure.

    On the other hand, if the affinity is higher, the B cell is “protected” by the intervention of specific T helper cells. Again, this is a programmed response to a specific signal (the higher affinity, measured against the retained hapten), and has no immediate advantage, except in view of what can happen in the future (a new encounter with the invading microorganism). Again, it is an intelligent response to the interpretation of a signal.

    I am not implying here that any active intelligence is working in the cells. The process is embedded as an algorithm, and it can go on because it was programmed to do so, exactly like a computer program will go on even if it is not “actively intelligent” (IOWs, conscious and cognitive) in that moment.

    But, as a computer program performs passively intelligent algorithms, so does the biological system which generates the affinity maturation.

    In no way there is a “natural selection” here. And if you say that the environment selects like in darwinian natural selection, because after all the environment includes an antigen presenting cell, a measure system, a system which actively generates controlled variation in a specific part of the gene, a system to destroy the bad results (apoptosis) and a system to promote the good results (specific T helper cells), and that we can consider all that exactly like a fitness function in a natural system, well, then I will be very disappointed by you.

  15. 15
    Dionisio says:

    More references to research papers related to the subject discussed here in this thread are posted in the thread “Mystery at the heart of life” starting @ post #212:

    http://www.uncommondescent.com.....ent-546460

  16. 16
    Dionisio says:

    I am not implying here that any active intelligence is working in the cells. The process is embedded as an algorithm, and it can go on because it was programmed to do so, exactly like a computer program will go on even if it is not “actively intelligent” (IOWs, conscious and cognitive) in that moment.

    But, as a computer program performs passively intelligent algorithms, so does the biological system which generates the affinity maturation.

    esattamente!

    The interwoven mechanisms could have been intelligently setup a priori. That’s the challenge to your interlocutors. How else can they explain the appearance of the amazingly complex choreographies orchestrated within the biological systems, which can handle even stochastic scenarios?

    🙂

  17. 17
    DNA_Jock says:

    gpuccio, prepare to be disappointed.

    So you agree that affinity maturation involves random (with respect to fitness) mutation and differential reproduction. Good.

    In affinity maturation, the process is an intelligent selection in all senses.

    I am not implying here that any active intelligence is working in the cells.

    So you are using the word “intelligent”, when what you actually mean is “complicated”. A fairly common mistake hereabouts, I guess.

    What is the minimum level of complexity for such a RM+DR system that would confer a selectable advantage? Or, to put it another way, how do you suppose that the cell might “measure” the affinity of its antibody for a hapten? What would be a simple way for the cell to translate affinity into differential reproduction?

    Consider the feeling mutual.

  18. 18
    littlejohn says:

    #17-

    I believe what gpuccio means by intelligent, is that the process in intentional, and therefore we infer intelligence behind the intention. After all, none of these programmed molecular rearrangements appear to occur outside of living cells, do they?

  19. 19
    DNA_Jock says:

    littlejohn,

    I would be very surprised if gpuccio means that the process is “intentional”, given his “no active intelligence is working within the cells” comment. I would agree that he thinks it is “intended”.

    But thank you for offering the novel “intelligent” = “does not occur outside living cells”.

    Very interesting, but not…

  20. 20
    gpuccio says:

    DNA_Jock:

    I am disappointed.

    I don’t mean “complicated”. I mean that there is nothing natural in an algorithmic decision based on a direct measure, and implemented by specific processes (apoptosis, T cell support) which are in no way “naturally” related to the outcome. That means organization, and a lot of relationships between algorithmic parts which are not natural at all.

    Intelligent selection is a process where a property is measured by the system, and the system reacts in a programmed way to the measure.

    Natural selection is a process where a reproductor becomes better at reproduction, and therefore reproduces better, using better the resources in the environment.

    If you cannot see the difference, your mental bias is much more serious than I suspected. And I am disappointed.

  21. 21
    littlejohn says:

    DNA_Jock

    I did not mean to imply that intelligence could not or does not exist outside living cells, rather, I am unaware of the occurrence of programmed molecular rearrangements taking place outside living cells, such as the programmed DNA rearrangements connected with the immune system.

    It could very well be that I am misunderstanding gpuccio, and I am definitely unclear about your interpretation, seemingly saying that he views the process as intended, but not intentional?

  22. 22
    Dionisio says:

    Can anyone point to any set of papers explaining how the entire mechanisms gpuccio described in the OP got setup to work the way they do?

    One option is that the interwoven mechanisms could have been intelligently setup a priori.

    Is there a detailed explanation for the appearance of the amazingly complex choreographies orchestrated within the biological systems, which can handle even stochastic scenarios?

  23. 23
    gpuccio says:

    To all:

    Just to clarify, intelligent selection is an algorithmic procedure based on measurement of a predefined property, and selection, active selection of the result according to the logical (binary) outcome of the measurement.

    Obviously, all algorithms that I know of, based on IS, are designed. I don’t believe that “spontaneous”, non designed systems may work by intelligent selection as I have defined it.

    However, anyone who believes differently can show how that can happen.

    The ATP binding protein in Szostak’s paper is the result of intelligent selection.

    The famous algorithm proposed by Elizabeth in TSZ is based on IS.

    None of these are example of natural selection.

    In natural selection it is not the system which measures or rewards. There is an active reproductor which uses environmental resources, and can use them better. That’s all. No measure, no selection. No “fitness function”. Just function.

  24. 24
    DNA_Jock says:

    Intelligent selection is a process where a property is measured by the system, and the system reacts in a programmed way to the measure.

    Can we delete the phrase “in a programmed way” from your definition? It doesn `t seem to belong…
    A simple ‘yes’ or ‘no’ will suffice.

    Just to clarify, intelligent selection is an algorithmic procedure based on measurement of a predefined property, and selection, active selection of the result according to the logical (binary) outcome of the measurement.

    That’s a different definition altogether. Why “predefined”? Can we delete that from your definition?
    Surely you did not mean to restrict the outcomes to “logical (binary)” outcomes? A sniper selects from many windage adjustments based on the wind speed and direction observed. Even in Texas.
    And surely passive selection can be just as “intelligent” as active selection, e.g. I choose to not pull someone out of the way of an oncoming train?

    I am disappointed that you did not deign to respond to my questions @17.
    There’s a lot of it about, I guess.

    P.S. your continued refusal to engage on the results of Szostak`s work and Liddle`s algorithm because the examples were designed continues to crack me up.

  25. 25
    sparc says:

    It doesn’t make sense for any immunologist to join this kind of “if you have a hammer everything looks like a nail” discussion because you will just continue to claim that the immune system is intelligently designed and try to obfuscate mutation and selection as the major forces forming the antibody repertoire.

  26. 26
    Me_Think says:

    Here is a brief discription of how Ebola virus works

    Multiple IgG antibodies bind to GP epitopes in close proximity, allowing the binding of C1 to the Fc region of the antibodies. This complex binds C1q ligands on the cell surface and stabilizes the interaction between the virus and its receptor, increasing the likelihood of viral attachment.while antibodies normally protect the body, this virus is able to use them for faster and easier attachment to target cells.VP35 is able to disrupt this pathway just as it begins by competing with RIG-1 for the binding of dsRNA.
    VP35 is also able to counteract the antiviral action of interferon in infected cells by suppressing the pathway regulated by double-stranded RNA-dependent protein kinase PKR. It accomplishes this goal by inhibiting phosphorylation of PKR and eIF-2?.
    The second matrix protein, VP24, suppresses interferon production as well. The binding of IFN-?/? and IFN-? to their respective receptors activates STAT complexes, a family of transcription factors that regulate immune system gene expression. Normally, STAT1:STAT2 heterodimers and STAT1 homodimers are transported to the nucleus by karyopherin ?1 and activate numerous genes involved in antiviral activities (Fig 11). However, VP24 competes with STAT1 to bind karyopherin ?1, blocking nuclear accumulation and leading to inhibition of IFN signaling.
    Monocytes/macrophages in the lymphoid tissues are early and sustained targets of this deadly virus. Since these cells usually elicit the response cascade in the acute phage of inflammation, their early infection helps Ebola evade the immune system while subsequently spreading throughout the host. In addition, infected macrophages release increased amounts of nitric oxide (NO), a gaseous hormone that normally functions in cell communication.

    It’s working shows how intelligent it is. Obviously it is being controlled and directed by an ID agent. ID agents are real baddies. They kill people just for fun. they started the 2014 outbreak by killing a 2 year old child. Do you agree with this conclusion ?

  27. 27
    gpuccio says:

    sparc:

    1) I don’t understand what you mean with the hammer and nail “metaphor”. Could you please clarify?

    2) I will certainly go on “claiming” that the immune system is intelligently designed, and will go on giving arguments in that sense, because I believe that is true. I supposed we were here to discuss these things. You, please, go on claiming what you believe, and giving arguments for your beliefs. If you like.

    3) I am still waiting for references about the evolution of AID, or any other argument in favor of a neo darwinian explanation of the systems I described. Your contribution will be appreciated. If it comes.

  28. 28
    gpuccio says:

    Me_Think:

    I have no doubts that viruses are designed.

  29. 29
    gpuccio says:

    DNA_Jock:

    I suppose there are 3 different point here. Let’s go in some order:

    a) Your questions at #17. I confess that I have not answered because I am not sure I understand them. I will try anyway, and you correct me if it is the case.

    You ask:

    “What is the minimum level of complexity for such a RM+DR system that would confer a selectable advantage? Or, to put it another way, how do you suppose that the cell might “measure” the affinity of its antibody for a hapten? What would be a simple way for the cell to translate affinity into differential reproduction?”

    Not sure what “DR” means. And what is the meaning of the rest? The high affinity generated by the system is somatic, and is not transmitted in reproduction. What is transmitted is the whole system which generates it. And it is certainly very complex. I don’t know if there is any simpler way to get to the same result. Probably not.

    Does that answer your questions? And I say, again, that I am not “using the word “intelligent”, when what I actually mean is “complicated””. Not at all. In this context, I am using the word “intelligent selection” in a very specific sense, as I will try to clarify in next post.

  30. 30
    Joe says:

    Mwe Think:

    Obviously it is being controlled and directed by an ID agent.

    Why, because you are too stupid to think of something else? Why can’t it, as an intelligent agency, be controlling itself? And why can’t it be that Darwinian processes turned a good virus into a killing virus?

  31. 31
    Joe says:

    sparc,

    If you don’t like the design inference wrt the immune system then just step up and demonstrate that blind and unguided processes can produce it. Ya see we infer it was intelligently designed in part because there aren’t any known blind and unguided processes that can produce such a system.

    So have at it as your whining isn’t going to change anything.

  32. 32
    Dionisio says:

    #25 sparc

    “It doesn’t make sense for any immunologist to join this kind of “if you have a hammer everything looks like a nail” discussion because you will just continue to claim that the immune system is intelligently designed and try to obfuscate mutation and selection as the major forces forming the antibody repertoire.”

    Is whining the best argument you can present at this discussion? Can’t you do better than this?

    Can you point to any set of papers explaining how the entire mechanisms gpuccio described in the OP got setup to work the way they do?

    One option is that the interwoven mechanisms could have been intelligently setup a priori.

    What is your strong argument against it?

    Is there a detailed explanation for the appearance of the amazingly complex choreographies orchestrated within the biological systems, which can handle even stochastic scenarios?

    This thread was made after you questioned gpuccio’s insightful comments in kf’s thread. Do you need to be reminded of your question again?

    I mistakenly overestimated your knowledge and expected to see this new thread flooded with strong arguments from you. That’s why I suggested to start a separate thread, specially to discuss the issues you had questioned in gpuccio’s comments within kf’s thread.

    Even gpuccio thanked you for your comment that triggered this separate thread.

    And now all you can do is whine and complain?

    You have disappointed me. Now I see I had exaggerated expectations. Your question to gpuccio in the kf’s thread gave me the wrong impression.

    Oh, well. What else is new? Your comrades have done the same before too.

    Well, fasten your seatbelt. It ain’t gonna get easier than this. As more research is done, shedding more light on the elaborate cellular and molecular choreographic orchestrations seen in biological systems, the discussion will get more intensive. All arguments will be thoroughly scrutinized.

    🙂

  33. 33
    Me_Think says:

    gpuccio @ 28,

    I have no doubts that viruses are designed.

    [..by ID agents.]
    Ok, so you are not averse to admitting ID agents, which guide the viral processes are bad and they have no qualm about killing a child, objective morality be damned.

    My second question, if I may, What is that you want to achieve in this OP if you already believe the system is designed and you have rejected [evolution] and selection (@ 14) as a parameter ? Have you – to exclude super natural ID explanation- exhausted research of chemical, structural and hydrodynamics of the system ? I am sure you have used the SwissModel or Chimera to generate protein (hapten can’t work without protein. It has to be attached) models and examined various energy parameters and possible binding site. May be you examined ramachandran plots too…. you know if you haven’t done any of those and have understood the dynamics, you can’t really claim everything is designed by intelligence, right?

    If I throw a ball, it will follow the path which has the least Kinetic – potential energy difference. It is pretty intelligent. Does it mean the ball calculates all the possible paths in the milliseconds after the ball is released into air and chooses the correct path which minimizes KE-PE ? The force on a point on that path can be calculated by the integral of the negative potential on a point on that path, does it mean the ball knows advanced maths? or can you conclude the ball has consciousness ? Isn’t your conclusions in the OP somewhat similar ?

  34. 34
    Dionisio says:

    #29 gpuccio

    The high affinity generated by the system is somatic, and is not transmitted in reproduction. What is transmitted is the whole system which generates it. And it is certainly very complex. I don’t know if there is any simpler way to get to the same result. Probably not.

    That’s a clear statement based on careful analysis of the available evidences. Your interlocutors seem to base their arguments on old misconceptions and misleading presuppositions. They definitely should try better next time. 🙂

  35. 35
    Joe says:

    Me Think:

    Ok, so you are not averse to admitting ID agents, which guide the viral processes…

    That is NOT what he said. Obviously you have issues.

    My second question, if I may, What is that you want to achieve in this OP if you already believe the system is designed and you have rejected [evolution] and selection (@ 14) as a parameter ?

    Natural selection has proven to be impotent. Only true believers like you still cling to it.

    BTW ID doesn’t require the supernatural. You are so confused that it has become amusing watching you contort reality.

  36. 36
    Dionisio says:

    #33 Me_Think

    Are whining and complaining your best arguments for this serious discussion?

    You may benefit from reading carefully my post #32 addressed to sparc, but mostly applicable to you and your party comrades too.

    C’mon, give it another try. You should do better than this poor performance you have shown here so far.

    Onlookers/lurkers are watching what’s going on. They want to read a serious discussion. Don’t let them down. Bring up your strong arguments.

    🙂

  37. 37
    Me_Think says:

    Joe,
    You are late to the party. Check my comment #26. GP replied to my comment @28 and I am taking it further from there. You can’t claim Ebola (It’s a virus, Joe) is designed by ID agent and escape from the conclusion that ID agent is thus responsible for deaths.

  38. 38
    Me_Think says:

    Dionisio @ 36
    Read my comment #33 again. I am sure you will find the relevance after a few reads. Have you understood all those – swiss, chimera, kinetic energy – potential energy bit ?

  39. 39
    DNA_Jock says:

    Gpuccio @29:

    You [DNA_Jock] ask:

    What is the minimum level of complexity for such a RM+DR system that would confer a selectable advantage? Or, to put it another way, how do you suppose that the cell might “measure” the affinity of its antibody for a hapten? What would be a simple way for the cell to translate affinity into differential reproduction?

    Not sure what “DR” means. And what is the meaning of the rest? The high affinity generated by the system is somatic, and is not transmitted in reproduction. What is transmitted is the whole system which generates it. And it is certainly very complex. I don’t know if there is any simpler way to get to the same result. Probably not.

    DR means ‘differential reproduction’. Of the B cells. Trying to avoid begging the question of IS vs NS…

    Does that answer your questions?

    Yes, thank you. Despite the fact that you ducked questions 2 and 3 completely and re-wrote the first question I asked — “What is the minimum level of complexity for such a RM+DR system that would confer a selectable advantage?” — substituting the question you prefer, i.e. “is [there] any simpler way to get to the same result”, your response of “I don’t know…Probably not.” lets me know all I need to: you aren’t interested in actually thinking about the system, and how it might have arisen. Your choice.

    And I say, again, that I am not “using the word “intelligent”, when what I actually mean is “complicated””. Not at all. In this context, I am using the word “intelligent selection” in a very specific sense, as I will try to clarify in next post.

    I look forward to your clarification, since (as I noted in 24), you have given two different definitions, both of which carry curiously teleological baggage. You wouldn’t be trying to beg the question now, would you?

  40. 40
    DNA_Jock says:

    Me_Think:

    Here is a brief description of how Ebola virus works

    ROFLMAO.
    I had a much more benign example in mind…

  41. 41
    Joe says:

    Me Think:

    You can’t claim Ebola (It’s a virus, Joe) is designed by ID agent and escape from the conclusion that ID agent is thus responsible for deaths.

    LoL! YOU can’t because you don’t have any reasoning capability. I know ebola is a virus. I also know that it could have easily become deadly due to Darwinian processes acting on a non-deadly virus.

    Perhaps you also think that all deaths by car means the car designers caused the deaths.

  42. 42
    Dionisio says:

    Here are two of the posts that triggered the creation of this separate discussion thread:

    Posts #58 and 59 by sparc in kf’s thread:

    http://www.uncommondescent.com.....ent-546295

    The author of those two ‘challenging’ posts has not presented any strong arguments against gpuccio’s original comments. Not yet. We’re still waiting…

    Oh, well… what else is new?

    🙂

  43. 43
    Me_Think says:

    Joe @ 41

    Perhaps you also think that all deaths by car means the car designers caused the deaths.

    🙂 You think the ID agent designed Ebola virus to be benevolent and there was a mutiny by some agents who changed it to bad virus ?!

  44. 44
    Joe says:

    Me Think:

    You think the ID agent designed Ebola virus to be benevolent and there was a mutiny by some agents who changed it to bad virus ?!

    So you are admitting that you are willfully ignorant. Fine but your willful ignorance is not an argument.

    No agents are required to change it, Me Think. Grow up and learn how to read.

  45. 45
    Andre says:

    Me_Think

    The Virus is found in fruit bats, it properly has a function for them but is deadly for humans, now if people ate infected meat that was not properly prepared how is that a designer’s fault? The same applies to HIV, it spread because of inadequate preparation of food, and you blame the designer? LOL…..

    Just goes to show that whiners like you only want a personal genie that will poof into existence for your every whim, but won’t take the responsibility for anything you do……

  46. 46
    Joe says:

    Me Thinks wants all car designers to be held responsible for deaths relating to the cars they designed.

    What’s up with that?

  47. 47
    Dionisio says:

    #38 Me_Think

    Read my comment #33 again. I am sure you will find the relevance after a few reads.

    Your comment #33 does not seem to answer my questions in #32:

    Can you point to any set of papers explaining how the entire mechanisms gpuccio described in the OP got setup to work the way they do?

    One option is that the interwoven mechanisms could have been intelligently setup a priori.

    What is your strong argument against it?

    Is there a detailed explanation for the appearance of the amazingly complex choreographies orchestrated within the biological systems, which can handle even stochastic scenarios?

    Science researchers keep working hard to understand how the biological systems function and what they do, hence they don’t have time to squander on senseless OOL debates. That’s left to others.

    I’m personally more interested in the research papers that shed light on the functioning of the interwoven mechanisms seen in the biological systems. Not so interested in OOL debates. But if someone offers strong, comprehensive, logically coherent explanations about the origin of those interwoven mechanisms, I would enjoy reading them too.

    🙂

  48. 48
    gpuccio says:

    DNA_Jock:

    So, the second point:

    b) What do I mean by “intelligent selection”? I thought is was obvious, after having discussed the point and the definition practically for years, and probably with you too. But evidently I am not able to express my ideas clearly. So I will try again.

    First of all, please do not stick to the word “intelligent”. I use it here in a specific context, to define a type of selection which is different from natural selection (and, indeed, much more common).

    To be clear, I do not imply by the word neither of the following:

    1) That a conscious intelligence is active during the process of IS.

    2) That a conscious intelligence is the source of the process itself.

    Point 1 has already been clarified. Point 2 deserves some further reflection: it means, and I want that to be clear, that I do not imply that a process of intelligent selection is, by definition, designed. I certainly believe that all processes of IS that I know are designed, but as I said in my post #23, it is perfectly possible in principle (while not true in what we can observe) that a system which uses IS may originate from non design processes. I quote myself:

    “Obviously, all algorithms that I know of, based on IS, are designed. I don’t believe that “spontaneous”, non designed systems may work by intelligent selection as I have defined it.

    However, anyone who believes differently can show how that can happen.”

    So, it should be clear that when I say that a process uses intelligent selection, I am not logically implying that it is designed.

    Is that clear?

    So, what do I mean by “intelligent selection”?

    Let’s begin with “selection”. I am referring to a very specific context, which is the one we are usually discussing here: some process which acts on the results of RV, and determines a differential outcome of that result (let’s call it suppression or enhancement).

    So, here I am not using “selection” as a general synonim of “choice”, as you seem to imply in your post. I quote you:

    “A sniper selects from many windage adjustments based on the wind speed and direction observed. Even in Texas.
    And surely passive selection can be just as “intelligent” as active selection, e.g. I choose to not pull someone out of the way of an oncoming train?”

    That’s why “selection”, in the specific sense I give here, is binary: it is a process which can give one of two outcomes: suppression or enhancement (I am not considering here the simple fact that both suppression and enhancement can be of various degrees, or partially stochastic, ans so on, because that is not relevant for the discussion I am having here: the point is, the selection happens between the two categories: suppression or enhancement of the RV).

    So, what I am saying is that we have two different kinds of processes:

    1) Natural selection: in a system, reproducing beings compete for the system’s resources. RV generates better reproducers, which expand, suppressing (more or less) the previous population.

    2) Intelligent selection (or we could call it in different ways, if you object to “intelligent: specific, true, non natural, and so on): we have a system with reproducing beings. Those beings have properties which are not directly connected to reproduction. The system has complex configurations that can measure one of those properties. Controlled RV changes the degree of that property. The system measures the variation. The system can react with two different behaviours to the measure: one of them suppresses the reproduction of the reproducing beings, the other one enhances it. The system implements one or the other according to the binary result of the measure. Therefore, the reproduction of the reproducers is suppressed or enhanced according to the variation of the property, even if the property itself gives no reproductive advantage.

    In the second type of process, the connection between the property and the differential reproduction is guaranteed by a complex configuration of the system, which implements an algorithm with different steps and logical connections. IOWs, the whole process is vastly symbolic.

    That’s what I mean when I say that the system is active in Intelligent Selection.

    Let’s consider the RV part. In natural selection, it is just a random error in procedures optimized not to err. In Intelligent selection, it is controlled: it is an error which is “realized” by specific structures in the system, and is applied to specific regions. The scenario is completely different from the random error in a procedure, and obviously suggests an intentional error to generate diversification. So, even if the variation is random, it is at the same time controlled (for example, AID will not generate variation out of the variable region of the interested genes).

    I must stop here, for the moment.

  49. 49
    gpuccio says:

    Me_Think:

    The inference of design is about cognitive complexity, and has nothing to do with benevolence or malevolence. So, I infer design according to ID theory, and not according to benevolence issues.

    I will answer your other points as soon as I have time.

  50. 50
    Dionisio says:

    #42 follow-up

    Apparently two of his comrades attempted to help him but failed too.

    posts 48 and 49 put them to think. Maybe next time they’ll try better?

    Why is it so difficult for them to answer the easy questions in post #47?

    The game clock is ticking… the ball is in their court.

    🙂

  51. 51
    gpuccio says:

    Dionisio:

    To sum it up:

    sparc has not given any references about the evolution of AID. He probably thinks that it is my duty to explain it in darwinian terms.

    DNA_Jock states:

    “you aren’t interested in actually thinking about the system, and how it might have arisen. Your choice.”

    Yes, my choice. My choice is that I have been thinking a lot about the system, and how it might have arisen, and I have concluded, guided by ID theory, that it is designed. I am so interested that I have made a post about it, and I am trying to follow-up with the discussion however difficult it may be in these busy days (for me). I have decided that the two systems I have described exhibit tons of functional information, well beyond 500 bits, 1000 bits, and much more. No doubts about their designed origin.

    But DNA_Jock seems to believe that it is my duty to explain in darwinian terms what, IMO, can never be explained in darwinian terms. And that I am really culpable for not trying.

    What am I missing?

  52. 52
    gpuccio says:

    Me_Think:

    “What is that you want to achieve in this OP if you already believe the system is designed and you have rejected [evolution] and selection (@ 14) as a parameter ?”

    I want to show two examples of highly engineered systems in biological beings for which a design inference is practically beyond any doubt.

    “Have you – to exclude super natural ID explanation- exhausted research of chemical, structural and hydrodynamics of the system ?”

    Design is certainly not supernatural. And it uses chemical, structural and hydrodinamic properties to achieve a purpose. Moreover, I never reason in terms of natural and supernatural.

    “I am sure you have used the SwissModel or Chimera to generate protein (hapten can’t work without protein. It has to be attached) models and examined various energy parameters and possible binding site. May be you examined ramachandran plots too…. you know if you haven’t done any of those and have understood the dynamics, you can’t really claim everything is designed by intelligence, right?”

    Wrong. What you say makes no sense in this discussion. If you have an argument, make it as clearly as possible.

    “If I throw a ball, it will follow the path which has the least Kinetic – potential energy difference. ”

    Yes, and so?

    “It is pretty intelligent.”

    No. It obeys laws, which could be considered intelligent or not, but that would bring us to discuss fine tuning of the universe, which is not the purpose of this discussion.

    “Does it mean the ball calculates all the possible paths in the milliseconds after the ball is released into air and chooses the correct path which minimizes KE-PE ?”

    No. It means that it obeys the laws of mechanics. Has your discussion fallen so low?

    “The force on a point on that path can be calculated by the integral of the negative potential on a point on that path, does it mean the ball knows advanced maths?”

    No.

    “or can you conclude the ball has consciousness ?”

    No.

    “Isn’t your conclusions in the OP somewhat similar ?”

    No.

    And, in case you have not understood, I do think that viruses are designed.

    Any other easy and silly question?

  53. 53
    DNA_Jock says:

    Gpuccio,
    If, as you note,

    To be clear, I do not imply by the word neither of the following:
    1) That a conscious intelligence is active during the process of IS.
    2) That a conscious intelligence is the source of the process itself.

    Then let`s call it something other than “intelligent selection”. How about “gpuccio selection” (GPS)?
    The remainder of your post 48 does nothing to define GPS; rather you offer your characterization of the antibody affinity maturation process, as being complicated. The whole bit about “reproduction of the reproducing beings” seems completely superfluous to any definition of GPS.
    So far, you have offered two definitions of GPS, which (when stripped of their teleological baggage) are:

    [GPS] is a process where a property is measured by the system, and the system reacts to the measure.

    [GPS] is an algorithmic procedure based on measurement of a property, and selection of the result according to the outcome of the measurement.

    How are these for definitions of GPS?

    “you aren’t interested in actually thinking about the system, and how it might have arisen. Your choice.”
    [emphasis in original]

    Yes, my choice. My choice is that I have been thinking a lot about the system, and how it might have arisen, and I have concluded, guided by ID theory, that it is designed. I am so interested that I have made a post about it, and I am trying to follow-up with the discussion however difficult it may be in these busy days (for me). I have decided that the two systems I have described exhibit tons of functional information, well beyond 500 bits, 1000 bits, and much more. No doubts about their designed origin.
    But DNA_Jock seems to believe that it is my duty to explain in darwinian terms what, IMO, can never be explained in darwinian terms. And that I am really culpable for not trying.
    What am I missing?

    You are missing the fact that design theory 101 states that before you conclude design, you must first assess the relevant chance hypothesis. That is, you must make a good faith effort to try to explain the object in Darwinian terms. Based on your confusion over and re-phrasing of my questions at 17, it is clear that you have not made any such effort. So yes, you are really culpable for not trying.
    I couldn’t have put it better myself.

  54. 54
    gpuccio says:

    DNA_Jock:

    Disappointed has become an euphemism.

    Yes, I have given a definition of Intelligent Selection (as I will go on calling it). You have given nothing, except gratuitous denial like “teleological baggage”. To quote you, your choice.

    I have no intentions of trying to “explain the object in Darwinian terms”. My chance hypothesis is a chance hypothesis, not a myth. You, who go on observing the myth, do your part. If you want. Again, your choice.

    I understand that in your world your ideas are true until those who don’t believe in them succeed in proving them true. Again, your choice.

    I believed you had arguments, even wrong ones. Obviously, you don’t. Disappointment and boredom. And believe me, I am not happy saying it.

  55. 55
    gpuccio says:

    DNA_Jock:

    By the way, I forgot point 3:

    “P.S. your continued refusal to engage on the results of Szostak`s work and Liddle`s algorithm because the examples were designed continues to crack me up.”

    Sorry that you are cracked up. Very simply:

    a) I have never refused to engage on the results of those two “things”. I have clearly said what I think. One (Szostak’s) is a methodological cheat, the other (Elizabeth’s) a completely wrong reasoning.

    b) With different intentions and responsibilities, the error is more or less the same. And it is not, in any way, that the two things are “designed”. The error, as I have explained many times in detail, is that both use Intelligent Selection to derive concepts about Natural Selection.

    Ah, but I forgot: you don’t understand what Intelligent Selection is. So, I understand why you have no problems with those two things.

    But, at least, don’t insist in saying that I criticize them “because they were designed”. That is simply not true.

  56. 56
    DNA_Jock says:

    Sorry gpuccio, but your “IS” remains a rather slippery entity, whose definition changes expediently:

    At 48, you claim:

    To be clear, I do not imply by the word neither of the following:

    1) That a conscious intelligence is active during the process of IS.

    2) That a conscious intelligence is the source of the process itself.

    Yet on November 7th you summarized your complaint against Szostak and Liddle as follows:

    IS requires a conscious intelligent agent who recognizes some function as desirable, sets the context to develop it, can measure it at any desired level, and can intervene in the system to expand any result which shows any degree of the desired function. IOWs, both the definition of the function, the way to measure it, and the interventions to facilitate its emergence are carefully engineered. It’s design all the way.

    Oh. Dear.

    I stand by my previous statements.

  57. 57
    gpuccio says:

    DNA_Jock:

    I am very proud that you keep such good trace of my statements.

    However, sorry to disappoint you, but there is no conflict in my statements, only different contexts.

    Let’s try this way. IS is a process where the measurement of a specific function, and the response according to the binary outcome, are embedded in the procedure and bear no simple “natural” relationship to the measured property itself.

    To be more clear, the apoptosis or amplification of the B mutated cells according to the variation in affinity to the antigen is in no way a “natural” result of the variation itself. Cells with a higher affinity do not reproduce better. It is the system which recognizes the potential utility of that property and supports the cells bearing that property (in the form of specific T helper cells). IOWs, is is the configuration of the system, aimed at measuring and responding through specific engineered algorithms, which determines the connection between the property and the enhanced survival (or death).

    Not so in natural selection, where the variation itself confers a reproductive advantage to the cell in an environment which is not structured to measure it or respond to it.

    Another difference, as I have explained, is that the random variation is targeted in IS, and completely random in NS.

    Now, it is absolutely true that such a kind of IS is always the result of the design by a conscious intelligent agent, as I have stated. But, again, that is not by definition or by logical necessity: it’s simply that all the examples we know of are designed.

    That is an empirical observation, which is certainly the consequence of the true fact that non design systems are unable to generate such controlled and complex procedures, for the inherent limitations outlines by ID theory. Only consciousness can do those things.

    However, that conclusion is not a logical a priori necessity for me. It is the result of observation and good scientific reasoning.

    That’s why I state:

    “I do not imply by the word IS that a conscious intelligence is the source of the process itself”.

    It is perfectly true. I do not imply it in the definition of the word: I infer it from empirical observations of reality.

    I recommend that you read again what I say in my post #48, as a comment to the second point, a point that you have quoted accurately avoiding to quote the comment. However, here it is:

    Point 2 deserves some further reflection: it means, and I want that to be clear, that I do not imply that a process of intelligent selection is, by definition, designed. I certainly believe that all processes of IS that I know are designed, but as I said in my post #23, it is perfectly possible in principle (while not true in what we can observe) that a system which uses IS may originate from non design processes. I quote myself:

    Obviously, all algorithms that I know of, based on IS, are designed. I don’t believe that “spontaneous”, non designed systems may work by intelligent selection as I have defined it.

    However, anyone who believes differently can show how that can happen.

    Emphasis added.

    I hope that your quote mining and your bad tricks are done in good faith. I hope it for you.

    So, show how IS, as I have defined it, and as we see it at work in the immune system, can originate without design. If you want. But it is you who must show it. Not me.

  58. 58
    Dionisio says:

    gpuccio,

    You asked me what are you missing?

    As far as I can see, nothing.

    You’ve explained things clear enough for anyone to understand it, as long as the willingness to understand is there. However, trying to explain anything to someone who is not interested in understanding or having a serious discussion is a waste of time, if it were not for the onlookers/lurkers who could benefit from reading your explanation vs. your interlocutors’ senseless gibberish. Why is it so difficult for them to answer the easy questions in post #47?

    I lack your patience and pedagogical skills to explain difficult things in such easy terms as you do. I’m learning from reviewing your comments, and thinking about the information processing aspects of the biological mechanisms and systems we discuss.

    Thank you.

  59. 59
    Dionisio says:

    gpuccio

    In my post #1 within this thread, there’s a reference to a recent paper (last quarter of 2014), which provides much information about AID.

    In post #8 ba77 provided several interesting references related to the discussed subject.

    Posts #9-13 contain more references to papers related to the discussed subject.

    Post #15 links to another series of references to related papers posted in another thread.

    Most of those referenced papers shed light on the functioning of the discussed mechanisms.

    What references have your interlocutors provided in return, in order to support their claim that the interwoven mechanisms you have explained came up through Darwinian processes?

  60. 60
    Dionisio says:

    gpuccio,

    Is there a known biological predecessor of the mechanisms you described in the OP?
    Did it have more or less algorithmic steps, more or less components, simpler or more complex configuration?
    Is there a way to describe how to ‘evolve’ from the preceding setup to the current one?
    Then, what preceded the predecessor?
    And so on…
    I have not read anything on this. My main interest is in learning about the functioning of the existing interconnected mechanisms within the biological systems. The OOL debate is not high in my list of preferences. I’m not so concerned about how the systems originated. I’m more concerned about how they work and what they do in their current state.
    Thank you.

  61. 61
    Me_Think says:

    gpuccio @ 52

    Wrong. What you say makes no sense in this discussion. If you have an argument, make it as clearly as possible.

    Well, that sums up your attitude – you have no problem accepting that the ball obeys the laws of mechanics but refuse to examine the dynamics of the system which could have evolved from it’s primordial state as a result of the response to temporal changes over the years in hapten – immune response system. Since hapten depends on the protein for taxis and functioning, the modelling and visualizations tools that I mentioned in my post are very, very relevant in examining what you think is designed system.
    The default hypothesis is Nature did it, not ID agent did it. You need to eliminate all natural explanation before applying your CSI or it’s variants. The question is – have you done that ? The the answer is there for everyone to see – NO you haven’t.

  62. 62
    Dionisio says:

    Can anyone answer the easy questions in post #47?

  63. 63
    Me_Think says:

    Dionisio @ 62
    I haven’t come across any, as I haven’t been searching for whether biological system could have been designed by ID. Since you and GP have been at it, may be you could provide the answer – which might be available in ID journals or cutting edge ID labs.

  64. 64
    Dionisio says:

    #63 Me_Think

    Here are the questions in post #47:

    1. Can you point to any set of papers explaining how the entire mechanisms gpuccio described in the OP got setup to work the way they do?

    One option is that the interwoven mechanisms could have been intelligently setup a priori.
    2. What is your strong argument against it?

    3. Is there a detailed explanation for the appearance of the amazingly complex choreographies orchestrated within the biological systems, which can handle even stochastic scenarios?

    Here are the correct answers:

    1. No, there and not such papers, as far as I’m aware of.

    2. No strong argument.

    3. No, there is not.

    I don’t think ID folks are concerned about the ‘step-by-step’ details.
    I think they just state that it was intelligently designed.

  65. 65
    DNA_Jock says:

    Ha ha gpuccio. Really?
    In the context of defending your use of your term of art “intelligent selection”, against my criticism that

    you are using the word “intelligent”, when what you actually mean is “complicated”.

    you said:

    What do I mean by “intelligent selection”? I thought is was obvious, after having discussed the point and the definition practically for years, and probably with you too. But evidently I am not able to express my ideas clearly. So I will try again.

    First of all, please do not stick to the word “intelligent”. I use it here in a specific context, to define a type of selection which is different from natural selection (and, indeed, much more common).

    To be clear, I do not imply by the word neither of the following:

    1) That a conscious intelligence is active during the process of IS.

    2) That a conscious intelligence is the source of the process itself.

    But you have previously defined your term of art as requiring a conscious intelligent agent.
    So your use of the word DOES imply such an agent. You DO imply it in your (previous) definition of the word. It matters not one iota whether the definition is based on some universal empirical observation or not. The agent is implied by your use of the word, given your definition.
    Jeez, how lame can you get?

    So, show how IS, as I have defined it, and as we see it at work in the immune system, can originate without design. If you want. But it is you who must show it. Not me.

    Which definition are we using, the one that requires a conscious intelligent agent, or the one that doesn’t? And what’s with the stipulation “as we see it at work in the immune system”?
    If you are going to conclude “design”, then you have to try to come up with the Darwinian explanation. (All possible chance explanations, actually. Another problem for design theory. Oh dear.) Frankly, I don’t know jack about immunology, but it appears that you know less.
    If you would settle on one of the definitions of GPS that I provided, then maybe I could have a go, but the “as we see it at work in the immune system” is quite the escape hatch. You seem to lack confidence.

    You accuse me of quote-mining and “bad tricks”, but my crime appears to be that I failed to reference a particular part of a rambling post, that you are apparently quite proud of. No suggestion that I quoted you out of context. All I did was point out your inconsistencies.

  66. 66
    Dionisio says:

    Can anyone answer the questions in post #64 differently than the suggested correct answers?

  67. 67
    Dionisio says:

    #66 follow-up

    No, no one can answer those questions differently than the suggested correct answers.

  68. 68
    Dionisio says:

    #67 addendum

    That’s it. 🙂

  69. 69
    bornagain77 says:

    Dionisio, you may appreciate this:

    Optimized Design Models Explain Biological Systems by Jeffrey Tomkins, Ph.D. – Jan. 2015
    Excerpt: When this basic but complex engineering model is applied to biological systems, researchers have found tremendous efficiency—none of the resources are wasted. In a recent study, the cell’s systems were tested using the model bacterium Escherichia coli (E. coli). In the best-characterized cellular sensing system known to man, E. coli, the chemotaxis network was evaluated.1
    2014. Optimal resource allocation in cellular sensing systems. Proceedings of the National Academy of Sciences.,,,
    ,,,researchers compared the function of gene networks in E. coli to the man-made architecture of the Linux computer operating system.2 Expressed (turned on) genes in E. coli were considered analogous to called computer programs in the Linux operating system. The researchers found that both the biological and computer systems had the hallmark of design principles, with three different levels of regulatory hierarchy:
    1) master regulators
    2) middle managers
    3) bottom-level workhorse genes/programs
    However, the similarity ended there. The genome of E. coli was found to be much more streamlined, efficient, and condensed in its information processing! Conversely, the man-made computer system contained a much larger amount of called code producing a much smaller amount of end results. In fact, the Linux operating system was literally bloated with middle-level managers—much like many other inefficient man-made systems.,,,
    ,,,research using design-based principles of prediction, even with a seemingly “simple” bacterium, are proving that cellular systems and genomes are not only far better explained by optimized engineering, but their systems far exceed the capabilities of mankind’s own design genius.
    http://www.icr.org/article/opt.....biological

    Optimal resource allocation in cellular sensing systems – 2014
    Excerpt: Cells continually have to sense their environments to make decisions—to stay put or move, to differentiate or proliferate, or even to live or die. However, they are thwarted by noise at the cellular scale. Cells use signaling networks to filter this noise as much as possible and sense accurately. To operate these networks, resources are required: time, protein copies, and energy. We present a theory for the optimal design of cellular sensing systems that maximize sensing precision given these resources. It reveals a new design principle, namely that of optimal resource allocation. It describes how these resources must be allocated so that none are wasted. We show that the chemotaxis network of Escherichia coli obeys this principle.
    http://www.pnas.org/content/111/49/17486.abstract

    (Comparing Computer Operating Systems to Regulatory Networks in E-Coli) What Is The Genome? It’s Not Junk! – Dr. Robert Carter – video
    http://www.metacafe.com/watch/8905583/

    Comparing genomes to computer operating systems – Van – May 2010
    Excerpt: we present a comparison between the transcriptional regulatory network of a well-studied bacterium (Escherichia coli) and the call graph of a canonical OS (Linux) in terms of topology,,,
    http://www.ncbi.nlm.nih.gov/pubmed/20439753

  70. 70
    Dionisio says:

    BA77
    Yes, those are very interesting references. Thank you for sharing them.

  71. 71
    gpuccio says:

    DNA_Jock:

    I am afraid I am losing faith in your good faith. Sad.

    Intelligent selection is definable and recognizable for its formal characteristics as a process (which I have describe in detail many times here), and which make it completely different from natural selection.

    Natural selection can be explained in non design terms very easily, and therefore we all accept that it is a non design process. Intelligent selection, as far as I know, cannot be explained in non design terms, and is always the result of design (empirical observation which leads to inference).

    Using examples of Intelligent Selection to derive conclusions about Natural Selection is methodological error or cheat, because they are two different things, whatever their possible origin.

    It’s as simple as that.

    My point is that, out of any discourse about origin, the formal characteristics of natural selection and intelligent selection are completely different, and therefore the two processes can be easily distinguished objectively by anyone who is not on an agenda.

    And believe me, I am not interested in a personal competition with you, a person that I have appreciated and esteemed, about how much we know of immunology or how much confidence we have. I am grateful for your contributions, good and bad.

  72. 72
    gpuccio says:

    Me_Think:

    In no way I “refuse to examine the dynamics of the system which could have evolved”. You believe that those dynamics exist. So, you give me those dynamics, and I will happily examine them.

    This aspect of the discussion has become really funny. I just paste here what I wrote to DNA_Jock: I understand that in your world your ideas are true until those who don’t believe in them succeed in proving them true.

    Live happy in your win-win situation.

  73. 73
    DATCG says:

    lol BA77, was going to reference that link to Optimal Resource Allocation. Repeating here to breakout some of it in Bold for emphasis…

    We present a theory for the optimal design of cellular sensing systems that maximize sensing precision given these resources. It reveals a new design principle, namely that of optimal resource allocation. It describes how these resources must be allocated so that none are wasted. We show that the chemotaxis network of Escherichia coli obeys this principle.

    This is beautiful… They’re looking at this from a perspective as a Designed System. Therefore they question why specific functions behave and work as they do, either by limits or due to resources.

    Here, we consider the interplay among cellular resources, network design, and performance in a canonical biochemical function, namely sensing the environment.

    Living cells can measure chemical concentrations with extraordinary precision (1?–3), raising the question what sets the fundamental limit to the accuracy of chemical sensing (1). Cells measure chemical concentrations via receptors on their surface. These measurements are inevitably corrupted by noise that arises from the stochastic arrival of ligand molecules by diffusion and from the stochastic binding of the ligand to the receptor. Berg and Purcell pointed out that the sensing error is fundamentally bounded by this noise extrinsic to the cell, but that cells can reduce the error by taking multiple independent measurements (1). One way to increase the number of measurements is to add more receptors (1, 4). Another is to take more measurements per receptor over time; here, the cell infers the concentration not from the instantaneous number of ligand-bound receptors, but rather from the average receptor occupancy over an integration time T (1, 4??????–11).

    This time integration has to be performed by the signaling networks that transmit the information from the surface of the cell to its interior (10). Although the work of Berg and Purcell and subsequent studies identify time and the number of receptors as resources that limit the accuracy of sensing, the fundamental limits that have emerged ignore the cost of making and operating the signaling network. Making proteins is costly; producing proteins that confer no benefit to the cell can slow down bacterial growth (12). Moreover, many networks are driven out of thermodynamic equilibrium by the continuous turnover of fuel molecules such as ATP, leading to the dissipation of heat (13???–17). In fact, one can estimate that the fuel needed to operate a sensory network is comparable to that to make new components after cell division (SI Text).

    In this manuscript, we present a theory for the optimal design of sensing systems, which maximizes sensing precision given the available cellular resources.

    Design Heuristic offers insight for future…

    The design principle of Eq. 5 can also be used to construct optimal synthetic networks that minimize resource consumption.

    Finally, the process of sampling a time series, like the receptor state over time, defines a specific, familiar computation that could be conducted by any machine;

  74. 74
    DATCG says:

    Here is the web site for discovering Design Principles by
    Dr. Pieter Rein ten Wolde…

    Biochemical Networks and Cell Computer


    Biochemical Networks

    Group leader: Prof. dr. Pieter Rein ten Wolde

    Biochemical networks are the central processing units of life. They can perform a variety of computational tasks analogous to electronic circuits. Their design principles, however, are markedly different: in a biochemical network, computations are performed by molecules that chemically and physically interact with each other. The aim of the Biochemical Networks group and group leader Pieter Rein ten Wolde is to unravel their design principles using a combination of database analyses, theory and computer simulation.

    Cell Computer and Optimal Design

    Cells are able to measure these chemical concentrations with unprecedented precision thanks to receptor proteins on their surface, which bind to the surrounding molecules. A network of chemical reactions subsequently transmits the signal into the cell.

    These networks are the information processing machines of a living cell, comparable with a computer. Just like a computer, the cellular system needs time, energy and storage capacity to function. A large difference between a computer and a cellular measurement system is that cellular processes are very noisy, as a result of which it was not yet clear how cells can measure concentrations with such a high precision.

    The AMOLF researchers have now developed a theory that describes the accuracy of a concentration measurement based on the number of proteins present, the time and the energy that the cell invests in each measurement.

    Optimal design

    The researchers first looked at passive cellular detection systems, which consume no energy. In these systems the amount of receptor proteins, the proteins that bind the surrounding molecules, limits the number of measurements the cell can perform. The cell computer takes an average of this number to determine the overall molecule concentration.

    To obtain a more accurate estimate of the concentration, the cellular system must remember measurements from the past. However, this requires time, energy and other proteins to store the information. To the researchers’ surprise, these three resources determine the accuracy of the measurements like links in a chain. The precision is limited by the resource that is the least present.

    This observation led the researchers to a design principle not previously identified for this type of system: in an optimal measurement system all of the links are equally strong. The network that enables the bacterium E. coli to find food was found to obey this principle.

    The researchers expect that this design logic of cellular systems can also be used to develop efficient synthetic systems and materials.

  75. 75
    Me_Think says:

    gpuccio @ 72

    This aspect of the discussion has become really funny. I just paste here what I wrote to DNA_Jock: I understand that in your world your ideas are true until those who don’t believe in them succeed in proving them true.

    Well, your logic cracks me up too.
    In case you didn’t notice , you are the one who is claiming ID agent did it, which is not the scientific view. If you are saying your view is scientific and yet you claim ID agent is guiding the process, then you need to prove that natural dynamics of the system could not have done it. Instead you are blithely admitting you haven’t examined the dynamics of the system but somehow conclude it is designed , which – I remind you again- is not the scientific view. If you are arguing from a metaphysical viewpoint, your thinking may be right.

  76. 76
    gpuccio says:

    Me_Think:

    Very, very bad epistemology. That’s not how empirical science works.

    Have you ever heard of inference to the best explanation?

    But why waste time? We agree in being cracked up one from the other. That’s very fine.

  77. 77
    gpuccio says:

    BA and DATG:

    Thank you for the very good contributions! 🙂

  78. 78
    Me_Think says:

    gpuccio @ 76

    Have you ever heard of inference to the best explanation?

    Abductive reasoning is exactly what I am talking about! You need to eliminate all natural reasons before you come to the conclusion that the process is designed. What you have said so far proves you haven’t done that.

  79. 79
    Me_Think says:

    DATCG @ 73
    Pretty much every natural process and it’s interactions can be described in design terms, that doesn’t mean they are designed by ID agents with a handy Mac. Here is an example of ball I gave earlier:

    If I throw a ball, it will follow the path which has the least Kinetic – potential energy difference. It is pretty intelligent. Does it mean the ball calculates all the possible paths in the milliseconds after the ball is released into air and chooses the correct path which minimizes KE-PE ? The force on a point on that path can be calculated by the integral of the negative potential on a point on that path, does it mean the ball knows advanced maths? or can you conclude the ball has consciousness ?

  80. 80
    gpuccio says:

    Me_think:

    “You need to eliminate all natural reasons before you come to the conclusion that the process is designed.”

    No. And design is a natural explanation.

  81. 81
    DATCG says:

    Gpuccio,

    Thanks for the great post and Dionisio for that paper. Very interesting from a possible Design Inference and as a Design Heuristic.

    Checked out the link you gave as well. Here is one Infographic on B Cell memory…

    FIGURE 4 | Memory B cell evolution.

    Ready templates and pre-cursors “help” instruct movement to Germinative Center for processing reactions. Likely a pre-programmed function.

    a | Cues from pre-germinal centre (pre-GC) cognate T follicular helper (TFH) cells instruct antigen-primed B cells to initiate the GC reaction. It is likely that the commitment to antibody class is pre-programmed at this initial juncture and that all classes of B cells can seed the primary GC response.

    Control of Cell Cycle crucial for B cell dynamics. Regulatory functions of BCL-6 poorly understood still. AID and UNG requirement prior to programmed – Directed hypermutation, enhancing B Cells for specific foreign antigens. “Error Prone DNA Polymerase”(or badly named Highly Functional Design?) introduces mutations in to variable regions – necessary hotspots.

    b | Molecular control of the cell cycle is an integral component of dark-zone B cell dynamics and involves the expression of B cell lymphoma 6 (BCL-6), although the ways in which BCL-6 contributes to this regulation remain poorly resolved. The expression and activity of activation-induced cytidine deaminase (AID) and uracil DNA glycosylase (UNG) are required to initiate somatic hypermutation (SHM)(programmed process), which is targeted to single-stranded DNA. Following uracil excision, the DNA is processed by error-prone(badly named) DNA polymerases to introduce point mutations into the variable regions(hot spots) of the rearranged antibody genes. Class-switch recombination (CSR) can also occur during this dark-zone phase using AID to target DNA cleavage to antibody switch regions; the DNA double strand breaks that are generated trigger the DNA damage machinery, which completes the CSR event. The associations between cell cycle control, SHM and CSR are not clearly resolved in vivo.

    Not enough time to cover all steps in the figure, but think readers get the gist of a highly programmable Immune Response System with modular components and systems architecture, complete with preprogrammed sub-routines and more network features.

    Continuous monitoring – scanning…

    c | To scan folicullar dendritic cells (DCs) for antigens, GC B cells continuously move along follicular DC processes that are laden with mature immune complexes. These interactions are more similar to stromal cell-associated trafficking behavior than to stable immune synapse-like interactions. The affinity of the B cell receptor (BCR) for antigens may influence antigen uptake and peptide–MHC class II presentation at this juncture of development. Programmes of gene expression for molecules that are able to modify cognate contact may also be differentially induced as a result of BCR signal strength during follicular DC scanning.

    More interactive programming events…

    D | B cells then make contact for a longer duration with cognate GC TFH cells in the light zone, and this can be visualized directly in vivo. As in earlier, pre-GC events, these contacts must focus around T cell receptor (TCR)–peptide–MHC class II interactions and can be modified by a multitude of intercellular exchanges of molecular information. There is still little detailed analysis of these interactions in vivo. We depict the classes of molecules that can be associated with this crucial programming event, but the organization of these interactions and their precise developmental imprint are not yet clear.

    Re-Entry and Refine process

    E | Antigen presentation by B cells can influence re-entry into the dark zone and the re-initiation of BCR diversification (which involves cell proliferation, SHM and CSR).

    Germinal Cell Exit, Long Lived memory plasma cell compartments, Highest programmed Affinities, or apoptosis.

    F | GC cognate contact can also initiate B cell exit from the GC into the distinct non-secreting memory B cell and post-GC long-lived memory plasma cell compartments. BLIMP1, B lymphocyte-induced maturation protein 1; CR2, complement receptor 2; CXCR5, CXC-chemokine receptor 5; IFN?, interferon-?; IL, interleukin; PD1, programmed cell death protein 1; TH, T helper.

    Essentially, a controlled recognition and defense release system. That does not need to know all the specifics of foreign objects, but captures specific information of the newly recognized foreign objects, utilizing pre-programmed subroutines, dynamically updating programs with specific antigen information, with database, repository for retrieval purposes of highly targeted response by finely tuned identifiers.

    Have a good one 🙂

  82. 82
    Me_Think says:

    gpuccio @ 80

    No. And design is a natural explanation.

    No design by ID is not AT ALL a natural explanation.

  83. 83
    DATCG says:

    Me_Think,

    I use to believe in Darwinian/neo-Darwinian explanations. No longer do. I see a long series of failures now.

    And I disagree with your a priori assumption posted above, that “Nature Did It” by default. Times change. While I was taught what you claim, we might be moving back to a Design Paradigm, a best explanation as Design Inference.

    Maybe you can show how random mutations and natural selection over time create a modular, programmable system with novel creativity for Memory B Cell. I think it will be a problem doing so.

    Scientist today are breaking away from neo-Darwinian explanations for such systems – see The Third Way. They’re pushing neo-Darwinian explanations aside as being just one part of evolution, not the entire answer. Many see the limitations and failures of Neo-Darwinism. Don’t know if you agree with them or not.

    To me, it seems random mutations would be deleterious and cause loss of function in this highly coordinated system. Not help create novel functions. A few wrong mutations selected in highly conserved regions might limit or impair the process. Or worse, cause disease and/or catastrophic failure.

    I agree with Gpuccio. It is upon you to give Darwinian or neo-Darwinian processes as a solution. Or “The Third Way.” Whatever the proposed solution is now. It appears to be in disarray.

    Currently, experiments done by Richard Lenski after over 60,000 mutations and 25 years show very little. The improbability of random mutations and natural selection as strong selection process for new novel functions – machinery like we see in this network process – is not convincing to me.

    My opinion is – thinking of molecular functions as Design processes, modularity, programs, systems – are a better heuristic for research purposes of discovery and teaching as a learning concept.

    You guys have a good one, off for now.

  84. 84
    bornagain77 says:

    DATCG at 74, as to ‘Cell Computer’, you may find it interesting that cells also accomplish ‘quantum computation’ that far exceeds anything man has yet accomplished in regards to quantum computation:

    Quantum Information/Entanglement In DNA – short video
    https://vimeo.com/92405752

    Here is a paper that proved that protein folding belongs to the physics of the quantum world and that protein folding does not belong to the physics of the classical world:

    Physicists Discover Quantum Law of Protein Folding – February 22, 2011
    Quantum mechanics finally explains why protein folding depends on temperature in such a strange way.
    Excerpt: Their astonishing result is that this quantum transition model fits the folding curves of 15 different proteins and even explains the difference in folding and unfolding rates of the same proteins.
    That’s a significant breakthrough. Luo and Lo’s equations amount to the first universal laws of protein folding. That’s the equivalent in biology to something like the thermodynamic laws in physics.
    http://www.technologyreview.co.....f-protein/

    Moreover, We now have evidence of quantum computation being performed in DNA and protein molecules.

    Quantum Dots Spotlight DNA-Repair Proteins in Motion – March 2010
    Excerpt: “How this system works is an important unanswered question in this field,” he said. “It has to be able to identify very small mistakes in a 3-dimensional morass of gene strands. It’s akin to spotting potholes on every street all over the country and getting them fixed before the next rush hour.” Dr. Bennett Van Houten – of note: A bacterium has about 40 team members on its pothole crew. That allows its entire genome to be scanned for errors in 20 minutes, the typical doubling time.,, These smart machines can apparently also interact with other damage control teams if they cannot fix the problem on the spot.
    http://www.sciencedaily.com/re.....123522.htm

    Of note: DNA repair machines ‘Fixing every pothole in America before the next rush hour’ is analogous to the traveling salesman problem. The traveling salesman problem is a NP-hard (read: very hard) problem in computer science; The problem involves finding the shortest possible route between cities, visiting each city only once. ‘Traveling salesman problems’ are notorious for keeping supercomputers busy for days.

    NP-hard problem – Examples
    Excerpt: Another example of an NP-hard problem is the optimization problem of finding the least-cost cyclic route through all nodes of a weighted graph. This is commonly known as the traveling salesman problem.
    – per wikipedia

    Yet it is exactly this type of ‘traveling salesman problem’ that quantum computers excel at:

    Speed Test of Quantum Versus Conventional Computing: Quantum Computer Wins – May 8, 2013
    Excerpt: quantum computing is, “in some cases, really, really fast.”
    McGeoch says the calculations the D-Wave excels at involve a specific combinatorial optimization problem, comparable in difficulty to the more famous “travelling salesperson” problem that’s been a foundation of theoretical computing for decades.,,,
    “This type of computer is not intended for surfing the internet, but it does solve this narrow but important type of problem really, really fast,” McGeoch says. “There are degrees of what it can do. If you want it to solve the exact problem it’s built to solve, at the problem sizes I tested, it’s thousands of times faster than anything I’m aware of. If you want it to solve more general problems of that size, I would say it competes — it does as well as some of the best things I’ve looked at. At this point it’s merely above average but shows a promising scaling trajectory.”
    http://www.sciencedaily.com/re.....122828.htm

    Since it is obvious that there is not a material CPU (central processing unit) in the DNA, or cell, busily computing answers to this monster logistic problem, in a purely ‘material’ fashion, by crunching bits, then it is readily apparent that this monster ‘traveling salesman problem’, for DNA repair, is somehow being computed by ‘non-local’ quantum computation within the cell and/or within DNA.
    As well, We also have evidence of quantum computation solving the ‘travelling salesman problem’ within protein folding: It is known that proteins do not find their final folded form by random processes:

    The Humpty-Dumpty Effect: A Revolutionary Paper with Far-Reaching Implications – Paul Nelson – October 23, 2012
    Excerpt: Anyone who has studied the protein folding problem will have met the famous Levinthal paradox, formulated in 1969 by the molecular biologist Cyrus Levinthal. Put simply, the Levinthal paradox states that when one calculates the number of possible topological (rotational) configurations for the amino acids in even a small (say, 100 residue) unfolded protein, random search could never find the final folded conformation of that same protein during the lifetime of the physical universe. Therefore, concluded Levinthal, given that proteins obviously do fold, they are doing so, not by random search, but by following favored pathways. The challenge of the protein folding problem is to learn what those pathways are.
    http://www.evolutionnews.org/2.....65521.html

    Confronting Science’s Logical Limits – John L. Casti – 1996
    Excerpt: It has been estimated that a supercomputer applying plausible rules for protein folding would need 10^127 years to find the final folded form for even a very short sequence consisting of just 100 amino acids. (The universe is 13.7 x 10^9 years old). In fact, in 1993 Aviezri S. Fraenkel of the University of Pennsylvania showed that the mathematical formulation of the protein-folding problem is computationally “hard” in the same way that the traveling-salesman problem is hard.
    http://www.cs.virginia.edu/~ro.....Limits.pdf

    That no one really has a firm clue how proteins are finding their final folded form is made clear by the immense time (a few weeks) it takes for a few hundred thousand computers, which are linked together, to find the final folded form of a single protein:

    A Few Hundred Thousand Computers vs. (The Folding Of) A Single Protein Molecule – video
    https://www.youtube.com/watch?v=lHqi3ih0GrI

    The reason why finding the final form of a folded protein is so hard for supercomputers is that it is, as with DNA, like the ‘traveling salesman’ puzzle, which are ‘Just about the meanest problems you can set a computer (on) ‘.

    DNA computer helps traveling salesman – Philip Ball – 2000
    Excerpt: Just about the meanest problems you can set a computer belong to the class called ‘NP-complete’. The number of possible answers to these conundrums, and so the time required to find the correct solution, increases exponentially as the problem is scaled up in size. A famous example is the ‘travelling salesman’ puzzle, which involves finding the shortest route connecting all of a certain number of cities.,,,
    Solving the traveling-salesman problem is a little like finding the most stable folded shape of a protein’s chain-like molecular structure — in which the number of ‘cities’ can run to hundreds or even thousands.
    http://www.nature.com/news/200.....13-10.html

    And protein folding is found to be ‘NP-complete’

    Combinatorial Algorithms for Protein Folding in Lattice
    Models: A Survey of Mathematical Results – 2009
    Excerpt: Protein Folding: Computational Complexity
    4.1
    NP-completeness: from 10^300 to 2 Amino Acid Types
    4.2
    NP-completeness: Protein Folding in Ad-Hoc Models
    4.3
    NP-completeness: Protein Folding in the HP-Model
    http://www.cs.brown.edu/~sorin.....survey.pdf

    Thus we have very good evidence that proteins must be finding their final folded form by some method of quantum computation. ,,,, If so, as it seems exceedingly likely to be so, then this far exceeds anything man has yet accomplished in regards to quantum computation although billions of dollars have been spent trying to build better quantum computers!

  85. 85
    Me_Think says:

    DATCG @ 83

    I use to believe in Darwinian/neo-Darwinian explanations. No longer do. I see a long series of failures now.

    ID is just a list of complaints against Darwinism.
    I have tried understanding ID but I find no answers to:
    1) What is the mechanism by which ID agent manages billions of processes in trillions of organism? How does the agent get inside the organism right up to cell level and manages to fix/direct/ create new metabolism, pathways, mutation, protein foldings ?

    2) What is ID agent – is it a being, an energy or a field ?

    I assume it is a ‘being’ so I don’t know how it could penetrate up to cell level in trillions of organisms to manage billions of processes.
    If it is field, we should have detected it unless it is like dark matter, but in that case it can’t interact with matter/cells.
    If you assume it is energy, again we could have detected it unless it is dark energy, which of course can’t interact with matter freely.
    Frankly I don’t understand why ID would appeal to you.
    What’s more, no one on ID side seems to be bothered by these questions at all. They pretend it is irrelevant so you will never get an answer for those questions which could be a start of ID theory.

  86. 86
    DNA_Jock says:

    Gpuccio:

    Intelligent selection is definable and recognizable for its formal characteristics as a process (which I have describe in detail many times here), and which make it completely different from natural selection.

    And yet you seem curiously reticent about providing a single, operational definition. Strange, that.

    Using examples of Intelligent Selection to derive conclusions about Natural Selection is methodological error or cheat, because they are two different things, whatever their possible origin.

    It’s as simple as that.

    No. For any example, you need to explain why a designed experiment is a poor model of the natural process. Your criticisms of Keefe & Szostak fail, as we have discussed previously.

    Dionisio summed up the ID approach thus:

    I don’t think ID folks are concerned about the ‘step-by-step’ details.
    I think they just state that it was intelligently designed.

    Yup. That’s about the size of it.

  87. 87
    Dionisio says:

    gpuccio,

    Perhaps your interlocutors could benefit from thinking seriously about the following quote:

    “I don’t know” is more likely to be the reply of an expert.
    -Chandler Fulton [http://www.bio.brandeis.edu/faculty/fulton.html]

    🙂

    They seem to have difficulties admitting that the ‘official’ doctrine in biological sciences can’t describe in a comprehensive and logically coherent manner the origin of most biological systems. Humility does not seem very common in their party.

    I appreciate the effort you have made to explain in a clear manner some important principles that apply to the processes described in your OP for this thread.

    Too bad that some folks don’t want to understand what you wrote.

  88. 88
    bornagain77 says:

    as to: “ID is just a list of complaints against Darwinism.”

    Aside from the ‘complaint’ that unguided material processes, (i.e. Darwinian processes), have never been observed to generate non-trivial levels of the jaw dropping levels of integrated functional information/complexity we are finding in the cell, ID, unlike Darwinism, as ‘inference to the best explanation’, makes positive predictions and testable claims for biological science:

    A Positive, Testable Case for Intelligent Design – Casey Luskin – March 2011 – several examples of cited research
    http://www.evolutionnews.org/2.....45311.html

    In fact ID, unlike Darwinism, provides a fruitful heuristic in biological science:

    “Certainly, my own research with antibiotics during World War II received no guidance from insights provided by Darwinian evolution. Nor did Alexander Fleming’s discovery of bacterial inhibition by penicillin. I recently asked more than 70 eminent researchers if they would have done their work differently if they had thought Darwin’s theory was wrong. The responses were all the same: No.,,, In the peer-reviewed literature, the word “evolution” often occurs as a sort of coda to academic papers in experimental biology. Is the term integral or superfluous to the substance of these papers? To find out, I substituted for “evolution” some other word – “Buddhism,” “Aztec cosmology,” or even “creationism.” I found that the substitution never touched the paper’s core. This did not surprise me. From my conversations with leading researchers it had became clear that modern experimental biology gains its strength from the availability of new instruments and methodologies, not from an immersion in historical biology.,,,
    Darwinian evolution – whatever its other virtues – does not provide a fruitful heuristic in experimental biology. This becomes especially clear when we compare it with a heuristic framework such as the atomic model, which opens up structural chemistry and leads to advances in the synthesis of a multitude of new molecules of practical benefit.”
    Philip S. Skell – (the late) Emeritus Evan Pugh Professor at Pennsylvania State University, and a member of the National Academy of Sciences.
    http://www.discovery.org/a/2816

    “It has become clear in the past ten years that the concept of design is not merely an add-on meta-description of biological systems, of no scientific consequence, but is in fact a driver of science. A whole cohort of young scientists is being trained to “think like engineers” when looking at biological systems, using terms explicitly related to engineering design concepts: design, purpose, optimal tradeoffs for multiple goals, information, control, decision making, etc. This approach is widely seen as a successful, predictive, quantitative theory of biology.”
    David Snoke*, Systems Biology as a Research Program for Intelligent Design

    podcast: “David Snoke: Systems Biology and Intelligent Design, pt. 1”
    http://intelligentdesign.podom.....9_09-07_00
    podcast: David Snoke: Systems Biology and Intelligent Design, pt. 2
    http://intelligentdesign.podom.....0_01-07_00

    How the Burgeoning Field of Systems Biology Supports Intelligent Design – July 2014
    Excerpt: Snoke lists various features in biology that have been found to function like goal-directed, top-down engineered systems:
    *”Negative feedback for stable operation.”
    *”Frequency filtering” for extracting a signal from a noisy system.
    *Control and signaling to induce a response.
    *”Information storage” where information is stored for later use. In fact, Snoke observes:
    “This paradigm [of systems biology] is advancing the view that biology is essentially an information science with information operating on multiple hierarchical levels and in complex networks [13]. ”
    *”Timing and synchronization,” where organisms maintain clocks to ensure that different processes and events happen in the right order.
    *”Addressing,” where signaling molecules are tagged with an address to help them arrive at their intended target.
    *”Hierarchies of function,” where organisms maintain clocks to ensure that cellular processes and events happen at the right times and in the right order.
    *”Redundancy,” as organisms contain backup systems or “fail-safes” if primary essential systems fail.
    *”Adaptation,” where organisms are pre-engineered to be able to undergo small-scale adaptations to their environments. As Snoke explains, “These systems use randomization controlled by supersystems, just as the immune system uses randomization in a very controlled way,” and “Only part of the system is allowed to vary randomly, while the rest is highly conserved.”,,,
    Snoke observes that systems biology assumes that biological features are optimized, meaning, in part, that “just about everything in the cell does indeed have a role, i.e., that there is very little ‘junk.'” He explains, “Some systems biologists go further than just assuming that every little thing has a purpose. Some argue that each item is fulfilling its purpose as well as is physically possible,” and quotes additional authorities who assume that biological systems are optimized.,,,
    http://www.evolutionnews.org/2.....87871.html

    Systems Biology as a Research Program for Intelligent Design – David Snoke – 2014
    http://bio-complexity.org/ojs/.....O-C.2014.3

    In fact, ID is falsifiable, whereas neo-Darwinism has no rigid falsification criteria:

    “In so far as a scientific statement speaks about reality, it must be falsifiable; and in so far as it is not falsifiable, it does not speak about reality.”
    Karl Popper – The Two Fundamental Problems of the Theory of Knowledge (2014 edition), Routledge
    http://izquotes.com/quote/147518

    It’s (Much) Easier to Falsify Intelligent Design than Darwinian Evolution – Michael Behe, PhD
    https://www.youtube.com/watch?v=_T1v_VLueGk

    The Law of Physicodynamic Incompleteness – David L. Abel
    Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”
    If only one exception to this null hypothesis were published, the hypothesis would be falsified. Falsification would require an experiment devoid of behind-the-scenes steering. Any artificial selection hidden in the experimental design would disqualify the experimental falsification. After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided.
    The time has come to extend this null hypothesis into a formal scientific prediction:
    “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.”
    https://www.academia.edu/9957206/The_Law_of_Physicodynamic_Incompleteness_Scirus_Topic_Page_

  89. 89
    gpuccio says:

    DNA_Jock:

    My criticisms of Keefe & Szostak remains perfectly valid.

    Szostak’s experiment is a poor model of the natural process because it has the formal properties of IS, not of NS: selection of a property by measurement, and controlled variation + amplification in cycles of and re-selection based on new measurements.

    It could be a good model of what happens in affinity maturation, but not of NS. The measured property has no relationship with fitness and survival, and therefore could never be managed by NS. On the other hand, it can be chosen, measured and amplified by the IS algorithm designed by the authors, like in all cases of protein engineering.

    So, again, and for clarity, it is a bad paper not because the experiment is designed (all experiments are designed), but because it is badly designed: it does not model what it tries to model.

    But again, I have no intention to convince you, least of all to go on with a discussion which seems to have lost any constructive aspect. If you agree, we could leave it at that.

  90. 90
    gpuccio says:

    Me_Think:

    1) What is the mechanism by which ID agent manages billions of processes in trillions of organism? How does the agent get inside the organism right up to cell level and manages to fix/direct/ create new metabolism, pathways, mutation, protein foldings ?”

    Why trillions? It is reasonable that the process of design happens in a limited number of organisms, for example when a new species is engineered. Would you say that the designer of a printer has to “get inside” millions of printers only because millions of that printer are sold after it has been designed?

    The consciousness of the designer “gets inside” at the cellular level in exactly the same way as our personal consciousness gets inside the cells in our brain, and operates changes in them. A very natural interface, probably at quantum level.

    2) What is ID agent – is it a being, an energy or a field ?

    A conscious being, certainly. Like us. Consciousness is the pre-requisite of design (indeed, design is defined as a process where conscious representations are outputted to matter). But the designer’s consciousness can certainly operate through fields and energy.

    If it is field, we should have detected it unless it is like dark matter, but in that case it can’t interact with matter/cells.
    If you assume it is energy, again we could have detected it unless it is dark energy, which of course can’t interact with matter freely.

    You seem so sure that our understanding of physics is complete, even in issues, like dark matter and dark energy, where by definition (see the word “dark”) it is really lacking.

    Dark energy was not even a concept, until a few years ago. Now it is a concept, indeed a question, for which we have really no satisfying answers.

    You seem so sure that our paradigms of physics will not undergo drastic shifts in the next few (or many) years. So were the scientists of the end of the ninteenth century, just before quantum mechanics and relativity.

    I am sure of the opposite.

  91. 91
    bornagain77 says:

    gpuccio, I think Casey Luskin had your post in mind when he loaded this podcast:

    podcast – “The Intelligent Design of the Immune System”
    http://intelligentdesign.podom.....1_04-08_00
    On this episode of ID the Future, Dr. Donald L. Ewert continues to explain why the vertebrate adaptive immune system does not use “random” or “chance” processes like Darwinian evolution to generate antibody diversity. Instead, he argues that the immune system is intelligently designed. Listen in as Dr. Ewert shares one of the most interesting stories in science, the generation of antibody diversity.

  92. 92
    EugeneS says:

    GP,

    I can only marvel at your patience. It is amazing how people may be unwilling to see the obvious. This is not to mean the subject matter of the post but the outcomes and conclusions. Nothing comes out of nothing, and absurdity raised to the n-th power is still absurdity as niwrad aptly points out ). Some people don’t want to be friends with common sense sometimes…

  93. 93
    Me_Think says:

    gpuccio @ 90

    Why trillions? It is reasonable that the process of design happens in a limited number of organisms, for example when a new species is engineered.

    Because there are billions of processes which need intervention from time to time. A primordial template is not enough. Just the proteins foldings (which are impossible according to ID ) per minute in trillions of cells will number billion. I am being very conservative.

    The consciousness of the designer “gets inside” at the cellular level in exactly the same way as our personal consciousness gets inside the cells in our brain, and operates changes in them. A very natural interface, probably at quantum level.

    Consciousness does not change structure and processes. fMRIs don’t show glial cells permanently changing, nor do MEG show permanent cortical neuron change in response to feeling/ thinking talking and actions, and certainly consciousness has no influence on metabolisms, mutation and protein folding. In any case conscious is not an external entity. It is emergent (I know you don’t agree, but that’s ok).

    But the designer’s consciousness can certainly operate through fields and energy

    Then it has to be a new type of energy which not only encompasses entire universe (like magnetic field/ gravity) but can zoom into trillions of organisms at microscopic level (unlike anything).

    You seem so sure that our understanding of physics is complete, even in issues, like dark matter and dark energy, where by definition (see the word “dark”) it is really lacking.

    We already know what dark matter properties should be (a lot of things in cosmology is already ‘known’ before it’s discovery) – it is a Weakly interacting massive particle, that’s the reason we are not able to detect it at the energy levels available to us. Weakly interacting particles, obviously, can’t interact easily with matter.Again we do know dark energy density is too low ( order of 10^-27 kg per cubic meter) to be of use as matter interacting energy.

    So were the scientists of the end of the ninteenth century, just before quantum mechanics and relativity

    We have our Standard model and beyond that we have SUSY. What do you see in those which could be candidate for ID ? No scientists, past or present, ever said anything other than a field, energy or matter will emerge. Those are the basics.

  94. 94
    Dionisio says:

    As far as I understand it, the ID proponents simply state, based on empirical evidence and logical reasoning, that the origin of many things we observe in nature can only be attributed to an intelligent design cause.

    They don’t seem to care much, at least at this point, about the detailed ‘step-by-step’ process of intelligent design, or about the nature of the designer(s), or the timing of such design, etc.

    I might be wrong on this. Perhaps I have misunderstood their postulates. But that’s how I see it.

    gpuccio is in my opinion one of the most eloquent ID proponents in this blog, specially in the discussions associated with biology. Unfortunately some of his interlocutors don’t seem interested in having mutually enriching discussions. But I have benefitted from reading many of his insightful posts here.

  95. 95
    Me_Think says:

    EugeneS @ 92

    Nothing comes out of nothing, and absurdity raised to the n-th power is still absurdity as niwrad aptly points out )

    Universe comes out of Nothing. Thinking a word raised to nth power will compute to anything else is absurd 🙂

  96. 96
    bornagain77 says:

    “Universe comes out of Nothing.”

    Check and mate!

  97. 97
    Me_Think says:

    bornagain77 @ 96
    ???? Edit: I thought you weren’t a Krauss fan. Good that you seem to agree Quantum fluctuation and not the ID agent created universe 🙂

  98. 98
    Joe says:

    Me Think:

    1) What is the mechanism by which ID agent manages billions of processes in trillions of organism? How does the agent get inside the organism right up to cell level and manages to fix/direct/ create new metabolism, pathways, mutation, protein foldings ?

    2) What is ID agent – is it a being, an energy or a field ?

    Neither of those are part of ID. Thank you for continuing to expose your ignorance.

    Science has demonstrated that in the absence of designer input or direct observation the only possible way to make any scientific determination into the specific process used or the designers’ identity, is by studying the design and all relevant evidence. That is how it works in archaeology and forensics. And it is very telling the Me Think is ignorant of how science operates.

  99. 99
    Joe says:

    Me Think:

    I assume it is a ‘being’ so I don’t know how it could penetrate up to cell level in trillions of organisms to manage billions of processes.

    Strawman. Do programmers and computer designers reside inside of computers directing all of the processes?

    ID appeals to us because blind and undirected processes are not up to the task and yet we exist. Human curiosity wants to know how our existence came to be.

  100. 100
    bornagain77 says:

    as to “Good that you seem to agree Quantum fluctuation and not the ID agent created universe”

    Actually, thinking quantum fluctuations are uncaused is absurd. There is no such thing as a uncaused effect. i.e. every effect must have a cause! Moreover, since ‘quantum fluctuations’ are necessary to explain the universe’s initial inhomogeneity, then obviously one cannot also use the same ‘quantum fluctuations’ to explain why the universe had its initial extremely homogenous state in the first place.

    Overall structure of the universe seeded by Heisenberg’s Uncertainty Principle:

    Cosmology: Late news from the Big Bang – Feb. 5, 2015
    Excerpt: The Planck Consortium has now published new analyses of data returned by the eponymous space telescope. The telescope on board of the Planck satellite has measured the distribution of the cosmic microwave background radiation (CMB), which, in essence, tells us what the Universe looked like about 400,000 years after the Big Bang. These latest findings are in complete agreement with the predictions of Mukhanov’s theory – for example, his calculation of the value of the so-called spectral index of the initial inhomogeneities. As Jean-Loup Puget, Principal Investigator for the HFI-instrument on the Planck satellite, stated: “The Planck data confirm the basic predictions that quantum fluctuations are at the origin of all structures in the Universe.” Mukhanov, who first published his model in 1981 and joined the Physics Faculty at LMU in 1997, says “I couldn’t hope for a better verification of my theory.”
    Messages from the remote past
    For Mukhanov, the idea that quantum fluctuations must have played a role in the very earliest phase of the history of the Universe is implicit in Heisenberg’s Uncertainty Principle. Heisenberg showed that there is a specific limit to the precision with which the position and the momentum of a particle can be determined at any given moment. This in turn implies that the initial matter distribution will inevitably exhibit minute inhomogeneities in density. Mukhanov’s calculations first demonstrated that such quantum fluctuations could give rise to density differences in the early Universe, which in turn could serve as seeds for the galaxies and their clusters. Indeed, without quantum fluctuations, whose nature and magnitude Mukhanov quantitatively characterized, the observed distribution of matter in the Universe would be inexplicable.
    http://phys.org/news/2015-02-c.....s-big.html

    Of related note:

    Quantum physics just got less complicated – Dec. 19, 2014
    Excerpt: Patrick Coles, Jedrzej Kaniewski, and Stephanie Wehner,,, found that ‘wave-particle duality’ is simply the quantum ‘uncertainty principle’ in disguise, reducing two mysteries to one.,,,
    “The connection between uncertainty and wave-particle duality comes out very naturally when you consider them as questions about what information you can gain about a system. Our result highlights the power of thinking about physics from the perspective of information,”,,,
    http://phys.org/news/2014-12-q.....cated.html

    John 1:1
    In the beginning was the Word, and the Word was with God, and the Word was God.

    As to the question of whether the cause of the universe is personal or whether it is impersonal, the best cause for any effect in the universe, and for the universe itself, is, and always has been, a personal agent:

    A Professor’s Journey out of Nihilism: Why I am not an Atheist – University of Wyoming – J. Budziszewski
    Excerpt page12: “There were two great holes in the argument about the irrelevance of God. The first is that in order to attack free will, I supposed that I understood cause and effect; I supposed causation to be less mysterious than volition.
    If anything, it is the other way around. I can perceive a logical connection between premises and valid conclusions. I can perceive at least a rational connection between my willing to do something and my doing it. But between the apple and the earth, I can perceive no connection at all. Why does the apple fall? We don’t know. “But there is gravity,” you say. No, “gravity” is merely the name of the phenomenon, not its explanation. “But there are laws of gravity,” you say. No, the “laws” are not its explanation either; they are merely a more precise description of the thing to be explained, which remains as mysterious as before. For just this reason, philosophers of science are shy of the term “laws”; they prefer “lawlike regularities.” To call the equations of gravity “laws” and speak of the apple as “obeying” them is to speak as though, like the traffic laws, the “laws” of gravity are addressed to rational agents capable of conforming their wills to the command. This is cheating, because it makes mechanical causality (the more opaque of the two phenomena) seem like volition (the less). In my own way of thinking the cheating was even graver, because I attacked the less opaque in the name of the more.
    The other hole in my reasoning was cruder. If my imprisonment in a blind causality made my reasoning so unreliable that I couldn’t trust my beliefs, then by the same token I shouldn’t have trusted my beliefs about imprisonment in a blind causality. But in that case I had no business denying free will in the first place.”
    http://www.facebook.com/l.php?.....=iAQHzw14O

    “to say that a stone falls to earth because it’s obeying a law, makes it a man and even a citizen”
    – CS Lewis

    “In the whole history of the universe the laws of nature have never produced, (i.e. caused), a single event.”
    C.S. Lewis – doodle video
    https://www.youtube.com/watch?v=_20yiBQAIlk

    If you disagree that agency is the best explanation as to being the cause for the universe, and for every effect in the universe, then I invite you to take up Talbott’s challenge and explain biological systems without using terms that invoke agency: Stephen Talbott points out that it is impossible to describe the complexities of biological life without illegitimately using words that invoke agent causality:

    The ‘Mental Cell’: Let’s Loosen Up Biological Thinking! – Stephen L. Talbott – September 9, 2014
    Excerpt: Many biologists are content to dismiss the problem with hand-waving: “When we wield the language of agency, we are speaking metaphorically, and we could just as well, if less conveniently, abandon the metaphors”.
    Yet no scientist or philosopher has shown how this shift of language could be effected. And the fact of the matter is just obvious: the biologist who is not investigating how the organism achieves something in a well-directed way is not yet doing biology, as opposed to physics or chemistry. Is this in turn just hand-waving? Let the reader inclined to think so take up a challenge: pose a single topic for biological research, doing so in language that avoids all implication of agency, cognition, and purposiveness1.
    One reason this cannot be done is clear enough: molecular biology — the discipline that was finally going to reduce life unreservedly to mindless mechanism — is now posing its own severe challenges. In this era of Big Data, the message from every side concerns previously unimagined complexity, incessant cross-talk and intertwining pathways, wildly unexpected genomic performances, dynamic conformational changes involving proteins and their cooperative or antagonistic binding partners, pervasive multifunctionality, intricately directed behavior somehow arising from the interaction of countless players in interpenetrating networks, and opposite effects by the same molecules in slightly different contexts. The picture at the molecular level begins to look as lively and organic — and thoughtful — as life itself.
    http://natureinstitute.org/txt.....ell_23.htm

    This working biologist agrees completely with Talbott:

    Life, Purpose, Mind: Where the Machine Metaphor Fails – Ann Gauger – June 2011
    Excerpt: I’m a working biologist, on bacterial regulation (transcription and translation and protein stability) through signalling molecules, ,,, I can confirm the following points as realities: we lack adequate conceptual categories for what we are seeing in the biological world; with many additional genomes sequenced annually, we have much more data than we know what to do with (and making sense of it has become the current challenge); cells are staggeringly chock full of sophisticated technologies, which are exquisitely integrated; life is not dominated by a single technology, but rather a composite of many; and yet life is more than the sum of its parts; in our work, we biologists use words that imply intentionality, functionality, strategy, and design in biology–we simply cannot avoid them.
    Furthermore, I suggest that to maintain that all of biology is solely a product of selection and genetic decay and time requires a metaphysical conviction that isn’t troubled by the evidence. Alternatively, it could be the view of someone who is unfamiliar with the evidence, for one reason or another. But for those who will consider the evidence that is so obvious throughout biology, I suggest it’s high time we moved on. – Matthew
    http://www.evolutionnews.org/2.....nt-8858161

  101. 101
    Joe says:

    If I throw a ball, it will follow the path which has the least Kinetic – potential energy difference.

    I bet it will follow the path in which the thrower threw it. If I throw a baseball into a wind it will not turn itself around and go downwind, ie the path of the least Kinetic – potential energy difference.

  102. 102
    Me_Think says:

    Joe @ 98,99

    Me_Think @ 85: What’s more, no one on ID side seems to be bothered by these questions at all. They pretend it is irrelevant so you will never get an answer for those questions which could be a start of ID theory.

  103. 103
    Joe says:

    Me Think- You are wrong and I have explained why. Your willful ignorance still means nothing here.

    The start of ID was producing methodologies to determine intelligent design from nature, operating freely. We have that. Your position still doesn’t have any methodology, unless bald declaration is a methodology.

    ID is about the detection and study of intelligently designed objects. structures and events in nature. Your questions cannot be answered until we first determine intelligent design and then study it along with all relevant evidence.

    Why are you proud to be scientifically ignorant?

  104. 104
    Joe says:

    AGAIN:

    Science has demonstrated that in the absence of designer input or direct observation the only possible way to make any scientific determination into the specific process used or the designers’ identity, is by studying the design and all relevant evidence. That is how it works in archaeology and forensics.

    Reality is too much for Me Think to grasp…

  105. 105
    Me_Think says:

    Joe @ 104
    That’s very very old argument , Joe. It is called the explanatory filter argument and has been discussed threadbare at panda’s thumb. You may want to head over there. My question is how does ID agent influence and change process inside the cell and what is ID agent ? I know it is studiously ignored by IDers.

  106. 106
    Joe says:

    LoL! Me Think your ignorance of science is amusing. Why should anyone care what a willfully ignorant troll has to say?

    Why would ID do anything different than what is being done in successful design-centric venues?

    My question is how does ID agent influence and change process inside the cell and what is ID agent ?

    How do programmers influence and change process inside a computer?

    I know it is studiously ignored by IDers.

    It doesn’t have anything to do with ID and your ignorance, while amusing, still means nothing.

  107. 107
    Joe says:

    Me Think- If the posters at the panda’s thumb could support their position ID would fade away. That they can’t and instead must attack ID with their ignorance tells us all we need to know- that our opponents are ignorant cowards.

  108. 108
    Me_Think says:

    Joe @ 106

    How do programmers influence and change process inside a computer?

    You consider software as hardware ?. Programmers can’t change the hardware inside physically using C++ (that’s a programming language). Cell, protein folding mutations, pathways are hardware changes, Joe.

  109. 109
    Joe says:

    Me Think:

    You consider software as hardware ?

    How did you get from what I posted? Software can change hardware paths due to different gates being activated, by software.

    Programmers can’t change the hardware inside physically using C++ (that’s a programming language).

    Programmers can change the hardware inside of a field programmable gate array or any PAL. And programmers can have the computers’ output change what it is doing.

    Cell, protein folding mutations, pathways are hardware changes, Joe.

    Guided by software.

  110. 110
    Me_Think says:

    =>Cell, protein folding mutations, pathways are hardware changes, Joe.

    =>Guided by software

    BioC++ version 1.2 running on Mac Edit: which control nano contraptions in cell to guide the protein foldings, mutations, Metabolic pathways.. etc? and presumably it is run by ID agent from his plush office? He has a central server to control all the process in trillions of cells? and cells are connected to the network by wifi ?

  111. 111
    bornagain77 says:

    Check and mate!

    Searching for Bobby Fischer (10/10) Movie CLIP – Josh Offers a Draw (1993) HD
    https://www.youtube.com/watch?v=k9pFp6iRVM0

  112. 112
    Dionisio says:

    BA77

    I assume your post 111 relates to your post 96?

    🙂

  113. 113
    bornagain77 says:

    Yes, but it could just as well apply to any argument the atheist/materialist makes. i.e. It never ends well for the atheist. 🙂

  114. 114
    Me_Think says:

    Dionisio @ 112

    to BA77 I assume your post 111 relates to your post 96?

    Of course. what BA77 doesn’t know is Poe could have drawn by playing 7.h5 !!! It always ends well for us. We aren’t dumb like Poe

  115. 115
    gpuccio says:

    EugeneS

    Thank you for the kind words. 🙂

  116. 116
    gpuccio says:

    Dionisio:

    You are certainly a friend, and I appreciate your initiative and enthusiasm and work. This OP, in particular, is as much your work as mine. 🙂

  117. 117
    Dionisio says:

    BA77

    Yes, as in the vid clip you posted. 🙂

    Didn’t accept the draw offer, but later was forced to bite the bullet and admit defeat.

    We could witness a similar situation here soon. 🙂

  118. 118
    bornagain77 says:

    MT Nice, so the lesson is, Never let Darwinists do science and never let Hollywood directors select chess sequences since both types live in a dream world and are not concerned with reality 🙂

    “An alternate endgame position had been composed by Pal Benko. It was supposed to have been used in the film, but was rejected on the day before the scene was filmed because it did not use the theme that Josh overused his queen.”
    http://en.m.wikipedia.org/wiki.....by_Fischer

    Pal Benko (Hungarian: Benk? Pál; born July 14, 1928) is a chess grandmaster, author, and composer of endgame studies and chess problems.
    http://en.m.wikipedia.org/wiki/Pal_Benko

  119. 119
    gpuccio says:

    Me_Think at #93:

    When you contribute arguments, I really appreciate it.

    So:

    Because there are billions of processes which need intervention from time to time. A primordial template is not enough. Just the proteins foldings (which are impossible according to ID ) per minute in trillions of cells will number billion. I am being very conservative.

    First of all, why do you say that “proteins foldings are impossible according to ID?”.

    Protein foldings follow biochemical laws, exactly like the thrown ball. It is true that many foldings require special help (see chaperones), but that is another story.

    What is difficult (but not “impossible”, it only requires great computational resources) is to predict the folding from the primary structure.

    I don’t agree that there are billions of processes “which need intervention from time to time”, but I am not there counting. The design of biological beings, and of the existing genome and proteome and so on is certainly a huge task, but I see no reason to believe that it is in the range of design and designers (probably better then we are).

    Foldings just happen, once the correct structures have been designed (including chaperones).

    Consciousness does not change structure and processes. fMRIs don’t show glial cells permanently changing, nor do MEG show permanent cortical neuron change in response to feeling/ thinking talking and actions, and certainly consciousness has no influence on metabolisms, mutation and protein folding. In any case conscious is not an external entity. It is emergent (I know you don’t agree, but that’s ok).

    I don’t agree on anything, anything, in this paragraph. And yes, that’s OK. 🙂

    Then it has to be a new type of energy which not only encompasses entire universe (like magnetic field/ gravity) but can zoom into trillions of organisms at microscopic level (unlike anything).

    Maybe. What about gravity before the first theory of gravitation?

    We already know what dark matter properties should be (a lot of things in cosmology is already ‘known’ before it’s discovery) – it is a Weakly interacting massive particle, that’s the reason we are not able to detect it at the energy levels available to us. Weakly interacting particles, obviously, can’t interact easily with matter.Again we do know dark energy density is too low ( order of 10^-27 kg per cubic meter) to be of use as matter interacting energy.

    I agree about dark matter. I think that at present we have no reasonable idea about dark energy, so I would be more cautious if I were you (but I am not).

    But my point was, and is: there are many things that we literally don’t know, that we have probably never observed, or that we have observed and not understood. What was dark energy before the observations that brought it to our interest? Nothing, not even a question.

    Very simply said: reductionism is a very bad human habit. Always has been, always will be.

    We have our Standard model and beyond that we have SUSY. What do you see in those which could be candidate for ID ? No scientists, past or present, ever said anything other than a field, energy or matter will emerge. Those are the basics.

    Thank you for kindly providing a very good example of absolute reductionism. It’s a pleasure to cooperate with you! 🙂

  120. 120
    Dionisio says:

    #114 Me_Think

    Your comparison makes no sense.

    At least the two kids played seriously.

    You and your comrades don’t seem to care much about having any serious discussion. You seem to be more interested in mocking and ridiculing.

    That’s alright. We’re on the winning side of the story anyway. Time will tell. Just wait and see.

    We ain’t seen nothing yet. More research papers are coming in the days, weeks, months ahead. The big picture is getting clearer: amazingly elaborate cellular and molecular choreographic orchestrations within the biological systems, that can only be the product of intelligent design.

    Laugh now, while you still can. Who knows how long before you and your comrades will be forced to admit you were wrong. By then it might be too late. Think about it.

    Today you still have time to run away from your mistaken presuppositions and join the winning side of history. It’s not too late yet. Consider this seriously.

    🙂

  121. 121
    bornagain77 says:

    gpuccio you state:

    “Protein foldings follow biochemical laws, exactly like the thrown ball.”

    Actually, as touched on briefly in post 84, protein folding is now shown to belong the world of quantum physics, not to the world of classical physics (i.e. not like a ‘thrown ball’):

    Physicists Discover Quantum Law of Protein Folding – February 22, 2011
    Excerpt: First, a little background on protein folding. Proteins are long chains of amino acids that become biologically active only when they fold into specific, highly complex shapes. The puzzle is how proteins do this so quickly when they have so many possible configurations to choose from.
    To put this in perspective, a relatively small protein of only 100 amino acids can take some 10^100 different configurations. If it tried these shapes at the rate of 100 billion a second, it would take longer than the age of the universe to find the correct one. Just how these molecules do the job in nanoseconds, nobody knows.,,,
    Their astonishing result is that this quantum transition model fits the folding curves of 15 different proteins and even explains the difference in folding and unfolding rates of the same proteins.
    That’s a significant breakthrough. Luo and Lo’s equations amount to the first universal laws of protein folding. That’s the equivalent in biology to something like the thermodynamic laws in physics.
    http://www.technologyreview.co.....f-protein/

  122. 122
    Joe says:

    Me Think- The software controls the 1s and 0s, which are physical signals designed to produce specific results. Those 1s and 0s would be akin to proteins and all other cellular communications.

  123. 123
    gpuccio says:

    BA:

    OK, no problem, let’s say that folding follows laws, whatever they are. 🙂

  124. 124
    bornagain77 says:

    gpuccio, actually, as briefly touched on in post 84, there is a bit more to this ‘quantum protein folding’ that makes it much more interesting to the whole ID vs. Darwinism controversy than to just say that protein folding ‘follow laws whatever they are’ and leave it at that.
    In order for proteins to find their final folded form, and DNA to accomplish repair as quickly as it does, by the method of quantum computation, it is first necessary for quantum entanglement/information to be present in proteins and DNA so as to be able to be used as a ‘quantum information channel’ in order to perform the quantum computation:

    Quantum Entanglement and Information – substantive revision Sat Feb 7, 2015
    Excerpt: Quantum entanglement is a physical resource, like energy, associated with the peculiar nonclassical correlations that are possible between separated quantum systems. Entanglement can be measured, transformed, and purified. A pair of quantum systems in an entangled state can be used as a quantum information channel to perform computational and cryptographic tasks that are impossible for classical systems.
    http://plato.stanford.edu/entries/qt-entangle/

    and when we look at the literature we find evidence for quantum entanglement in both DNA and proteins

    Coherent intrachain energy migration in a conjugated polymer at room temperature. – 2009
    ABSTRACT The intermediate coupling regime for electronic energy transfer is of particular interest because excitation moves in space, as in a classical hopping mechanism, but quantum phase information is conserved. We conducted an ultrafast polarization experiment specifically designed to observe quantum coherent dynamics in this regime. Conjugated polymer samples with different chain conformations were examined as model multichromophoric systems. The data, recorded at room temperature, reveal coherent intrachain, (intra – within, on the inside), electronic energy transfer. Our results suggest that quantum transport effects occur at room temperature when chemical donor-acceptor bonds help to correlate dephasing perturbations.
    http://www.researchgate.net/pu.....emperature

    Quantum entanglement in hot systems – 2011
    Excerpt: The authors remark that this reverses the previous orthodoxy, which held that quantum effects could not exist in biological systems because of the amount of noise in these systems.,,, Environmental noise here drives a persistent and cyclic generation of new entanglement.,,, In summary, the authors say that they have demonstrated that entanglement can recur even in a hot noisy environment. In biological systems this can be related to changes in the conformation of macromolecules.
    http://quantum-mind.co.uk/quan.....t-systems/

    etc..etc..

    DNA Can Discern Between Two Quantum States, Research Shows – June 2011
    Excerpt: — DNA — can discern between quantum states known as spin. – The researchers fabricated self-assembling, single layers of DNA attached to a gold substrate. They then exposed the DNA to mixed groups of electrons with both directions of spin. Indeed, the team’s results surpassed expectations: The biological molecules reacted strongly with the electrons carrying one of those spins, and hardly at all with the others. The longer the molecule, the more efficient it was at choosing electrons with the desired spin, while single strands and damaged bits of DNA did not exhibit this property.
    http://www.sciencedaily.com/re.....104014.htm

    Quantum Information/Entanglement In DNA – short video
    https://vimeo.com/92405752

    What is a insurmountable problem for Darwinists is that ‘non-local’ quantum entanglement conclusively demonstrated that ‘information’ in its pure ‘quantum form’ is completely transcendent of any time and space constraints (Bell, Aspect, Leggett, Zeilinger, etc..). That this beyond space and time ‘information’ should be found in molecular biology on such a massive scale, in every DNA and protein molecule, is a direct empirical falsification of Darwinian claims.
    It is not possible for the ‘non-local’ quantum entanglement ‘effect’ in biology to be explained by a material (matter/energy) cause since the quantum entanglement effect falsified material particles as its own causation in the first place! (Aspect, Zeilinger), Appealing to the probability of various ‘random’ configurations of material particles, as Darwinism does, simply will not help since a timeless/spaceless cause must be supplied which is beyond the capacity of the material particles themselves to supply!

    Looking beyond space and time to cope with quantum theory – 29 October 2012
    Excerpt: “Our result gives weight to the idea that quantum correlations somehow arise from outside spacetime, in the sense that no story in space and time can describe them,”
    http://www.quantumlah.org/high.....uences.php

    Closing the last Bell-test loophole for photons – Jun 11, 2013
    Excerpt:– requiring no assumptions or correction of count rates – that confirmed quantum entanglement to nearly 70 standard deviations.,,,
    http://phys.org/news/2013-06-b.....otons.html

    etc.. etc..

    In other words, to give a coherent explanation for an effect that is shown to be completely independent of any time and space constraints one is forced to appeal to a cause that is itself not limited to time and space! i.e. Put more simply, you cannot explain a effect by a cause that has been falsified by the very same effect you are seeking to explain! Improbability arguments of various ‘special’ configurations of material particles, which have been a staple of the arguments against neo-Darwinism, simply do not apply since the cause is not within the material particles in the first place!

    And although Naturalists have proposed various, far fetched, naturalistic scenarios to try to get around the Theistic implications of quantum non-locality, none of the ‘far fetched’ naturalistic solutions, in themselves, are compatible with the reductive materialism that undergirds neo-Darwinian thought.

    “[while a number of philosophical ideas] may be logically consistent with present quantum mechanics, …materialism is not.”
    Eugene Wigner
    Quantum Physics Debunks Materialism – video playlist
    https://www.youtube.com/watch?list=PL1mr9ZTZb3TViAqtowpvZy5PZpn-MoSK_&v=4C5pq7W5yRM

    Why Quantum Theory Does Not Support Materialism By Bruce L Gordon, Ph.D
    Excerpt: The underlying problem is this: there are correlations in nature that require a causal explanation but for which no physical explanation is in principle possible. Furthermore, the nonlocalizability of field quanta entails that these entities, whatever they are, fail the criterion of material individuality. So, paradoxically and ironically, the most fundamental constituents and relations of the material world cannot, in principle, be understood in terms of material substances. Since there must be some explanation for these things, the correct explanation will have to be one which is non-physical – and this is plainly incompatible with any and all varieties of materialism.
    http://www.4truth.net/fourtrut.....8589952939

    Thus, as far as empirical science itself is concerned, Neo-Darwinism is falsified!

  125. 125
    bornagain77 says:

    gpuccio, since you touched on consciousness and the brain earlier, you may appreciate this paper I found recently:

    ,,, zero time lag neuronal synchrony despite long conduction delays – 2008
    Excerpt: Multielectrode recordings have revealed zero time lag synchronization among remote cerebral cortical areas. However, the axonal conduction delays among such distant regions can amount to several tens of milliseconds. It is still unclear which mechanism is giving rise to isochronous discharge of widely distributed neurons, despite such latencies,,,
    Remarkably, synchrony of neuronal activity is not limited to short-range interactions within a cortical patch. Interareal synchronization across cortical regions including interhemispheric areas has been observed in several tasks (7, 9, 11–14).,,,
    Beyond its functional relevance, the zero time lag synchrony among such distant neuronal ensembles must be established by mechanisms that are able to compensate for the delays involved in the neuronal communication.
    Latencies in conducting nerve impulses down axonal processes can amount to delays of several tens of milliseconds between the generation of a spike in a presynaptic cell and the elicitation of a postsynaptic potential (16). The question is how, despite such temporal delays, the reciprocal interactions between two brain regions can lead to the associated neural populations to fire in unison (i.e. zero time lag).,,,
    http://www.ncbi.nlm.nih.gov/pm.....MC2575223/

    The following paper appeals to a ‘non-local’, (i.e. beyond space and time), cause to try to explain the synchronization in neural circuits,,,

    Nonlocal mechanism for cluster synchronization in neural circuits – 2011
    Excerpt: The findings,,, call for reexamining sources of correlated activity in cortex,,,
    http://arxiv.org/abs/1103.3634

    of supplemental interest to proteins in general, the entire protein is involved in ‘ringing’ when struck by light::

    Proteins ‘ring like bells’ – June 2014
    As far back as 1948, Erwin Schrödinger—the inventor of modern quantum mechanics—published the book “What is life?”
    In it, he suggested that quantum mechanics and coherent ringing might be at the basis of all biochemical reactions. At the time, this idea never found wide acceptance because it was generally assumed that vibrations in protein molecules would be too rapidly damped.
    Now, scientists at the University of Glasgow have proven he was on the right track after all.
    Using modern laser spectroscopy, the scientists have been able to measure the vibrational spectrum of the enzyme lysozyme, a protein that fights off bacteria. They discovered that this enzyme rings like a bell with a frequency of a few terahertz or a million-million hertz. Most remarkably, the ringing involves the entire protein, meaning the ringing motion could be responsible for the transfer of energy across proteins.
    The experiments show that the ringing motion lasts for only a picosecond or one millionth of a millionth of a second. Biochemical reactions take place on a picosecond timescale and the scientists believe that evolution has optimised enzymes to ring for just the right amount of time. Any shorter, and biochemical reactions would become inefficient as energy is drained from the system too quickly. Any longer and the enzyme would simple oscillate forever: react, unreact, react, unreact, etc. The picosecond ringing time is just perfect for the most efficient reaction.
    These tiny motions enable proteins to morph quickly so they can readily bind with other molecules, a process that is necessary for life to perform critical biological functions like absorbing oxygen and repairing cells.
    The findings have been published in Nature Communications.
    Klaas Wynne, Chair in Chemical Physics at the University of Glasgow said: “This research shows us that proteins have mechanical properties that are highly unexpected and geared towards maximising efficiency. Future work will show whether these mechanical properties can be used to understand the function of complex living systems.”
    http://www.gla.ac.uk/news/headline_334344_en.html

  126. 126
    Dionisio says:

    BA77

    Interesting references. Thank you.

    More on the brain and neuroscience in this thread:

    http://www.uncommondescent.com.....ent-547013

  127. 127
    gpuccio says:

    BA:

    I am extremely interested in quantum effects in biology, as you, know, and I am convinced that they are very important in the consciousness/brain interface (which, IMO, is essentially similar to the consciousness/biological matter interface in biological design).

    Quantum effects are probably crucial also in many other biological processes, including protein folding and, as you argue, the possible transfer of information in biological molecules.

    So, thank you for all your contributions, which I have downloaded and am reading carefully.

    I think, however, that the point remains that protein folding, as far as we know, is governed by laws. Those laws may not be only classical, they may include quantum effects and they can also include quantum information effects. I agree with you on that.

    I don’t think, at the present state of our understanding, that protein folding implies a consciousness/matter quantum interaction just to happen. I think that proteins and their environments are a complex designed system which implements protein folding as it is necessary, through all the laws and the information transfers which are necessary for that to happen.

    Even if many other factors must be considered, there is certainly a very strong connection between protein sequence and protein folding. Therefore, the design of the correct sequence is certainly a major component to ensure correct folding.

  128. 128
    bornagain77 says:

    gpuccio, the most important point to consider in all this is not the question of whether protein folding is governed primarily by the sequential arrangement of amino acids in proteins or by the quantum information/entanglement in proteins, but the most important point to consider in all this is that finding quantum information/entanglement in proteins, (and DNA), directly falsifies the neo-Darwinian contention that information is merely ’emergent’ from a material basis.
    Remember, Quantum Information/Entanglement is shown to be its own a physical resource separate from the whims of matter-energy.

    Quantum Entanglement and Information
    Quantum entanglement is a physical resource, like energy, associated with the peculiar nonclassical correlations that are possible between separated quantum systems. Entanglement can be measured, transformed, and purified. A pair of quantum systems in an entangled state can be used as a quantum information channel to perform computational and cryptographic tasks that are impossible for classical systems. The general study of the information-processing capabilities of quantum systems is the subject of quantum information theory.
    http://plato.stanford.edu/entries/qt-entangle/

    Moreover, this falsification of the reductive materialistic claim of neo-Darwinism, (i.e. the claim that information is merely ’emergent’ from a material basis), is achieved by direct empirical evidence. The falsification of neo-Darwinian claims does not rely on probabilistic calculations of the rarity of functional sequences in sequence space in order to achieve its falsification of neo-Darwinian claims.
    In fact, completely contrary to the neo-Darwinian view that information is merely ’emergent’ from a material basis, physicists have now, by using the ‘quantum information channel’ of entanglement for quantum teleportation, reduced material to quantum information!
    (of note: energy is completely reduced to quantum information, whereas matter is semi-completely reduced, with the caveat being that matter can be reduced to energy via e=mc2).

    How Teleportation Will Work –
    Excerpt: In 1993, the idea of teleportation moved out of the realm of science fiction and into the world of theoretical possibility. It was then that physicist Charles Bennett and a team of researchers at IBM confirmed that quantum teleportation was possible, but only if the original object being teleported was destroyed. — As predicted, the original photon no longer existed once the replica was made.
    http://science.howstuffworks.c.....ation1.htm

    Quantum Teleportation – IBM Research Page
    Excerpt: “it would destroy the original (photon) in the process,,”
    http://researcher.ibm.com/view_project.php?id=2862
    etc.. etc..

    Thus not only is information not ’emergent’ from a energy-matter basis, as is presupposed in neo-Darwinism, but in actuality both energy and matter are ultimately reducible to a information basis as is presupposed in Christian Theism (John1:1-4).

    John 1:1-4
    In the beginning was the Word, and the Word was with God, and the Word was God. He was in the beginning with God. All things were made through Him, and without Him nothing was made that was made. In Him was life, and the life was the light of men.

    As to the question of whether sequential ‘digital’ information or quantum information is primary, classical ‘digital’ information is found to be a subset of ‘non-local’ (i.e. beyond space and time) quantum entanglement/information by the following method:

    Quantum knowledge cools computers: New understanding of entropy – June 2011
    Excerpt: No heat, even a cooling effect;
    In the case of perfect classical knowledge of a computer memory (zero entropy), deletion of the data requires in theory no energy at all. The researchers prove that “more than complete knowledge” from quantum entanglement with the memory (negative entropy) leads to deletion of the data being accompanied by removal of heat from the computer and its release as usable energy. This is the physical meaning of negative entropy. Renner emphasizes, however, “This doesn’t mean that we can develop a perpetual motion machine.” The data can only be deleted once, so there is no possibility to continue to generate energy. The process also destroys the entanglement, and it would take an input of energy to reset the system to its starting state. The equations are consistent with what’s known as the second law of thermodynamics: the idea that the entropy of the universe can never decrease. Vedral says “We’re working on the edge of the second law. If you go any further, you will break it.”
    http://www.sciencedaily.com/re.....134300.htm

    Thus, although I’m certainly not contesting that sequential ‘functional’ information in biology is important, sequential information is found to be a subset of quantum information/entanglement. Moreover, sequential information is also found to be less robust in its falsification of neo-Darwinian claims than quantum information is as far as empirical science itself is concerned.

  129. 129
    Dionisio says:

    BA77
    RE: the IBM Research document you referred to:

    Quantum Teleportation – IBM Research Page
    Excerpt: “it would destroy the original (photon) in the process,,”
    http://researcher.ibm.com/view_project.php?id=2862
    etc.. etc..

    In the third sentence of the second paragraph note this:

    (perhaps unltimately leading to a “quantum internet”),

    Did they mean ‘ultimately’ ?

    Perhaps before embarking on that thrilling adventure to teleportation, they might want to assign part of their budget to improving their proofreading abilities?

    🙂

  130. 130
    Dionisio says:

    BA77

    Does this relate to your post #128 too?

    http://www.uncommondescent.com.....ent-546761

  131. 131
    Dionisio says:

    Even if many other factors must be considered, there is certainly a very strong connection between protein sequence and protein folding. Therefore, the design of the correct sequence is certainly a major component to ensure correct folding. GP @ 127

    Yes, that’s a good point. The mechanisms to guarantee such sequence consistently must be setup a priori. How is that explained in the official doctrine in biology?

  132. 132
    bornagain77 says:

    Thanks for your link at 126 Dionisio:

    Mechanisms of Zero-Lag Synchronization in Cortical Motifs – April 24, 2014
    Abstract Excerpt: Zero-lag synchronization between distant cortical areas has been observed in a diversity of experimental data sets and between many different regions of the brain. Several computational mechanisms have been proposed to account for such isochronous synchronization in the presence of long conduction delays: Of these, the phenomenon of “dynamical relaying” – a mechanism that relies on a specific network motif – has proven to be the most robust with respect to parameter mismatch and system noise. Surprisingly, despite a contrary belief in the community, the common driving motif is an unreliable means of establishing zero-lag synchrony.,,,
    We call this manner of facilitating zero-lag synchrony resonance-induced synchronization, outline the conditions for its occurrence, and propose that it may be a general mechanism to promote zero-lag synchrony in the brain.
    Discussion Excerpt:,,,It seems reasonable to propose that resonance-induced synchronization will prove important for other neuronal systems, such as dendritic oscillations in single-neuron dynamics [51], and indeed other physical and biological systems of any domain characterized by weak interactions.
    http://journals.plos.org/plosc.....bi.1003548

    Not to gripe too much Dionisio, but doesn’t that seem just a bit redundant? i.e. Different areas of the brain are synchronized with zero delay because they are in zero delay resonance?
    Not that I’m qualified in the least to judge their level of work, but it seems to me that they have basically used the effect of zero delay resonance to try to explain the effect of zero delay synchronization.

    What am I missing?

    As far as I can tell, other than establishing the material conditions that are necessary for zero lag synchronization to occur in the brain, they have not really explained how the zero lag synchronization in the brain is possible.

  133. 133
    Dionisio says:

    BA77

    I agree. That seems a little redundant, to put it nicely.

    I don’t think you’re missing anything. Rather it seems like they’re missing a more open-minded ‘out of the box’ approach to research.

    You and I know they’re going to experience more ‘surprises’ as they dig deeper into the biological systems and neuroscience, trying to understand how the amazingly complex interwoven mechanisms function as a whole. No time to think about OOL issues. 🙂

    BTW, see my post #130. Thank you.

    Also, note that starting at this post there are several references to recent neuroscience papers:
    http://www.uncommondescent.com.....ent-547006

    Definitely we ain’t seen nothing yet. 🙂

  134. 134
    gpuccio says:

    To all:

    Just to awaken a little bit the discussion, as sparc’s references about AID evolution are still lacking, I have made some quick research on my own.

    First of all, I reference here a recent paper which sums up what is known about the “evolution” of the adaptive immune system from a “darwinian” point of view. It is a good paper, so I invite those who are interested to read it, and to decide for themselves how much is known, and how much is explained.

    Here it is:

    http://www.jimmunol.org/conten.....9.full.pdf

    For a simple summary, you can also have a look at the “evolution” part of this wikipedia voice:

    http://en.wikipedia.org/wiki/A.....#Evolution

    I will not comment in detail for the moment. I will just add a couple of very general thoughts about AID, which was the original issue in sparc’s comments which originated this OP.

    First of all, just to give a general idea, the adaptive immune system, IOWs the immune system where specific receptors are generated for specific antigens, and whose affinity “evolves” after the first immune response, appears in jawed vertebrates, but a first form of “specific” immune system, largely based on different principles, can be observed in jawless vertebrates, like lampreys.

    AID follows well the general pattern of the appearance of the adaptive immune system. A form of AID is already present in the first jawed fishes, cartilaginous fishes (sharks).

    Human AID is a 198 AAs protein, and it has strong homology with the protein in sharks (Callorhinchus milii):

    73 identities, 93 positives, E = 1e-50

    The homology becomes much stronger if we consider bony fishes, like Danio rerio:

    127 identities, 154 positives, E = 9e-84

    Just to understand, jawed fishes (and therefore the adaptive immune system) appear about 500 million years ago, just after the Cambrian explosion, well known to us IDists. Jawless fishes are a little bit older.

    From jawed fishes on, AID remains there, and the homologies with the human protein become stronger and stronger: in mammals (mouse) we have 183 identities and 189 positives, E = 8e-134. Practically identical as in humans, 100 million years ago.

    What before jawed fishes? The paper I referenced tells us:

    “Acquired immune diversity appears to have evolved at a very early stage of vertebrate evolution, because an AID ortholog, Petromyzon marinus cytidine deaminase (PmCDA), was identified in a lamprey, P. marinus.”

    It is true. That protein in the lamprey has a detectable homology with the human protein:

    39 identities, 79 positives, E = 2e-13

    Certainly homology, but as you can see rather weak. The same lamprey protein has even weaker homology with the AID in sharks (Callorhinchus milii):

    24 identities, 42 positives, E = 2e-06

    So, what can we say? I would say that AID appears in a form very strongly related to modern versions, including human, in jawed vertebrates, together with the adaptive immune system. About 500 millions years ago.

    A precursor of AID, a cytidine deaminase with weak homology to AID, is present in jawless fishes (lampreys), whose origin can be traced more or less to the Cambrian explosion itself.

    Nothing relevant before that, as far as I know. But I am ready to consider any corrections and suggestions. That was only a quick search.

  135. 135
    Dionisio says:

    gpuccio

    I’m glad to see your latest post, which seems to answer my questions in post #60. Thank you.

  136. 136
    Dionisio says:

    Perhaps this time gpuccio’s post #134 will encourage sparc to present strong evidences supporting his own arguments?
    Does he need another kind of motivation?
    Or maybe some of his comrades will give him a hand?
    🙂

  137. 137
    Dionisio says:

    gpuccio,

    Does the presence of AID and other required enzymes answer all the main questions about the setting up and activation of the discussed mechanisms? Are there other issues to consider in addition to having those enzymes available?

  138. 138
    Dionisio says:

    gpuccio

    As far as you’re aware of, is there any tech documentation for a detailed, comprehensive, logically coherent explanation of the evolution from a first form of “specific” immune system, largely based on different principles, that can be observed in jawless vertebrates, like lamprey, to the adaptive immune system you described in your OP for this thread?

  139. 139
    gpuccio says:

    Aurelio Smith:

    If you have followed the history of this OP, you may know that its purpose was essentially to provide the opportunity to discuss more deeply my original post in KF’s thread about FSCI.

    I have tried to do that here, but not much biological contribution has come from those who seemed to be ready to show how the specific algorithms embedded in the immune system evolved.

    So, please, don’t consider this as a complete argument about ID: it is not. You can read my other OPs and discussions for that, or you can just detail better what are the points you are interested in, and we can discuss them here.

    Regarding the basic repertoire generation and affinity maturation mechanisms, that I have tried to detail in this thread, my main point is probably not so much that they are “complicated” (although they are, very complex, and any attempt to quantify the dFSCI in them would easily bring values much bigger than 500 – 1000 bits, allowing a design inference).

    My specific point is that they are astonishing examples of a very interesting form of algorithm, in two parts which form a whole plan:

    1) The VDJ generation of the basic repertoire is a very beautiful example of generation of a low-specificity high-sensitivity network of receptors, whose obvious purpose is to allow a first specific immunological response to the highest number of antigens which could be met by the organism, but are not yet known.

    2) The affinity maturation algorithm in the germinative center of the lymph node is a wonderful application of the same principles of protein engineering, based on targeted random variation + Intelligent Selection for a pre-defined property (affinity for a known antigen), that we effectively use in bottom up protein design.

    So, in this case it is not only the functional complexity (extremely high), but also and especially the extraordinary engineering beauty that I wanted to discuss.

    IOWs, if you have followed a previous OP of mine, here we are not only in front of a piece of English language; we are in front of a Shakespeare’s sonnet, in all its beauty.

  140. 140
    Dionisio says:

    gpuccio

    @140 in the last sentence ‘precious OP’ most probably meant ‘previous OP’ (although undoubtedly your OP is very precious, because it’s very insightful).

    The auto-correct feature embedded in the editor changed your text. Been there too. 🙂

    You may delete this post after you read it. It’s only for you.

  141. 141
    gpuccio says:

    Dionisio:

    Thank you, corrected! You have probably saved me from dire accusations of self flattery. 🙂

    There is no reason to delete your post. Thank you again!

  142. 142
    gpuccio says:

    Dionisio:

    “As far as you’re aware of, is there any tech documentation for a detailed, comprehensive, logically coherent explanation of the evolution from a first form of “specific” immune system, largely based on different principles, that can be observed in jawless vertebrates, like lamprey, to the adaptive immune system you described in your OP for this thread?”

    Rhetorical question?

    However: NO!

  143. 143
    gpuccio says:

    Dionisio:

    “Does the presence of AID and other required enzymes answer all the main questions about the setting up and activation of the discussed mechanisms? Are there other issues to consider in addition to having those enzymes available?”

    Obviously, AID is only part of the whole scenario.

  144. 144
    Curly Howard says:

    If you look at any random biological system in detail, doesn’t it appear to be irreducibly complex?

  145. 145
    Dionisio says:

    Apparently the interlocutors lack serious arguments against gpuccio’s OP and follow-up comments. It’s not going to get easier for them.

    We can look forward, with much anticipation, to reading newer research papers that will continue to shed more light on the biological systems, thus confirming the ID proposition and making it much harder for the interlocutors to come up with valid arguments.

    This match is over.

    Final score:

    gpuccio: 1
    interlocutors: 0

    🙂

  146. 146
    Dionisio says:

    Autoimmunity and antibody affinity maturation are modulated by genetic variants on mouse chromosome 12

    doi: 10.1016/j.jaut.2015.01.007.

    http://www.ncbi.nlm.nih.gov/pubmed/25623266

  147. 147
    Dionisio says:

    🙂

  148. 148
    DATCG says:

    from 85, Me_Think…

    Wow.. missed lot of post, but try to catch up.

    Me_Think said, ID is just a list of complaints against Darwinism.

    Much more than complaints, it is a list of failures. Failures now fully recognized and openly so by other non-ID scientist. Many Neo-Darwinist recognize the failure of Random Mutations and Natural Selection as mechanism to account for macro-evolutionary diversity.

    BA77 responded partly in #88 above for ID.

    But, part of moving on in science is recognizing failure of a theory. We are in the middle of an amazing revolution taking place in science today. A great time to observe, discover and discuss as scientist seek and find answers to old questions still not fully understood.

    From a group of non-ID scientist, known as the Altenberg 16, “complaining” about the failures of Neo-Darwinism and seeking new solutions.

    “A wave of scientists now questions natural selection’s role, though fewer will publicly admit it” (p. 20).

    “Basically I don’t think anybody knows how evolution works [emphasis added]” (Jerry Fodor, p. 34).

    “Oh sure natural selection’s been demonstrated … the interesting point, however, is that it has rarely if ever been demonstrated to have anything to do with evolution in the sense of long-term changes in populations. … Summing up we can see that the import of the Darwinian theory of evolution is just unexplainable caprice from top to bottom. What evolves is just what happens to happen [ellipsis in original]” (Stanley Salthe, p. 21 – PhD Zoology).

    “There are people spouting off as if we know the answer. We don’t know the answer” (Stuart Kauffman, p. 54 – theoretical biologist and complex systems researcher who studies the origin of life on Earth.)

    “Darwinism and the neo-Darwinian synthesis, last dusted off 70 years ago, actually hinder discovery of the mechanism of evolution” (Antonio Lima-de-Faria, p. 83 – Geneticist)

    “Do I think natural selection should be relegated to a less important role in the discussion of evolution? Yes I do” (Scott Gilbert, p. 221 – Biologist, Development Biology, former Chair Developmental and Cell Biology of the Society for Integrative and Comparative Biology)

    ““She [Lynn Margulis] sees natural selection as ‘neither the source of heritable novelty nor the entire evolutionary process’ and has pronounced neo-Darwinism ‘dead’, since there’s no adequate evidence in the literature that random mutations result in new species” (Mazur, p. 257)”

    Margulis – “biologist best known for her scientific theory on the origin of complex cells, called symbiogenesis.”

    “At that meeting [Francisco] Ayala agreed with me when I stated that this doctrinaire neo-Darwinism is dead. He was a practitioner of neo-Darwinism but advances in molecular genetics, evolution, ecology, biochemistry, and other news had led him to agree that neo-Darwinism’s now dead” (Lynn Margulis, p. 278 – Francisco Ayala – Evolutionary Biologist )

    “The point is, however, that an organism can be modified and refined by natural selection, but that is not the way new species and new classes and new phyla originated” (Massimo Piattelli-Palmarini, p. 314 – ).”

    Many of these scientist are offering “self-organization” as an alternative to the failed neo-Darwinian paradigm.

    “I think self-organization is part of an alternative to natural selection. Let me try to frame it for you. In fact, it’s a huge debate. The truth is that we don’t know how to think about it” (Stuart Kauffman, p. 291).”

    Darwinian Evolution is in a crisis right now. We’re in the middle of a hurricane 🙂 Watching the resulting flow around us. Think it’s an exciting time for all, no matter what side we are on.

    Michael Denton(PhD Biochemistry) identified this crisis with his landmark book Evolution: Theory in Crisis in 1985.

    Then there is The Third Way. Another group of scientist who have broken away from Neo-Darwinian theory as an answer who are non-ID scientist.

    The Third Way of Evolution

    James Shapiro for example…

    “An expert in bacterial genetics, he proposes the concept of Natural Genetic Engineering, a process described to account for novelty created in the process of biological evolution. Shapiro is an advocate of non-Darwinian evolution and is a critic of the modern synthesis.”

    The Third Way is anti-ID. So this is not just about what ID scientist and researchers “complain” about Darwinism. It’s much bigger than any ID complaints.

  149. 149
    Curly Howard says:

    This is some interesting stuff, but I think most of it goes over my head. Some things I have noticed though:
    “Hapten” is not “the immunologically active part of an antigen,” you’re thinking of “epitope.” A hapten is an experimental type of antigen.
    “The two branches of the immune system” are not “the B and T system.” They are the innate and adaptive systems.
    The initial BCR repertoire is certainly not “low affinity.” They are typically in the nanomolar range.
    Also the BCR repertoire is known to be at least 10^11, although the total number of B cells present at any one time is limiting as you said.

    For someone making a number of basic mistakes such as these, is it possible you don’t really know what you are talking about?

    Are you just pointing out how complex something is and claiming “that simply has to be designed.”

  150. 150
    DATCG says:

    #85 Me_Think…

    “I have tried understanding ID…”

    What papers have you read by Design Theorist?

    Conservation of Information

    Conservation of Information is a good start. ID is in it’s infancy, has a long ways to go I think. But they’re first having to answer critics on ability of Random Mutations and Natural Selection…

    BIO-Complexity is a peer-reviewed scientific journal

    PDF paper – on challenges to Darwinian explanation of protein origins…

    Enzyme Families–Shared Evolutionary History or Shared Design? A Study of the GABA-Aminotransferase Family

    “…but I find no answers to:”

    1) What is the mechanism by which ID agent manages billions of processes in trillions of organism?

    This assumes an agent must be actively present for a functional design to work or continue working. The mechanism’s are automated control systems, code repository, editors, symbolic messaging systems and recognition. To numerous to mention, including self-replication and error-correction, set in place and working as designed with available energy resources.

    I assume you’re stating as an active manager. The fascinating aspect of cellular architecture and animated life forms are self-contained maintenance and operation. That is why a Design Theoretical viewpoint going forward works so well in discovery of How-To in future benefit for all of us.

    But, a very rudimentary comparison to our own current technology is todays automation we see across many areas of design networked systems.

    Today’s cars and computers are a simple, but growing area of self-maintenance machines. Will be amazing to see what self-driven cars can do in future as part of self-maintenance. A futuristic scenario of a self-driven car that drives to a maintenance bay for inspection and repairs, then back. There will be a growing network of self-maintained transportation going forward. Starting with simplest design features to maintain and update energy resources and software codes.

    Computers update code 24/7 today without intelligent active management. The question is how far can we go in the future with self-replicating code and self-repair.

    How does the agent get inside the organism right up to cell level and manages to fix/direct/ create new metabolism, pathways, mutation, protein foldings ?

    As shown, an intelligent agent does not have to be present at the other end of the network for my PC to update new sets of code or sub-routines. From a network of mirrored databases, automated processes send updates breezing across tens of millions of PCs and MACS around the globe today.

    Again, rudimentary examples as we are no where near our future design capacity in AI or automation, self-regulatory Code, error correction and repair.

    So some concepts for ID I look to as precursors to a more robust theory going forward is Prescriptive Information or Active Information and Conservation of Information.

    Semantic
    Information has two subsets: Descriptive and Prescriptive.

    Identifying Sources of Active Information

    As Design Theory progresses in genetics, cellular architecture, biology and in our own automated attempts we will continue to discover new Design Principles and Limitations of Optimal Design.

    That’s one of the reasons why I referenced the work above on Optimal Design…

    Cell Computer – Design Principle Discovery

    To obtain a more accurate estimate of the concentration, the cellular system must remember measurements from the past. However, this requires time, energy and other proteins to store the information. To the researchers’ surprise, these three resources determine the accuracy of the measurements like links in a chain. The precision is limited by the resource that is the least present.

    This observation led the researchers to a design principle not previously identified for this type of system: in an optimal measurement system all of the links are equally strong. The network that enables the bacterium E. coli to find food was found to obey this principle.

    The researchers expect that this design logic of cellular systems can also be used to develop efficient synthetic systems and materials.

    There’s nothing about undirected process of evolution in Optimal Design Principles. Again, I think an important question is would random mutations help or decrease these highly tuned systems? Must these informational systems be conserved?

    What if random mutations degenerate such a finely tuned system? If so, how many mutations to a cliff-fall from simply impaired process to catastrophic failure.

    That is an important area of research. And helps us look at Conservation of Information as another Design Principle.

    Then there is the obvious research of metamorphosis. Intriguing and amazing technology to research of one body plan to another, from crawling to flight. Of rapid changes in form and function. A need for Prescriptive Information or Specified Complexity – Active Information?

    Active Information in MetaBiology

    Chaitin notes this when he writes [3], “The fitness landscape has to be very special for Darwinian evolution to work.” The environment for evolution to occur, therefore, has to be carefully designed. Indeed, in the paradigm of conservation of information, smooth landscapes can be source of significant active information [14]. Metabiology’s construction of smooth landscapes is accomplished by running all viable programs, a computationally expensive approach that is only possible because there are no resource limitations. While metabiology is fascinating, it falls short of demonstrating the abilities of undirected Darwinian evolution. Other programs have claimed to simulate Darwinian evolution. These
    incluvde AVIDA [11,23] and ev [12,33]. Like AVIDA and ev, metabiology makes use of external information sources to assist in the search. Like the simple Hamming oracle, the halting oracle can be mined for information with various degrees of sophistication. Evolution thus requires external sources of knowledge to work. The degree to which this knowledge is used can be assessed using the idea of active information.

    Chaitin states [3], “For many years I have thought that it is a mathematical scandal that we do not have proof that Darwinian evolution works.” In fact, mathematics has consistently demonstrated that undirected Darwinian evolution does not work.

  151. 151
    gpuccio says:

    Curly Howard:

    Thank you for the comments.

    You have correctly shown an error, and I am grateful for that: I used “hapten” while I was thinking “epitope”. I will correct it, and leave your post as trace of my error. The simple fact is, I was really thinking epitope, as the attached definition shows, but for some reason the wrong word came to my mind. I have noticed that it happens quite often to me sometimes, especially now that I am in a reasonably old age. Thank you for the correction.

    I don’t really agree on the other “errors”. You say:

    ““The two branches of the immune system” are not “the B and T system.” They are the innate and adaptive systems.”

    OK, but the B and T systems are certainly two branches. I should have said “the two branches of the adaptive immune system”, but the context was really clear. Aren’t you being a little fastidious here?

    You say:

    “The initial BCR repertoire is certainly not “low affinity.” They are typically in the nanomolar range.”

    But I was not using any absolute concept of “low”, I was just comparing it to the high affinity results of the maturation. I could have said “lower affinity”, but aren’t you being a little fastidious here?

    You say:

    “Also the BCR repertoire is known to be at least 10^11, although the total number of B cells present at any one time is limiting as you said.”

    That’s correct, but it should be obvious from the context that I was speaking of the BCR repertoire actually implemented in one individual by the VDJ racombination process, as I have explicitly stated:

    “No one knows exactly how big that repertoire is in each individual, but new techniques are helping much in studying it quantitatively. From what I have read, I would say that the size is probably somewhere between 10^6 and 10^9 (more or less the total number of B cells in an organism).”

    (emphasis added)

    You say:

    “For someone making a number of basic mistakes such as these, is it possible you don’t really know what you are talking about?”

    It is certainly possible, but I hope it is not true.

    However, thank you for the comments and the correction. I am always happy to correct and clarify. That’s why we discuss here.

    Then you say:

    “Are you just pointing out how complex something is and claiming “that simply has to be designed.””

    No, I don’t think so. But I will refer you to my answer to Aurelio Smith at #140 for this aspect.

    In your previous post, you say:

    “If you look at any random biological system in detail, doesn’t it appear to be irreducibly complex?”

    I am not sure what you mean. In a sense, most biological systems are irreducibly complex. But they are not random. Could you clarify your point, and give some examples?

    Just to be fair, you also say:

    “This is some interesting stuff”

    I take it as a compliment. 🙂

  152. 152
    Dionisio says:

    Curly Howard

    Thank you for your comments posted @145 & @150

    I’m sure gpuccio will gladly make any necessary clarifications or corrections to his text in response to your questions or suggestions.

    This whole thing is difficult for me to grasp. Hence I ask questions that some might consider trivial or elementary.

    In posts #32 and #47 I asked the following questions, which have not been answered by anyone (except gpuccio) so far in this discussion thread:

    1. Can you point to any set of papers explaining how the entire mechanisms gpuccio described in the OP got setup to work the way they do?

    One option is that the interwoven mechanisms could have been intelligently setup a priori.

    2. What is your strong argument against it?

    3. Is there a detailed explanation for the appearance of the amazingly complex choreographies orchestrated within the biological systems, which can handle even stochastic scenarios?

  153. 153
    gpuccio says:

    DATCG:

    Very good contributions, thank you.

    I find the distinction between descriptive information and prescriptive information a very important and clarifying point. It corresponds very well to the two basic experiences of a conscious being: meaning and purpose.

  154. 154
    gpuccio says:

    Dionisio:

    Thank you for the very interesting reference at #147.

    Of course, I have tried to describe here the essential structure of the two algorithmic processes actin in generating the basic BCR repertoire and in affinity maturation, but there is also the problem of their epigenetic activation and regulation (the procedures 🙂 ), about which i think we know almost nothing.

  155. 155
    gpuccio says:

    Dionisio:

    An interesting point that I had not the time to touch is that those processes have some connection with autoimmunity and lymphoid neoplasms. There is probably a price to be paid for using random variation, even in a controlled context.

  156. 156
    Dionisio says:

    Curly Howard

    RE: addendum to my post #153

    In post #60 I asked gpuccio the following questions:

    (4) Is there a known biological predecessor of the mechanisms you described in the OP?
    (5) Did it have more or less algorithmic steps, more or less components, simpler or more complex configuration?
    (6) Is there a way to describe how to ‘evolve’ from the preceding setup to the current one?
    (7) Then, what preceded the predecessor?
    And so on…

    Later, in posts #138 & #139 I asked gpuccio the following questions:

    (8) Does the presence of AID and other required enzymes answer all the main questions about the setting up and activation of the discussed mechanisms?

    (9) Are there other issues to consider in addition to having those enzymes available?

    (10) As far as you’re aware of, is there any tech documentation for a detailed, comprehensive, logically coherent explanation of the evolution from a first form of “specific” immune system, largely based on different principles, that can be observed in jawless vertebrates, like lamprey, to the adaptive immune system you described in your OP for this thread?

    gpuccio’s post #134, #143 & #144 answered the above questions.

    However, I would like to ask others the same questions, in case they disagree with -or want to expand on- what gpuccio wrote.

    You’re welcome to answer those questions too.

  157. 157
    Dionisio says:

    #155 gpuccio

    I think I see your point. The ‘elusive’ procedures keep coming back. 🙂

    However, I believe future research papers will strengthen your point about the procedures though. Let’s wait and see. Research seems to be intensifying at an accelerated pace lately. That’s good news, isn’t it?

  158. 158
    Dionisio says:

    #156 gpuccio

    Yes, agree, that’s an interesting observation. Thank you.

  159. 159
    DATCG says:

    Gpuccio, you need a Peer Review process. 😉 Certainly made a difference for Neo-Darwinism the last 70 years.

    “Darwinism and the neo-Darwinian synthesis, last dusted off 70 years ago, actually hinder discovery of the mechanism of evolution” (Antonio Lima-de-Faria, p. 83 – Geneticist).”

    On “branches” can understand why it’s confusing, but I understood you were talking about Adaptive Immune system from previous paragraph.

    Understanding Irreducible Complexity

    VENTER: Below ribosomes, yes: you certainly can’t get below that. But you have to have self-replication.
    CHURCH: But that’s what we need to do — otherwise they’ll call it irreducible complexity. If you say you can’t get below a ribosome, we’re in trouble, right? We have to find a ribosome that can do its trick with less than 53 proteins.

    VENTER: In the RNA world, you didn’t need ribosomes.

    CHURCH: But we need to construct that. Nobody has constructed a ribosome that works well without proteins.

    VENTER: Yes.

    SHAPIRO: I can only suggest that a ribosome forming spontaneously has about the same probability as an eye forming spontaneously.

    CHURCH: It won’t form spontaneously; we’ll do it bit by bit.

    SHAPIRO: Both are obviously products of long evolution of preexisting life through the process of trial and error.

    CHURCH: But none of us has recreated that any.

    SHAPIRO: There must have been much more primitive ways of putting together

    CHURCH: But prove it.

    In the end, Robert Shapiro’s statements said it all: We don’t know how the ribosome and its required proteins evolved, but we know that “Both are obviously products of long evolution of preexisting life through the process of trial and error.” This is a prime example of “evolution-of-the-gaps,” and it demonstrates that intelligent design could go a long way towards solving problems in 21st century biology. This also demonstrates that intelligent design proponents have worthwhile contributions to make and deserve a place at the table in these kinds of discussions.

    The argument is not: This is to complex to understand, thus Design. But once understood, it is an Irreducibly Complex System.

    Irreducible – Interdependent Elements – a) pull one part out, it stops functioning and the system fails, requires all parts to be in place before it can properly function

    “If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.”
    Charles Darwin, Origin of Species

    The scientist I quoted above – Non-ID theorist, all agree neo-Darwinian theory failed to uphold Darwin’s original claim of gradual modifications over time to account for macro-evolution in diversity of life forms.

    His theory “broke down.” So the search is on for another way, a “Third Way” or an ID way, or another way, but Neo-Darwinism is moved to a smaller role, no longer seen as sufficient for a full explanation of Macro Evolution.

  160. 160
    gpuccio says:

    DATCG:

    OK, just to avoid any misunderstanding, I changed “low affinity” to “lower affinity” and added “adaptive”.

    You know, when you receive from your peer reviewers this kind of requests (for what we could call “minor revisions”), you can usually be sure that the paper will be accepted. 🙂

  161. 161
    DATCG says:

    BA77, thanks.

    Will save links. Had not looked at Snoke on Systems yet(oh wow – great paper!) Curious if there been any other confirmations on the Protein Folding – proposed QM model.

    Gpuccio – thumbs up 😉

  162. 162
    Dionisio says:

    DATCG

    Interesting comments posted @149, 151 & 160.

    Thanks!

  163. 163
    Me_Think says:

    DATCG @ 151

    What papers have you read by Design Theorist?

    Conservation of Information

    Conservation of Information is a good start. ID is in it’s infancy, has a long ways to go I think. But they’re first having to answer critics on ability of Random Mutations and Natural Selection…

    Conservation of information & Axe’s landscapes works if you assume low dimension landscape where you reach the local maxima/minima and get trapped.
    Have you read ‘Arrival of fittest’ and Papers of Wagner ? Do you understand how hyper-dimensions can reduce search area? You can do your own calculation using Wagner’s matlab code or software included in his University of Zurich page ,if you want.

    BIO-Complexity is a peer-reviewed scientific journal

    Yes,it is an ID journal with ID proponents in it’s editorial board, with stated objective to promote ID, for testing the scientific merit of the claim that intelligent design (ID) is a credible explanation for life.

    This assumes an agent must be actively present for a functional design to work or continue working. The mechanism’s are automated control systems, code repository, editors, symbolic messaging systems and recognition. To numerous to mention, including self-replication and error-correction, set in place and working as designed with available energy resources.

    If ID is to be believed, pretty much every process – mutations, protein folding, creating new metabolisms, searching landscape, finding pathways etc require assistance. Some of these processes happen billions of time in Trillions of organisms. How would you explain the working without ID agent intervention ?

    Today’s cars and computers are a simple, but growing area of self-maintenance machines. Will be amazing to see what self-driven cars can do in future as part of self-maintenance. A futuristic scenario of a self-driven car that drives to a maintenance bay for inspection and repairs, then back. There will be a growing network of self-maintained transportation going forward. Starting with simplest design features to maintain and update energy resources and software codes

    You seem to assume ID agent has far superior technical capability than we have. That would be true only if you prove universe is designed by the agent. You can’t claim universe is designed and cite that as a proof that designer is a tech wizard.

  164. 164
    gpuccio says:

    Me_Think:

    You say:

    If ID is to be believed, pretty much every process – mutations, protein folding, creating new metabolisms, searching landscape, finding pathways etc require assistance. Some of these processes happen billions of time in Trillions of organisms. How would you explain the working without ID agent intervention ?

    You have strange ideas about ID.

    Mutations happen all the time without any design intervention. Only guided mutations would require intervention. They are a possible tool of biological design, but they certainly do not need to happen in trillions of organisms, billions of time. Why do you think that?

    Protein folding happens all the time without any design intervention, once all that is necessary for it to happen has been correctly designed.

    Creating new metabolisms and searching landscapes certainly requires design interventions, if the complexity to generate is high and original. But again, why would that happen “billions of time in trillions of organisms”?

    Moreover, many adaptive changes can certainly be achieved algorithmically. In that case, only the original algorithm needs to be designed, while further achievements are reached algorithmically, if necessary by processing new information from the outer environment.

    I suppose this thread is exactly about that kind of things.

  165. 165
    gpuccio says:

    Me_Think:

    You say:

    “You seem to assume ID agent has far superior technical capability than we have. That would be true only if you prove universe is designed by the agent.”

    Why? There are certainly ID agents who have far superior technical capability that I have, in many fields. That is certainly true even if the universe cannot be proved to be designed by them.

  166. 166
    Dionisio says:

    #164 Me_Think

    Are those your best arguments vs. DATCG’s interesting comments posted @149, 151 & 160?

    Can’t you do better than that?

    BTW, can you answer any of the questions in post #157?

    Also, have you seen sparc around? This discussion thread was triggered by his ‘challenging’ comments in another thread. But he has not produced any solid argument yet.

    Are you and your comrades having nightmares when you see the new research papers shedding more light on the biological systems these days?

    🙂

  167. 167
    gpuccio says:

    sparc, sparc:

    Where are you?

  168. 168
    Me_Think says:

    gpuccio @ 166

    Why? There are certainly ID agents who have far superior technical capability that I have, in many fields. That is certainly true even if the universe cannot be proved to be designed by them.

    That would matter only if you claim they built the universe!

  169. 169
    Me_Think says:

    Dionisio @ 167

    Are you and your comrades having nightmares when you see the new research papers shedding more light on the biological systems these days?

    Not at all. No one goes about doing research believing ID agents created all these using some high end tech gear. Ask the researchers who do all the research that you cite here – how many believe ID agents did it ?

  170. 170
    Me_Think says:

    gpuccio @ 165
    Missed the comment in my earlier posting spree.

    You have strange ideas about ID.

    All leanerd from UD.

    Mutations happen all the time without any design intervention.
    Protein folding happens all the time without any design intervention

    You are on the wrong side of ID debate 🙂

    why would that happen “billions of time in trillions of organisms”?

    All cellular processes have to happen in all the cells, right? Trillions include microbes too.

  171. 171
    Dionisio says:

    #170 Me_Think

    What about the rest of post 167?

    You answered (poorly) only the last of the 5 questions I asked you in that post.

    Why? Because it was the easiest to answer?

  172. 172
    DATCG says:

    Me_Think,

    You complained earlier that ID was only a list of complaints on Darwinism. Not true.
    So I showed links to ID peer-reviewed papers.

    There’s robust debate going on. Recently Miller responded to Michael Behe. Behe responded knocking down Miller’s points. There’s ongoing dialogue between the two. So, despite your protest, serious debate is being done by ID camp that forces neo-Darwinian camp to respond. Each are making scientific arguments.

    As to Wagner, only looked briefly. But now I’m curious. Are you agreeing Neo-Darwinism failed? Because looking at Wagner, he too notices this failure as a creative mechanism for new functions. Just curious where you stand. Guess you do, based on blurbs from Wagner’s book on Amazon…

    “Natural selection can preserve innovations, but it cannot create them. Nature’s many innovations—some uncannily perfect—call for natural principles that accelerate life’s ability to innovate.”

    Darwin’s theory of natural selection explains how useful adaptations are preserved over time. But the biggest mystery about evolution eluded him. As genetics pioneer Hugo de Vries put it, “natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest.”

    Can random mutations over a mere 3.8 billion years really be responsible for wings, eyeballs, knees, camouflage, lactose digestion, photosynthesis, and the rest of nature’s creative marvels? And if the answer is no, what is the mechanism that explains evolution’s speed and efficiency?

    —– Note: answer must be NO as Wagner proposes that he provides the “missing piece” or does he? —–

    So, I’ve posted about Lenski’s 60,000 experiments. What are we missing between Wagner’s model and Lenski’s reality? Other than possibility of Active Information being smuggled in by Wagner? Which, oddly enough I mentioned above.

    In Arrival of the Fittest, renowned evolutionary biologist Andreas Wagner draws on over fifteen years of research to present the missing piece in Darwin’s theory. Using experimental and computational technologies that were heretofore unimagined, he has found that adaptations are not just driven by chance, but by a set of laws that allow nature to discover new molecules and mechanisms in a fraction of the time that random variation would take.

    Well, least other scientist are admitting a missing link 😉
    Again though, how does this match reality of Lenski’s experiments?

    Wait – did they just state – “computational technologies that were heretofore unimagined?” Interesting.

    How does he ever get to a Ribosome?

    I quoted Venter and Church above. Both good scientist and well recognized, non-ID. They recognize the problem. Did he convince Church? Curious what he would think of Wagner’s miracle find.

  173. 173
    DATCG says:

    Me_Think,

    ID does not claim active intervention by a Designer. You’re attempting to force your own interpretations on ID.

    My simple example was to rebut your assertion against automation.

    To show design principles work today with automated solutions. You can say “trillions” as if that’s scary. That’s not an argument against design however. There are nearly 7 billion mobile phones and a billion PCs, not including MACS, Ipads, etc. So smart systems are going to be ubiquitous in the future from Smart TVs to every appliance in the home, car, business. All making trillions of transactions, communications and automated configuration upgrades.

    Left w/o human intervention, 24 hours, 7 days a week, billions of these devices get updated. Without hands on management. I do not have to be at my office for updates to be downloaded, installed and function with expanded code.

    This is a trivial example. Your argument is a non-starter.

    You seem to think we are limited in the future. When in just a few decades we’ve gone from a first computer to fully automated systems in billions of nano tech devices.

    Where will our Design systems be a hundred years from now?

    Are you stating automated solutions will stop improving? AI will halt? Designed systems in the future will not become more autonomous? With less human intervention? That we will not learn from cellular technology and the Immune system we’re discussing with new Design Principles?

    So, the research scientist I quoted above who discovered new Design Principles. They should just quit?

    Prescriptive Information – that’s the Hidden Principle. Active Information is the key and there for all to see. Unless Wagner can show origins of information with his new ideas.

    Guess I’m more hopeful in research scientist and engineers than you are, that we continue to progress for new solutions.

    Whether Wagner’s ideas add to this or not – cover the missing Gap in Neo-Darwinism – not sure. Time will tell. I need to take a closer look when I have more time.

    Again, I’m very curious, do you agree with Wagner? That random mutations and natural selection cannot create? Only preserve? If so, I think at least we’re agreeing in some areas.

    Have a good one, off for now.

  174. 174
    gpuccio says:

    Me_Think:

    “That would matter only if you claim they built the universe!”

    But biological ID does not claim that the biological designer(s) built the universe!

  175. 175
    gpuccio says:

    Me_Think:

    “You are on the wrong side of ID debate ”

    I am on the side of ID theory.

  176. 176
    gpuccio says:

    DATCG:

    I am not impressed by what I have seen about Wagner’s ideas. Not even really interested. My impression is that they are irrelevant and conceptually wrong. But it is only an impression, because I have not read much about the matter, nor is it in any of my priorities.

    But maybe Me_Think could do me a service, and try to summarize in a clear way what Wagner thinks he has demonstrated, and how. Maybe I could become interested. Maybe.

  177. 177
    Joe says:

    Me Think:

    Have you read ‘Arrival of fittest’ and Papers of Wagner ?

    The book doesn’t say anything about the arrival of the fittest, however it does refute keith s’s argument about unguided evolution producing an objective nested hierarchy.

    If ID is to be believed, pretty much every process – mutations, protein folding, creating new metabolisms, searching landscape, finding pathways etc require assistance.

    That is false. Computers do not require assistance in order to operate.

    This has been explained to Me Think so it is obvious that Me Think is a willfully ignorant troll on an agenda of misrepresentation.

  178. 178
    Dionisio says:

    #177 gpuccio

    But maybe Me_Think could do me a service, and try to summarize in a clear way what Wagner thinks he has demonstrated, and how. Maybe I could become interested. Maybe.

    My friend, sorry to disappoint you with what I’m going to tell you now. I hope you don’t have high expectations on his willingness to be serious in this blog. Just see my post #172.

    Do you really expect him to ‘try to summarize in a clear way‘ something?

    Do you recall any instance in this blog, where he has ‘tried to summarize in a clear way‘ anything?

    🙂

    I think he could learn how to summarize in a clear way, by reading carefully your OP for this thread, which is a summarized explanation of a paper you saw referenced in a post in another thread.

    PS. I’m learning to write provocative ‘click-bait’ comments. 🙂

  179. 179
    Dionisio says:

    180 comments posted in this thread so far. And sparc hasn’t contributed as we mistakenly expected he will do. What a disappointment.

    🙂

    BTW, Visited 515 times so far. Many more onlookers/lurkers than commenters.

  180. 180
    Dionisio says:

    DATCG

    Very insightful comments. Thank you.

  181. 181
    EugeneS says:

    Me_Think # 95,

    The universe – agreed, but that is an aside issue! I suppose I could have avoided your retort if I’d said, nothing comes out of nothing in this world.

    Anyhow, do you think that in biology things like that can happen post the Big Bang? Why do you think so (if you do)?

  182. 182
    Curly Howard says:

    My point is that you think claiming something is irreducibly complex is justified simply by pointing out how complicated a process is. It seems that your strategy is to simply regurgitate as many facts about a biological process, throw in some unrelated words that make things sound designed(algorithm), and call it irreducibly complex. All you are really doing is pointing to things that we don’t have an evolutionary explanation for yet and saying “look how complicated this is! How could it not be designed?”
    That’s what it seems like to me.

  183. 183
    Barry Arrington says:

    CH @ 183: “That’s what it seems like to me.”

    Which is evidence of an appalling lack of intellectual curiosity. Curly, you should actually take some time to engage with an argument before attempting to rebut it. The “strategy” you describe is not even close to Behe’s argument. That you are tilting at a strawman should give you pause. I doubt that it will.

  184. 184
    Curly Howard says:

    I’m not sure who Behe is, but I think the strategy I explained describes Gpuccio’s methods here in the above post quite well.

  185. 185
    gpuccio says:

    Curly Howard:

    You say:

    My point is that you think claiming something is irreducibly complex is justified simply by pointing out how complicated a process is. It seems that your strategy is to simply regurgitate as many facts about a biological process, throw in some unrelated words that make things sound designed(algorithm), and call it irreducibly complex. All you are really doing is pointing to things that we don’t have an evolutionary explanation for yet and saying “look how complicated this is! How could it not be designed?”
    That’s what it seems like to me.

    The what it seems like to you is wrong.

    I don’t know how much you know of ID in general and of my personal ideas about ID theory in particular, however, while inviting you to read my some of my other OPs and my post #140 to Aurelio Smith here, I would like to point at some simple concepts:

    a) ID is about the design inference in general, and in biology in particular.

    b) The single central concept in ID inference is CSI. The subset of CSI to which I refer to is dFSCI (digital Functionally Specified Complex Information). I have used and applied the concept many times, in detail, both to individual proteins and to English language, giving the pertinent computations and design inferences.

    c) Irreducible Complexity is a special form of functional complexity, as introduced by Behe. It applies to systems whose function depends critically on many different parts, each of them complex, and therefore the emergence of the final function cannot easily be explained by a gradual darwinian mechanism, based on natural selection of function.

    d) In this particular OP, I have not tried any explicit computation of dFSCI, because as I have explained many times the purpose of this “instant OP” was different. In the discussion, hoever, I have given some relevant facts about AID, which could be used to try a quantification of its minimal dFSCI, which would probably allow a design inference even for that single component. That the whole system is above the 150 bits of dFSCI that I use as a threshold for biological systems, or the 500 – 1000 bits that others, like Dembski and KF, use as universal thresholds, is rather obvious. It is equally obvious that the whole system also satisfies Behe’s requirements for irreducible complexity. But I have not even tried to discuss those aspects in detail here.

    e) My main point was to show the special engineered-like form of those two mechanisms, especially if considered as a whole. That I have tried to do, both in the OP and in the discussion.

    f) I don’t “throw in some unrelated words that make things sound designed”. I use the word “algorithm” to indicate a set of events which are strictly guided by rules including measures and logical choices, determined by explicit laws. There is nothing in my use of the word “algorithm” that points to design. Indeed, if you read my posts, you will see that design is a process which is not algorithmic, but designed things can certainly work in an algorithmic way.

    It is true that complex algorithms are always designed, but that is because they are complex.

    In this particular cases, however, what I wanted to do was to show some formal properties of the involved algorithms, especially controlled random variation and intelligent selection based on the active measure of a property and the active differential response to that measure, which are strongly suggestive of design for their intrinsic form, because they strongly resemble human algorithms, like those used in bottom-up protein engineering.

    However, it remains true that functional complexity remains the central concept for ID inference, and obviously these systems are functionally complex, and exhibit tons of dFSCI. But they are also specially beautiful and human-like.

    By the way, you seem to be, from the few lines you have written here, a careful and informed person. As I try to respect my peer reviewers, I would like to suggest, for your information, that using statements like:

    “look how complicated this is! How could it not be designed?”

    to mischaracterize ID theory, and pour scorn on it, is a very trivial and gross form of gossip, and in no way corresponds to truth.

  186. 186
    Curly Howard says:

    So would you say that the adaptive immune system as a whole is irreducibly complex?

  187. 187
    EugeneS says:

    “we don’t have an evolutionary explanation for yet”

    And that after some 150 years of effort. Evolution (NS+RV) does happen but its scale has been grossly overstated. It has a marginal effect nowhere near one that is advertised. No genuine novelty can possibly come out by Darwinian means. No matter how many times supporters of evolution on the grand scale repeat it, it does not become a fact. There is an ever growing skepticism about the powers of Darwinian evolution in science. This does not undermine the impact of the works of Darwin or anyone else from his school of thought. Nonetheless with all due respect, the scientific truth should be preferred to evolutionary speculative narration. The science of the 21 century requires a level of scrutiny Darwinian macro-evolution does not stand.

  188. 188
    gpuccio says:

    Curly Howard:

    My point here was about the two mechanisms described, but if parts of a system are IC, then the whole system has an IC core.

    Saying that a system is IC implies that there is an irreducibly complex core which is essential to the function of the system. Of course, the system can include parts which are not essential to the function, or which are shared with other functional systems.

    You should really read Behe, before discussing Irreducible Complexity.

  189. 189
    Curly Howard says:

    So what is the irreducibly complex core of the system that “generates a blind repertoire of lower affinity antibodies?”

  190. 190
    Curly Howard says:

    First off Eugene, molecular biology has only been around for half that time. Second, it seems you have no idea how difficult and time-consuming the process of research is. And third, the theory of evolution is only becoming stronger. It has been continuously furthered over those past 150 years despite its basic beginnings. It is accepted by the vast majority of those who study it as well as other fields in biology, including some of the smartest people I know. And it is even being integrated more into basic biology courses at the university level.

    This “ever growing skepticism” seems to only exist in your mind, or maybe here at UD.

  191. 191
    Silver Asiatic says:

    CH

    So would you say that the adaptive immune system as a whole is irreducibly complex?

    It’s not merely complexity that we’re looking at.
    Even at the most general, theoretical level, the immune system is irreducible.

    The building of an immune system where once there was none, would require the same disease to kill the organism.

    Showing the inter-connected range of strategies that a cell can use for an immune system, merely adds vast complexity to the process which is inexplicable in its simplest form.

    Becoming immune to disease is a means of preserving the organism – thus a prevention of evolutionary forces.

    A step-by-step development from non-immune to immune would require a non-functioning immune system, completely vulnerable to death, to eventually resist the same diseases that would kill it without the immune system.

    The system can only work when it is functioning correctly – to ward off disease.

    That doesn’t even touch on the massive physical changes needed to create a variable response to stimuli.

  192. 192
    Silver Asiatic says:

    CH

    And third, the theory of evolution is only becoming stronger.

    Ok, but supposedly before this time, it had no weaknesses – so how could it get stronger?

    We also shouldn’t overlook the fact that some scientists are calling for a new-new synthesis because the old-new one is not working.

  193. 193
    Dionisio says:

    gpuccio

    Reaching close to 200 posts in this discussion thread you started, after our friend KF suggested you convert your post on the affinity maturation into a separate OP. Looking back we can see KF knew what he was suggesting. What a vision!

    Can you imagine what would happen when we get an OP on the cell fate specification/determination mechanisms?
    Our interlocutors will have to sweat profusely in order to try and make a point. Can’t wait to see that. It must be fun. 🙂

  194. 194
    gpuccio says:

    Curly Howard:

    “So what is the irreducibly complex core of the system that “generates a blind repertoire of lower affinity antibodies?””

    Your request is rather exacting, because in writing this OP I had not prepared any detailed argumentation on this specific point. As I have said, my main attention was on other aspects.

    However, obviously, you have a right to ask. So, I will try to answer, at least in a general form. But I need a little bit of time to prepare a reasoned answer.

    So, please, stay in tune.

  195. 195
    Curly Howard says:

    Silver Asiatic, little of what you say makes sense or demonstrates even a general understanding of how biological processes work.

    “The building of an immune system where once there was none, would require the same disease to kill the organism.” This is wrong on numerous levels. First, disease does not necessarily equate to death. Also, you are ignoring a major function of the immune system: keeping symbiotic organisms in check. You are painting with too broad of brush strokes.

    Taking the first step in building an immune system would make an organism “more fit” in comparison to the other organisms of the population. This preserves the organism and in no way “prevents evolutionary forces.” It is the definition of an evolutionary force; a mutation that provides the basis from which natural selection can act. Look at Dscam in Drosophila, it consists of numerous possible exons functioning in development of the neural system. Some of the exons, however, have evolved to confer the ability to recognize pathogens and opsonize bacteria.

    When you say “the system can only work when it is functioning correctly,” you demonstrate your lack of knowledge on biology. There is a spectrum of function in every biological process seen across different species due to evolution. Organisms do not need a highly specialized immune system such that we have in order to survive and this is seen in nature. Just because an organism is susceptible to a pathogen, does not mean it will definitely be infected by that pathogen or die from the pathogen. New generations only need a slightly better mechanism of avoiding disease in order to increase survival.

  196. 196
    Curly Howard says:

    It’s unsettling to hear that you can so boldly make the claim that these systems are irreducibly complex without having actually identified the irreducible core of the systems, which is per your own definition. With every post you make it seems like your criteria for irreducible complexity amounts simply to “wow this is complicated, it must be irreducibly complex” as I originally stated.

    Ultimately, it seems to me that every biological system is irreducibly complex by your definition as there will always be some irreducible core required for function of every biological molecule. This is what makes it so easy for you to claim that this system or that system is irreducibly complex without any evidence, and also makes the argument inherently unscientific.

  197. 197
    gpuccio says:

    Curly Howard:

    All that because I asked for a little bit of time to prepare a reasoned answer? Wow!

    I consider your attitude simply unkind. Maybe I will comment on the IC of the system, but it will not be to answer your request.

    By.

  198. 198
    gpuccio says:

    Dionisio:

    Yes, the OP has been really a success, and the discussion interesting, although strongly “asymmetric” (and that is really an euphemism). Yes, KF has a great vision.

    I have found many new interesting data about AID. It is really an interesting actor.

    In the end, all is connected to epigenetic regulation.

    Here is an interesting paper, very recent:

    http://www.ncbi.nlm.nih.gov/pm.....-00642.pdf

    And another one:

    http://www.ncbi.nlm.nih.gov/pm.....-00534.pdf

  199. 199
    Dionisio says:

    gpuccio

    Yes, agree, that’s an euphemistic way to call this discussion: strongly ‘asymmetric’. 🙂

    For example, no one among the Darwinian interlocutors dared to answer any of the questions in post #157.
    I had much higher expectations about those folks. What a disappointment. 🙂

    Thank you for sharing those two recent papers.

    I’m still trying to ‘digest’ some of the interesting references that were posted in this discussion.

    il tempo vola!

    BTW, this is post #200!

  200. 200
    REC says:

    I wasn’t going to comment on this thread but your self-congratulatory posts have annoyed me. You’ve proved information can be increased in an evolutionary process, due to selection acting on random variation. Congrats for defeating ID theory.

    “Both use controlled random variation to generate diversity. The second process also uses intelligent selection based on existing information from the environment.”

    Here’s an easy proof. What is the total information content of the antibody producing genes in a fertilized egg? In an infant with an unstimulated immune system? In an adolescent with all vaccines and a few infections?

    In the latter, we’re talking more disease-fighting useful information than the human genome. An enormous antibody repertoire. All due to selection acting on random variation. Calling it “intelligent selection” or the system an “engineering process” can’t help you.

  201. 201
    Dionisio says:

    gpuccio

    Did you see the references in posts #1, 9-13, 15?

    BTW, at the end of post #179 I wrote this postscript

    PS. I’m learning to write provocative ‘click-bait’ comments. 🙂

    Now I see post #201 confirms my newly acquired skills! 🙂

    Note REC wrote:

    I wasn’t going to comment on this thread but your self-congratulatory posts have annoyed me.

    Yes!!! it worked!!! Yay!!! hurrah!!! 🙂

    I prefer the serious discussions, but now I realize that a little fun isn’t bad either.
    Specially when it’s provided by the interlocutors free of charge. 🙂

    Someone suggested that some of the interlocutors might be paid agents working for this blog, in order to make the Darwinists appear confused, misinformed and angry, and to keep us entertained? It’s difficult to believe that’s true. But who knows? However, if that were the case, how could one tell the real ones from the pretenders? 🙂

  202. 202
    gpuccio says:

    REC:

    Thank you for your comments, which allow us to go beyond the 200 posts limit, and to have a less asymmetric discussion. My self-congratulatory attitude is reinforced and comforted.

    Unfortunately, your “arguments” make no sense.

    You ask:

    “Here’s an easy proof. What is the total information content of the antibody producing genes in a fertilized egg? ”

    Very high. Extremely high. As high as to be able to generate the full organism.

    “In an infant with an unstimulated immune system?”

    Very high. Extremely high. And the information has changed form, obviously, and the embedded algorithms, both genetic and epigenetic, have taken their course. Essentially, the organism is the result of the information in the zygote, and there are certainly parts which have been influenced by randomness and by environmental inputs. Not yet antigenic, if we accept the “unstimulated” part (although, obviously, antigenic stimulation starts very early).

    “In an adolescent with all vaccines and a few infections?”

    Still very high. Extremely high. See previous point. Obviously, here the embedded algorithms have received some specific antigenic information from the environment, and reacted to that input according to the programmed responses which were already planned in the zygote.

    And so?

    The basic antibody repertoire is not “disease-fighting useful information” acquired by the organism. It is a useful resource already planned in the zygote, and dutifully developed by the growing organism. Considering it acquired information would be like considering my right hand an acquired tool, because certainly it was not in the zygote. I can’t follow your logic, if there is one.

    And there is no Intelligent Selection implied in the building of the basic repertoire, except in the process of negative elimination of anti-self reacting clones. The rest is a very efficient process of diversification by controlled random variation. There is nothing to be selected, because there is no information yet from the environment in the form of antigens.

    On the contrary, affinity maturation applies Intelligent Selection to tweak the existing resources against a specific outer information: the antigen. That is a process of modeling, but the process itself is obviously controlled by the same information that was already in the zygote.

    You say:

    “Calling it “intelligent selection” or the system an “engineering process” can’t help you.”

    I don’t think I need to be helped. The truth is very simple, and everyone can judge for oneself.

    So, with your permission, or without it, I will go on calling it “Intelligent Selection”, and the system an “engineering process”.

    Ans self-congratulating, obviously.

  203. 203
    gpuccio says:

    Dionisio:

    Good strategy!

    You know, an annoyed enemy is a good sign. 🙂

    Indeed, I usually try to be kind to my interlocutors, but there are limits…

  204. 204
    Dionisio says:

    gpuccio

    The two consecutive posts in this link seem interesting:

    http://www.uncommondescent.com.....ent-547437

  205. 205
    gpuccio says:

    Dionisio:

    Yes, very interesting indeed! Still new aspects of nucleosome architecture in epigenetic regulation. The scenario becomes more complex with each new day. 🙂

    I will read them carefully later, and comment.

  206. 206
    Dionisio says:

    gpuccio

    Maybe another OP in the oven?

    🙂

  207. 207
    Joe says:

    REC:

    the latter, we’re talking more disease-fighting useful information than the human genome. An enormous antibody repertoire. All due to selection acting on random variation.

    That is your opinion and only an opinion. For all you know it was intelligently designed that way.

    Calling it “intelligent selection” or the system an “engineering process” can’t help you.

    Why can’t it help us? Are you ignorant of what is being debated?

  208. 208
    Silver Asiatic says:

    Curly Howard

    First, disease does not necessarily equate to death.

    I’m talking about those cases where disease does equate to death. To reply that disease does not necessarily equate to death is dodging the difficult problem.
    Death-causing disease attacks organism. No immune system in place. Organism dies. No immune system can evolve step by step from that.

    Also, you are ignoring a major function of the immune system: keeping symbiotic organisms in check. You are painting with too broad of brush strokes.

    Keeping organisms in check is anti-evolutionary. Evolutionary change doesn’t care about preserving an organism. The organism will either die, or it could evolve to a point where it benefits from the disease and is not threatened by it. An immune system does just what you say – keeps the organism in check. Preserving an organism is a means of resisting evolutionary change. This is inexplicable in evolutionary terms.

    Taking the first step in building an immune system would make an organism “more fit” in comparison to the other organisms of the population.

    As above, the organism has to survive several generations against a disease that kills it. It cannot take the first step in that instance. If there are, for example, 20 steps required to resist a death-dealing disease, the population has to survive longer with a non-effective immune system. But the population also has competitors. If the disease is not deadly to competition, then no immune system will ever emerge.

  209. 209
    Dionisio says:

    gpuccio

    FYI – added a few references to recent papers in the same link indicated in post #205. You may want to review them at your convenience.

  210. 210
    Curly Howard says:

    So let’s take this very simple example silver:

    Species is susceptible to a bacterial pathogen.
    In one organism of the population a protein evolves that binds and blocks the pathogen.
    That organism is more likely to survive as is its offspring who also have this protein.

    How is that not an example of the first step in evolving an immune system?

    Keeping organism in-check is anti-evolutionary? Have you never heard of symbiosis? It’s a huge field in evolutionary biology. In no way does it violate evolution. If two species benefit each other under certain conditions then it will be beneficial for those organisms to coexist, typically with the multicellular host keeping a single-cellars organism in check to some degree.

    And no, an organism does not have to survive several generations, nor does there necessarily need to be 20 steps. Why not just one? As long as the gene remains in the population long enough for natural selection to work on it, it has the potential to provide the species with a very basic immune system. And I would expect a system that directly increases survival rate to spread quickly through a population over time.

  211. 211
    Box says:

    Curly Howard: Species is susceptible to a bacterial pathogen.
    In one organism of the population a protein evolves that binds and blocks the pathogen.
    That organism is more likely to survive as is its offspring who also have this protein.

    Obviously the new protein production must be regulated. IOW there is the necessity of a host of associated stuff that simultaneously needs to evolve with the new protein. And – you guessed it – that associated new stuff needs to be regulated as well. So it turns out that your “very simple example” is not simple at all.
    Arguably the most profound mystery of animal life is ‘homeostasis’.

  212. 212
    Curly Howard says:

    The protein does not necessarily need to develop its own regulation system. Co-opting the regulatory mechanisms of the protein it evolved from is quite possible and does not require “a host of associated stuff.” The highly regulated systems we see today are the product of many years of evolution.

    The only necessity would be appreciable amounts of this new pathogen-binding protein. It does not need to be highly regulated, only expressed continuously at low levels I would argue.

  213. 213
    Dionisio says:

    #213 Curly Howard

    Are you referring to the case in gpuccio’s OP or to an imaginary situation?

    What would trigger the production of every required protein at the right time and location and in the required amount?

    Can you explain how to get the mechanisms described in gpuccio’s OP?

    Thank you.

  214. 214
    DATCG says:

    Gpuccio,
    Thought you would appreciate this link. Work is already done for you on examples of IC. Well, at least in sharing the concept other than from Dr. Behe.

    A research paper shows Immune System molecular machinery being Irreducibly Complex with 12 parts, none of which can be removed without failure. Seems they understand the concept…

    Molecular Machine Irreducibly Complex

    “The structure of this biological machine is conceptually similar to an engineer’s blueprint, and it explains how each of the parts in this complex assemble into a functional complex that efficiently identifies viral DNA when it enters the cell,” Wiedenheft said. “This surveillance machine consists of 12 different parts and each part of the machine has a distinct job. If we’re missing one part of the machine, it doesn’t work.”

    Each part is essential for the machine to function. 🙂

    I posted links above by non-ID Scientist searching for and defining Design Principles – Cell Computer – on Optimal Resource management in the cell.

    Now, we see IC is a valid Design Principle of cellular technology. It should become accepted as such in the future. I suspect had it not been offered by an ID proponent as Dr. Behe, it would be far more acceptable today. Hopefully such bias will be dropped in the future.

  215. 215
    Box says:

    Curly Howard #213

    In effect you are saying that new proteins don’t ‘necessarily’ need regulating. I find that hard to believe for several reasons. One is that under materialism an organism is a bag of chemicals which performs a mysterious balancing act: an ever-changing ‘equilibrium’ is somehow being preserved. Now a new chemical is added to the mix. Why on earth doesn’t it need to be highly regulated – especially from a materialistic viewpoint?

    In reality organisms can deal with all sorts of new stuff, but that only proves that materialism is unable to describe life.

    Talbott: Scientists can damage tissues in endlessly creative ways that the organism has never confronted in its evolutionary history. Yet, so far as its resources allow, it mobilizes those resources, sets them in motion, and does what it has never done before, all in the interest of restoring a dynamic form and a functioning that the individual molecules and cells certainly cannot be said to “understand” or “have in view”.

  216. 216
    DATCG says:

    Dionisio, likewise, thanks 🙂 Enjoying this post as I have time.

    Curly,

    The Co-Option Model of Protein Evolution makes assumptions which must be tested. ID scientist Douglas Axe, Gauger, and Reeves have recently completed a series of test for the Co-Option Model to address Darwinist claims against Irreducible Complexity.

    Biologic Institute’s Groundbreaking Peer-Reviewed Science Has Now Demonstrated the Implausibility of Evolving New Proteins

    Links to research papers are provided in the article.

    Conclusion…

    Based on these results, we conclude that conversion to BioF2 function would require at least two changes in the starting gene and probably more, since most double mutations do not work for two promising starting genes. The most favorable recruitment scenario would therefore require three genetic changes after the duplication event: two to achieve low-level BioF2 activity and one to boost that activity by overexpression. But even this best case would require about 10^15 years in a natural population, making it unrealistic. Considering this along with the whole body of evidence on enzyme conversions, we think structural similarities among enzymes with distinct functions are better interpreted as supporting shared design principles than shared evolutionary histories.

    and wrap up…

    This new paper thus provides a robust disproof of the co-option model, overturning a cornerstone argument that evolutionists have long used when trying to answer ID arguments like irreducible complexity. By testing the co-option model, Biologic Institute is not just asking the right questions and doing innovative research that addresses key issues in the debate over Darwinian evolution and intelligent design. They’re also finding data that confirms that ID’s earliest arguments were right all along.

    Another paper is cited with possible ramification to Co-Option Model…

    The Extinction Dynamics of Bacterial Pseudogenes

    Pseudogenes have traditionally been viewed as evolving in a strictly neutral manner. In bacteria, however, pseudogenes are deleted rapidly from genomes, suggesting that their presence is somehow deleterious. The distribution of pseudogenes among sequenced strains of Salmonella indicates that removal of many of these apparently functionless regions is attributable to their deleterious effects in cell fitness, suggesting that a sizeable fraction of pseudogenes are under selection.

    Why it is important…

    Don’t miss the profound importance of this. What it means is that there is very likely a fitness cost associated with carrying an extra, useless copy of a gene, and therefore it can be advantageous to delete duplicate version. This has major implications for the co-option model of protein evolution, because it shows that producing a new protein does not involve “neutral evolution,” but rather requires steps that very likely will impose a deleterious effect upon the organism.

    So, when you say Co-Option is “quite possible.” What are you basing your statement on? These series of test by Biologic Institute shows the difficulty of such assumptions.

  217. 217
    Curly Howard says:

    Nowhere did I say that new proteins don’t need regulating. What I said was that they don’t need to be highly regulated. There will always be some form of regulation present and there is always a continuum of regulation when comparing the expression of different protein products. In this case the protein product needs little regulatory control to have its effect. Simply expressing the protein at low levels will provide the organism with the ability to block the pathogen. It is through evolution that a simple system like this can be continuously tweaked so that it becomes highly regulated and diversified into an immune system as complex as those we see today.

    Most of your “balancing act” nonsense doesn’t seem to have anything to do with this hypothetical.

  218. 218
    Curly Howard says:

    Datcg, I was not referring to any specific co-option model. I was assuming some type of alteration in in gene expression, such as exon switching as in the Dscam example I gave a while back.

    Anyways, I’ve started to skim the paper you linked to. Do you know how they made sure that the amino-acid changes they were making didn’t alter protein structure/folding in some unforeseen way? Did they get any atomic structures of their altered proteins? How do they know they weren’t creating a binding site that shutdown protein function?

  219. 219
    Dionisio says:

    Curly Howard

    Did you see my post #214?

    Please, would you mind to answer those questions?

    Thanks.

  220. 220
    Box says:

    Curly Howard #218,

    CH: Nowhere did I say that new proteins don’t need regulating. What I said was that they don’t need to be highly regulated.

    Why should we suppose that it can just be added to the mix in various amounts without disrupting the “equilibrium”, which we term homeostasis? Why is a – not highly regulated – new protein to be regarded as “no threat” to the balancing act that an organism – a bag of chemicals under materialism – performs?

    CH: There will always be some form of regulation present (..)

    Why would there “always” be regulation present for a new protein that the organism has never confronted in its evolutionary history?

    CH: (..) and there is always a continuum of regulation when comparing the expression of different protein products. In this case the protein product needs little regulatory control to have its effect.

    What do you even mean by “little regulatory control”? Just a little epigenetic control is necessary? Just a small amount of e.g. histone adjustment in order to express the new protein? Just the evolution of a few new tools (which in turn also need regulation) to break down the new protein are necessary to gain a little regulatory control over the new protein when concentrations are getting to high? Does the term ”little” make this evolutionary just-so-story any more likely?

    CH: Simply expressing the protein at low levels will provide the organism with the ability to block the pathogen.

    What part is “simple” about expressing the protein at low levels?

    CH: Most of your “balancing act” nonsense doesn’t seem to have anything to do with this hypothetical.

    Dear Curly H., if one’s position doesn’t make any sense, it is better to stay silent.

  221. 221
    Dionisio says:

    Curly Howard

    Did you ever respond to my post #157?

    Here’s the link:

    http://www.uncommondescent.com.....ent-547249

    If you did, please point to your post where I can read your comments on my post #157.
    Thanks.

  222. 222
    Dionisio says:

    #221 Box

    if one’s position doesn’t make any sense, it is better to stay silent.

    What if they believe their presuppositions make sense?

    🙂

  223. 223
    Curly Howard says:

    Box, how would the expression of this hypothetical new protein at low levels effect homeostasis? Why do you assume a new protein would disrupt homeostasis?

    There will always be some form of regulatory control of a gene that is expressed, whether it is a complex regulatory network or simply the ability to recruit RNA polymerase, there is some form or regulation.

    There are hundreds, probably thousands of ways in which a new protein could be regulated. In this hypothetical example I am assuming that the new protein co-opts some or all of the regulatory mechanisms of the protein it has evolved from.

    I agree, if your position doesn’t make sense, you should stay silent.

    You should heed your own advice.

  224. 224
    Box says:

    Dionisio #223,

    As you know, homeostasis – preserving the magical equilibrium – is a point I often raise. Besides hand waving of the sort that Curly Howard offers – “new proteins do not need to be highly regulated” – evolutionists are utterly unresponsive.
    I hold that a new protein without regulation is comparable to an extra set of wings for a fruit fly without attachment to the nervous system and without muscles.

  225. 225
    Silver Asiatic says:

    Curly Howard 211

    Thanks for your reply – and your follow up with Box and DATCG.

    Species is susceptible to a bacterial pathogen.
    In one organism of the population a protein evolves that binds and blocks the pathogen.
    That organism is more likely to survive as is its offspring who also have this protein.

    Ok, but in this case, the organism can survive attacks from the pathogen without needing an immune system. So, an organism that binds and blocks the pathogen will have an evolutionary advantage – yes, that works fine.

    However, pathogens will tend to kill the organism in many cases. So, in those cases, the pathogen will just kill the organisms and no evolution will result. Beyond that, an immune system blocks the pathogen to preserve the organism. But this makes the organism resistant to evolving new, more sophisticated features of its own. Why not evolve to eat the pathogen? Why should it block it?
    Why not evolve to become more like the pathogen? Why evolve a complex blocking mechanism – and why do so many organisms evolve the same kind of thing rather than merely evolve new features as speciation would expect and require?

    The reason it is anti-evolutionary is that the evolution story requires organisms to develop a massively diverse and increasingly complex variety of features. If the organism preserves itself in its present state – that halts the process of evolution.

    And no, an organism does not have to survive several generations, nor does there necessarily need to be 20 steps. Why not just one?

    I’m talking about cases whether the pathogen causes death and there is no immune system.
    You can’t build a new immune system if the organism dies – it can’t reproduce. Plus, you can’t build an immune system in one step. Several parts have to work together for the system to function. That’s why its irreducibly complex.

  226. 226
    Box says:

    Curly Howard: Box, how would the expression of this hypothetical new protein at low levels effect homeostasis? Why do you assume a new protein would disrupt homeostasis?

    I will repeat myself one more time. If you remain unresponsive then our discussion ends.

    Under materialism an organism is a bag of chemicals, which (miraculously) preserves an equilibrium. As far as we understand the process this is done by regulators which are in turn regulated by other regulators – without a “master-regulator” in sight. IOW everything is well organized and highly regulated.
    The entrance of a new protein is comparable to the appearance of a group of complete strangers with hammers in the main assembly hall of Lamborghini.
    You ask me “why do you assume a new protein would disrupt homeostasis?“, but in fact it is the other way around: it is evolutionists like you who assume – in defiance of basic logic – that the introduction of a new protein is possible without disrupting homeostasis.

  227. 227
    DNA_Jock says:

    Silver Asiatic, you appear to switch randomly between talking about individual organisms and populations of organisms. You seem deeply muddled.

    However, pathogens will tend to kill the organism in many cases. So, in those cases, the pathogen will just kill the organisms and no evolution will result.

    Actually, this is extremely rare. Pathogen infections have mortality rates between 1% and 99%, with almost all being in the lower half of that range. Ebola and untreated bubonic plague have ~50% mortality rates. Yes, a pathogen could cause the extinction of a species but that is very very rare. And bad news for the pathogen. Read up about predator-prey dynamics…

    Beyond that, an immune system blocks the pathogen to preserve the organism. But this makes the organism resistant to evolving new, more sophisticated features of its own.

    WTF? Why on earth?

    Why not evolve to eat the pathogen? Why should it block it?

    Organisms could do that too. Phagocytes.

    Why not evolve to become more like the pathogen?

    This makes no sense whatsoever. We should become more like ebola? Or trypanosomes? Or Yersinia? Which one would you pick? How would that help?

    Why evolve a complex blocking mechanism – and why do so many organisms evolve the same kind of thing rather than merely evolve new features as speciation would expect and require?

    Common descent.

  228. 228
    DNA_Jock says:

    Box wrote:

    You ask me “why do you assume a new protein would disrupt homeostasis?“, but in fact it is the other way around: it is evolutionists like you who assume – in defiance of basic logic – that the introduction of a new protein is possible without disrupting homeostasis.

    You do know that thousands of new proteins have been introduced into many different species (and expressed at extremely high levels) without any disruption of homeostasis? The entire biotechnology industry is based on this simple fact.
    Yikes.

  229. 229
    Box says:

    DNA-Jock #229,

    Yes, indeed reality contradicts any materialistic view on organisms. Read my post #216, from “In reality organisms can deal with all sorts of new stuff …”

  230. 230
    Dionisio says:

    #225 Box

    You have a good point. Thank you.

  231. 231
    DNA_Jock says:

    Box,

    Your original point was “Obviously the new protein production must be regulated.”

    But here you recognize that reality contradicts this view, and eliminates your objection to Howard’s scenario. So your complaint is that, according to your understanding of the “materialist” position, new protein production should require regulation.

    I think we can move on.

  232. 232
    Silver Asiatic says:

    DNA_Jock

    You do know that thousands of new proteins have been introduced into many different species (and expressed at extremely high levels) without any disruption of homeostasis?

    As Box pointed out, you’re merely restating the problem.

  233. 233
    Silver Asiatic says:

    DNA_Jock

    Actually, this is extremely rare. Pathogen infections have mortality rates between 1% and 99%, with almost all being in the lower half of that range.

    Topic: Building immune systems step-by-step before immune systems existed.
    Your response? Pathogen mortality rates are low among organisms that already have immune systems in place.

    Your assumptions are getting in the way of your explanations. You have to explain how and why the first immune systems were developed.

    Yes, a pathogen could cause the extinction of a species but that is very very rare.

    You know how many species went extinct before immune systems existed?

    This makes no sense whatsoever. We should become more like ebola? Or trypanosomes? Or Yersinia? Which one would you pick? How would that help?

    Muddled thinking?

    You begin your explanation of the origin of immune systems with how human beings would evolve.

    No, you have to start in a world where there are no immune systems, and then explain how they developed step-by-step.

    You’re defending the grand evolutionary story, remember? Bacteria became human beings. But they also developed immune systems to preserve the organism in its present state. Preservation of the current state is an obstacle to speciation. Adding to that, as Box pointed out, organisms exhibit homeostasis which preserves a equilibrium – and is thus a barrier to evolutionary change.

    With that, you might want to address to OP, DNA_Jock:

    You have it all here: molecular complexity, high control, multiple cellular interactions, irreducible complexity in tons, spacial and temporal organization, extremely efficient engineering. The process is so delicate that errors in it are probably the cause of many human lymphomas.

    Errors in the process are the cause of deadly diseases. That’s why the step-by-step evolution of the process doesn’t work.

    So, to sum up. two different complex algorithms act to ensure efficient immune responses.

    Step by step development of algorithms. That’s what you need to explain.

    Both processes are wonderful examples of sophisticated engineering and irreducibly complex systems, and they are completely different one from the other. Both processes work together in sequence in a sophisticated and irreducibly complex meta-system.

    Again, the origin of two processes working in sequence when previously there was none – that’s the challenge.

    Both use controlled random variation to generate diversity. The second process also uses intelligent selection based on existing information from the environment (the epitope conserved in the Follicular GC cell).

    My comments were far more simplistic than this. I’m just looking at the enormous gap in the explanatory power of evolutionary stories. There is no reason for this complex system to evolve in order to resist pathogens and preserve the organism.

  234. 234
    DNA_Jock says:

    Silver,

    Like I said, read up on predator-prey dynamics. Your inability to distinguish between a population and an individual organism is noted.

    Topic: Building immune systems step-by-step before immune systems existed.

    Not really. The topic is antibody affinity maturation.

    No, you have to start in a world where there are no immune systems, and then explain how they developed step-by-step.

    Reading up on innate immunity might help some, too.

  235. 235
    Box says:

    DNA_Jock #232,

    DNA_Jock: Your original point was “Obviously the new protein production must be regulated.”

    Yes, and it still is. If we assume the (unlikely) event of the coming into existence (by evolutionary means) of a new protein, then we must also assume the coming into existence of a matching set of regulators – like an extra set of wings for the fruit fly needs muscles and a connection to the nervous system.
    IOW the probability of the coming into existence of a matching set of regulators by evolutionary means needs to be factored in when we assess the probability of the coming into existence of a (functional) new protein by evolutionary means. And surely I agree with you that this does make evolution look even worse.

    DNA_Jock: But here you recognize that reality contradicts this view, and eliminates your objection to Howard’s scenario.

    If organisms find ways to regulate new proteins by non-evolutionary means – because an organism is something else than a bag of chemicals – then this doesn’t exempt evolutionary theory from factoring in the probability of the coming into existence of a regulatory apparatus by evolutionary means.
    IOW if an evolutionary biologist states “there are no non-chemical or non-evolutionary means”, then the coming into existence of a regulatory apparatus by evolutionary means need to be factored in for each new protein.

    DNA_Jock: So your complaint is that, according to your understanding of the “materialist” position, new protein production should require regulation.

    Now, there is no understanding of the materialist position which accommodates for unregulated new proteins; right? However there are many materialists who prefer not to think about that.

  236. 236
    DNA_Jock says:

    As to the stuff you added:

    You have it all here: molecular complexity, high control, multiple cellular interactions, irreducible complexity in tons, spacial and temporal organization, extremely efficient engineering. The process is so delicate that errors in it are probably the cause of many human lymphomas.
    Both processes are wonderful examples of sophisticated engineering and irreducibly complex systems, and they are completely different one from the other. Both processes work together in sequence in a sophisticated and irreducibly complex meta-system.
    Both use controlled random variation to generate diversity. The second process also uses intelligent selection based on existing information from the environment (the epitope conserved in the Follicular GC cell).

    Bafflegab that reduces to “it’s complicated, therefore design”, as I noted previously.
    Your incredulity is not evidence of anything except, perhaps…

  237. 237
    Silver Asiatic says:

    You’re supposed to offer some kind of explanation, DNA_Jock.

    I’d say, “it’s complicated, therefore evolution has a very big problem”.

  238. 238
    DNA_Jock says:

    You’re supposed to offer some kind of explanation, DNA_Jock.

    I’d say, “it’s complicated, therefore evolution has a very big problem”.

    I’m willing to say, “I don’t know” and let people who understand immunology far better than I do figure it all out. They have a pretty impressive track record. It’s the people who wish to conclude design who must, according to the Isaac Newton of Information Theory, eliminate all possible chance hypotheses.

    You are going to have to learn a lot more biology…

    It’s fun — enjoy!

  239. 239
    Zachriel says:

    Silver Asiatic: No, you have to start in a world where there are no immune systems, and then explain how they developed step-by-step.

    One of the first steps was the ability of the organism to distinguish between food and itself or other like organisms. Amoebas have this basic ability, and macrophages often resemble amoebas in their behavior.

  240. 240
    gpuccio says:

    To all:

    Sorry, I was busy. I will try to catch up with the discussion.

    By the way, have you looked at this post?

    http://www.uncommondescent.com.....a-article/

    The CRISPR issue is not only pertinent for neo Lamarkism. It is also pertinent to the discussion here, in a way.

    It seems that even prokaryotes have an “adaptive immune system” of a sort. Completely different, but many principles are the same.

    Fascinating.

  241. 241
    gpuccio says:

    Well, it seems that there is not much to catch up with. No arguments from the other side. Boring.

  242. 242
    gpuccio says:

    Here is a very simple description of the process of VDJ recombination, from the Wikipedia page:

    Process[edit]
    V(D)J recombination begins when V(D)J recombinase (through the activity of RAG1) binds an RSS flanking a coding gene segment (V, D, or J) and creates a single-strand nick in the DNA between the first base of the RSS (just before the heptamer) and the coding segment. This is essentially energetically neutral (no need for ATP hydrolysis) and results in the formation of a free 3′ hydroxyl group and a 5′ phosphate group on the same strand. The reactive hydroxyl group is positioned by the recombinase to attack the phosphodiester bond of opposite strand, forming two DNA ends: a hairpin (stem-loop) on the coding segment and a blunt end on the signal segment.[11] The current model is that DNA nicking and hairpin formation occurs on both strands simultaneously (or nearly so) in a complex known as a recombination center.[12][13][14][15]

    The blunt signal ends are flushly ligated together to form a circular piece of DNA containing all of the intervening sequences between the coding segments known as a signal joint (although circular in nature, this is not to be confused with a plasmid). While originally thought to be lost during successive cell divisions, there is evidence that signal joints may re-enter the genome and lead to pathologies by activating oncogenes or interrupting tumor suppressor gene function(s).

    The coding ends are processed further prior to their ligation by several events that ultimately lead to junctional diversity.[16] Processing beings when DNA-PK binds to each broken DNA end and recruits several other proteins including Artemis, XRCC4, DNA ligase IV, Cernunnos, and several DNA polymerases.[17] DNA-PK forms a complex that leads to its autophosphorylation, resulting in activation of Artemis. The coding end hairpins are opened by the activity of Artemis.[18] If they are opened at the center, a blunt DNA end will result; however in many cases, the opening is “off-center” and results in extra bases remaining on one strand (an overhang). These are known as palindromic (P) nucleotides due to the palindromic nature of the sequence produced when DNA repair enzymes resolve the overhang.[19] The process of hairpin opening by Artemis is a crucial step of V(D)J recombination and is defective in the severe combined immunodeficiency (scid) mouse model.

    Next, XRCC4, Cernunnos, and DNA-PK align the DNA ends and recruit terminal deoxynucleotidyl transferase (TdT), a template-independent DNA polymerase that adds non-templated (N) nucleotides to the coding end. The addition is mostly random, but TdT does exhibit a preference for G/C nucleotides.[20] As with all known DNA polymerases, the TdT adds nucleotides to one strand in a 5′ to 3′ direction.[21]

    Lastly, exonucleases can remove bases from the coding ends (including any P or N nucleotides that may have formed). DNA polymerases ? and ? then insert additional nucleotides as needed to make the two ends compatible for joining. This is a stochastic process, therefore any combination of the addition of P and N nucleotides and exonucleotlytic removal can occur (or none at all). Finally, the processed coding ends are ligated together by DNA ligase IV.[22]

    All of these processing events result in an antigen-binding region that is highly variable, even when the same gene segments are recombined. V(D)J recombination allows for the generation of immunoglobulins and T cell receptors to antigens that neither the organism nor its ancestor(s) need to have previously encountered, allowing for an adaptive immune response to novel pathogens that develop or to those that frequently change (e.g., seasonal influenza). However, a major caveat to this process is that the DNA sequence must remain in-frame in order to maintain the correct amino acid sequence in the final protein product. If the resulting sequence is out-of-frame, the development of the cell will be arrested, and the cell will not survive to maturity. V(D)J recombination is therefore a very costly process that must be (and is) strictly regulated and controlled.

    Irreducibly complex? You judge.

    I anticipate DNA_Jock and his creative criticism:

    “Bafflegab that reduces to “it’s complicated, therefore design””

  243. 243
    gpuccio says:

    So, the simple idea of our friends is: it’s not them that have to explain how that process appeared in vertebrates. The task is entirely ours (design fans). We have to eliminate all possible “chance hypotheses”.

    What chance hypotheses, you may ask. Not clear. All those hypotheses that we don’t know, and maybe never will know, which may include chance or not, or any possible mechanism of which we have no idea, but who can ever say?

    So, in the light of such a happy epistemology, if something were really designed, we could never, never know it. It is obviously impossible to falsify all possible unknown, unseen, unsuspected hypotheses.

    So, in the light of such a happy epistemology, if something were really designed, science will always believe that it is not, and nobody will ever think that there is any reason to explain it in a non design way.

  244. 244
    DNA_Jock says:

    What chance hypotheses, you may ask. Not clear. All those hypotheses that we don’t know, and maybe never will know, which may include chance or not, or any possible mechanism of which we have no idea, but who can ever say?

    Well, I didn’t say it would be easy. But you should take your complaints to the the Isaac Newton of Information Theory: he’s the one who came up with that requirement.
    The amusing thing is that no-one has even tried to quantify the chance hypothesis. Ever.
    Cue off-topic rant re strings over 500 bits…

  245. 245
    DATCG says:

    Gpuccio, yes, the CRISPR research is fascinating indeed.

    I agree, no arguments from other side other than a series of bluffs. And the mantra that blind, unguided events evolve – poof – from simple non-systems step by step into more specified, and directed complex systems.

    It can happen. They offer no evidence, but Double Standards are high. The ID scientist must prove it can’t evolve first.

    But, even when shown research by scientist a “disproof of concept” of the co-option model. they balk. They bluff. Suddenly the system is not so simple. It’s more precarious than we were told. The “simple” might have proteins folds wrong in the lab.

    Not that other labs have shown the research cannot be duplicated. Just a series of bluffs.

    Biologic Institute’s Groundbreaking Peer-Reviewed Science Has Now Demonstrated the Implausibility of Evolving New Proteins

    Instead of producing lab results of their own that counter the Biologic Institute’s research, bluffing is the answer.

    In science, once research has been done and conclusions offered, other scientist either duplicate the same series of test or show it cannot be duplicated.

    As shown, neo-Darwinist need to perform the same research. Biologic Institute has in fact provided a “disproof of concept” or they have not.

    If Neo-Darwinist can counter research done by Douglas Axe, Gauger and Reeves at Biologic Institute, they will have direct evidence of neo-Darwinian claims.

    So go for it Neo-Darwinist and stop bluffing.

  246. 246
    Curly Howard says:

    Silver, yes the pathogen will kill many organisms of that species as it has been for however many years, but it will not be able to kill this organism that has evolved this protein. This organism has increased its ability to survive as will its offspring. Evolution will certainly result, eventually the vast majority, if not all, of the population will express this protein. You’re not making any sense when you say “an immune system blocks the pathogen to preserve the organism. But this makes the organism resistant to evolving.” The ability to survive and thrive better than other organisms within your population or niche most certainly does not make you resistant to evolution. An increased ability to survive means you and your offspring will represent increasing proportions of the population who will also undergo evolutionary changes that either benefit survival or do not. The subpopulation with beneficial changes will again spread throughout the population.

    Evolving to block a pathogen is the simplest form of immune response I can think of. Antibodies still do it today against viruses and toxins, all the protein has to do is bind the pathogenic molecule. Nothing too complex about it.

    “Become more like the pathogen?” I have no idea what that means.

    Maybe they evolve the same kind of systems because these systems stem from the same precursors, although I’m not really sure what you are talking about when you say “evolve the same kind of thing.”

    No organism is preserving itself in its present state, organisms are constantly changing. Although different species change at different rates and to different degrees, depending on an infinite number of factors.

    “I’m talking about cases whether the pathogen causes death and there is no immune system.”
    No sh*t. That’s what we’ve been talking about, except for the fact that I’m arguing that one organism in this population develops a protein that has this most basic immune system function.

    In my hypothetical, the protein evolves from another protein through exon switching, so it is expressed at low levels along with the original protein. This new protein can bind and block a pathogen. How is that not the evolution of an immune system (however basic) in one step?

  247. 247
    Curly Howard says:

    Box, your homeostasis argument makes absolutely no sense. The word homeostasis and equilibrium in the context you are using them refers to any number of conditions including pH, temperature, concentration of oxygen, or CO2, osmolarity, etc. Changing these by a significant amount quickly results in death in most cases. My protein would have little effect on most of these and if it does have an effect, it would be negligible because there are plenty of other proteins already being expressed and floating around in the same place. The small change this new protein would cause would be completely washed out by what is already going on in the organism.

    Your Lamborghini assembly hall analogy is awful.

    I ask “why do you assume a new protein would disrupt homeostasis?” because there is absolutely no reason to assume the expression of an extra protein would disrupt homeostasis. In order for a new protein to shutdown homeostasis in a multicell organism, it would need to have a very specific and harmful effect. These are seen in toxins/poisons of certain predators/pathogens.

    If you are going to insist that this hypothetical protein will most certainly disrupt homeostasis, you are going to need to give me at least one specific example that makes physiological sense.

  248. 248
    Silver Asiatic says:

    Gpuccio @ 244

    So, the simple idea of our friends is: it’s not them that have to explain how that process appeared in vertebrates. The task is entirely ours (design fans). We have to eliminate all possible “chance hypotheses”.

    Excellent point – and brilliantly framed. We show our friends an impossibly sophisticated system and ask them to offer a convincing explanation of their own theory. They reply by putting the burden on us to eliminate chance hypotheses. Of course, the best chance hypothesis they’ve got is that there were some lucky mutations and “it just happened”. That’s irrefutable.

    So, in the light of such a happy epistemology, if something were really designed, we could never, never know it. It is obviously impossible to falsify all possible unknown, unseen, unsuspected hypotheses.

    Good point. Of course we will never know when we’ve eliminated the last possible chance hypothesis also — so design will always remain an open issue, as you stated so well.

    But I’ll still walk away from the discussion without having received a convincing explanation for what we know is happening in that cellular system.

  249. 249
    Upright BiPed says:

    Just skimming the thread…

    It’s unsettling to hear that you can so boldly make the claim that these systems are irreducibly complex without having actually identified the irreducible core of the systems

    These arguments against IC are dead. Dead.

    IC is required to translate information into a physical effect. The cell does not become organized without it.

  250. 250
    Curly Howard says:

    It was by gpuccio’s definition that an irreducibly complex system has an irreducibly complex core. I asked what it was, he admitted he hadn’t tried to identify it before he declared the system irreducibly complex. It couldn’t be more clear that his method for applying the idea of irreducible complexity amounts to “wow that’s complex! It has to be designed!”

  251. 251
    Upright BiPed says:

    As I said, I am only skimming the thread.

    And it remains true that IC counterarguments in biology are dead. The irreducible core of a translation apparatus is easily named and coherently understood.

  252. 252
    gpuccio says:

    UB:

    A very simple quote from Wikipedia (see post #243) is more than enough to show why the VDJ recombination (which is only part of the story) is Irreducibly Complex. Indeed, I wanted to make a more reasoned and documented argument, but as Curly Howard has promptly shown his malevolence and his inability to distinguish between a simple judgement and a detailed argumentation, why should I waste time for his sake? Wikipedia will suffice.

    Our interlocutors have really showed the worst of themselves in this thread. Zero arguments, not even attempts. However, CH and REC have succeeded in being unfair and rude, while DNA_Jock (a pale shadow of the discussant I remember from the recent past) has apparently chosen pseudo-obtusity as the best weapon. I suggest for him and his fellows the following formalization of thought which, if reasonably enforced, will certainly help neutralize all the disturbing ID anarchists before they annoy any more the scientific world:

    a) Definition: universal chance hypothesis: any possible hypothesis that could ever be formulated by any entity in the whole multiverse (indeed, in the whole multiverse of multiverses), and which can include all conceivable and inconceivable mechanisms and non mechanisms, including chance, determinism, compatibilism, magic and simple bad luck. Number of chance hypotheses: infinite. Cardinality of the set: at least aleph one.

    b) Statement: IDists must efficiently and possibly redundantly falsify all universal chance hypotheses before they can state anything.

    c) Statement: Non IDists can happily stick to their unsupported ideas unless and until IDists accomplish b).

    I hope our interlocutors will appreciate the epistemological help.

  253. 253
    gpuccio says:

    DATCG:

    Yes, the Gauger – Axe paper is very interesting, and a clear demonstration of how some unbiased research could easily clarify at least a few aspects of the ID neo darwinism debate, for example give better understanding of the protein functional space. But, obviously, those who have the resources have no motivation to do that. For them, those things are best left undecided.

  254. 254
    Box says:

    Curly Howard: Box, your homeostasis argument makes absolutely no sense.

    My argument is that new proteins needs regulation otherwise homeostasis will be disrupted. According to you this makes “absolutely no sense”, okay let’s hear it.

    Curly Howard: The word homeostasis and equilibrium in the context you are using them refers to any number of conditions including pH, temperature, concentration of oxygen, or CO2, osmolarity, etc. Changing these by a significant amount quickly results in death in most cases.

    Yes. And, I might add, also unregulated tiny amounts of new proteins can build up to significant amounts.

    Curly Howard: My protein would have little effect on most of these (…)

    Oh really?

    Curly Howard: (…) and if it does have an effect, it would be negligible (…)

    And why is that?

    Curly Howard: (…) because there are plenty of other proteins already being expressed and floating around in the same place. (…)

    Wait a minute here. Because there are plenty of other proteins already being expressed and floating around in the same place the effects of a new protein on homeostasis are negligible? Does that make sense?

    Curly Howard: The small change this new protein would cause would be completely washed out by what is already going on in the organism.

    “Completely washed out”? IOW there is so much going on in the cell, that one or two groups of extra (new) proteins don’t need regulation like all the other proteins, because … well … it is such a busy place … so … small amounts anyway … hardly noticeable when so much is going on already … and that’s why the ‘homeostasis argument’ makes absolutely no sense …
    BTW without regulation, how do you arrive at “small amounts”? And I have asked you before: What part is “simple” about expressing the protein at low levels?. Moreover if the cell has no tools to measure the right amount of the new protein and/or no tools to break down the new protein, why must we assume that the amount of the new protein – even if we assume low level expression – doesn’t keep building up intolerably over time?

    Curly Howard: Your Lamborghini assembly hall analogy is awful.

    I maintain that the comparison of a new protein with the appearance of a group of complete strangers with hammers in the main assembly hall of Lamborghini is apt. It is your “rebuttal” that the assembly hall is a busy place that doesn’t make any sense.

  255. 255
    gpuccio says:

    DNA_Jock:

    Always in the helping trend, here are a few synonyms that you could use in your future arguments, courtesy of Dictionary.com:

    Bafflegab: gobbledegook, abracadabra, artifice, cant, chant, charm, cheating, chicanery, conjuring, deceit, deception, delusion, flimflam, fraud, gibberish, hoax, humbug, imposture, incantation, jargon, juggling, legerdemain, magic, mummery, mystification, nonsense, occultism, rigmarole, spell, swindle, trick, trickery, hocus, magic words, monkey business, mumbo jumbo, open sesame, sleight of hands, smoke and mirrors

    Rant: yelling, raving, diatribe, harangue, oration, rhetoric, tirade, bluster, bombast, fustian, philippic, rhapsody, rodomontade, vociferation

    Ah, I love English! At least, let’s try to keep our language (ehm, gobbledegook) picturesque.

  256. 256
    gpuccio says:

    Dionisio:

    If you don’t mind, I would like to paste here one of your recent posts in the Mystery at the heart of life thread:

    Crystal structure of the CRISPR RNA–guided surveillance complex from Escherichia coli

    DOI: 10.1126/science.1256328

    Clustered regularly interspaced short palindromic repeats (CRISPRs) are essential components of RNA-guided adaptive immune systems that protect bacteria and archaea from viruses and plasmids.

    In Escherichia coli, short CRISPR-derived RNAs (crRNAs) assemble into a 405-kilodalton multisubunit surveillance complex called Cascade (CRISPR-associated complex for antiviral defense).

    Here we present the 3.24 angstrom resolution x-ray crystal structure of Cascade.

    Eleven proteins and a 61-nucleotide crRNA assemble into a seahorse-shaped architecture that binds double-stranded DNA targets complementary to the crRNA-guide sequence.

    Conserved sequences on the 3′ and 5′ ends of the crRNA are anchored by proteins at opposite ends of the complex, whereas the guide sequence is displayed along a helical assembly of six interwoven subunits that present five-nucleotide segments of the crRNA in pseudo–A-form configuration.

    The structure of Cascade suggests a mechanism for assembly and provides insights into the mechanisms of target recognition.

    http://www.sciencemag.org/content/345/6203/1473

    Definitely very pertinent. You are the best! 🙂

    Irreducibly Complex? Everyone judge for oneself.

    Here is some more detail form the EcoCyc site:

    Escherichia coli K-12 substr. MG1655 Enzyme: CRISPR-associated complex for antiviral defense
    Inferred from experiment
    Synonyms: Cascade

    Subunit composition of CRISPR-associated complex for antiviral defense = [CasA][CasB]2[CasC]6[CasD][CasE]
    Cascade subunit A = CasA (summary available)
    Cascade subunit B = CasB (summary available)
    Cascade subunit C = CasC (extended summary available)
    Cascade subunit D = CasD (summary available)
    crRNA endonuclease = CasE (summary available)

    Summary:
    CRISPR (clusters of regularly interspersed short palindromic repeats) loci are associated with defense against foreign DNA and occur widely in bacteria and archaea [Young08a]. The CRISPR locus of E. coli K-12 is transcribed into a large pre-crRNA. CasE alone or within the Cascade complex is required for processing of pre-crRNA into the mature crRNA. Processed crRNAs of approximately 57 nt copurify with Cascade. In the presence of Cas3, this complex gives rise to resistance against phages whose genomes have regions of complementarity to elements in the CRISPR repeat [Brouns08a].

    Cryo-EM structures of the Cascade complex before and after binding to a target sequence have been solved, showing that the bound crRNA is protected from degradation while still being available for base pairing with the target [Wiedenheft11]. Target nucleotide binding results in a concerted conformational change that may result in recruitment of the Cas3 nuclease [Jore11, Wiedenheft11].

    The 11 Cas proteins assemble with the crRNA into a ‘sea-horse’-shaped structure. CasE forms the head of the complex and binds the 3′ end of the pre-crRNA and positions it for cleavage; CasE, CasA and one subunit of CasC form the tail which contacts the 5′ end of crRNA. The 6 CasC subuits form a helical backbone which along with the 2 CasB subunits connects the head and tail. The crRNA is interwoven into the Cascade complex in a manner that presents segments for target DNA binding [Jackson14]. The crRNA-target DNA hybrid adopts a ribbon conformation rather than a helix; this conformation is facilitated by the structural disruption of base pairing at every 6th nucleotide in the hybrid molecule. Protein-nucleic acid interactions between the DNA-RNA hybrid and the Cascade complex (in particular the helical backbone) stabilise the ribbon conformation [Mulepati14].

    Cas3 as well as a mixture of CasC, CasD and CasE proteins catalyses ATP-independent annealing of RNA with DNA to form hybrid molecules of RNA base-paired into duplex DNA, also known as R-loops [Howard11]. The specificity of the CRISPR system is provided by the formation of R-loops [Jore11]. Strict complementarity between the target and the crRNA is only required in a seven-nucleotide seed region within the protospacer region of crRNAs [Semenova11].

    Review: [Horvath10]

    Molecular Weight: 405.0 kD

    By the way, just to know, for E. coli:

    Cas A: 502 AAs
    Cas B: 160 AAs
    Cas C: 363 AAs
    Cas D: 224 AAs
    crRNA endonuclease (CasE): 199 AAs

    Again, just to know.

  257. 257
    gpuccio says:

    Dionisio:

    More stuff:

    “Structures of the RNA-guided surveillance complex from a bacterial immune system”

    Nature 477, 486–489 (22 September 2011) doi:10.1038/nature10402

    Bacteria and archaea acquire resistance to viruses and plasmids by integrating short fragments of foreign DNA into clustered regularly interspaced short palindromic repeats (CRISPRs). These repetitive loci maintain a genetic record of all prior encounters with foreign transgressors1, 2, 3, 4, 5, 6. CRISPRs are transcribed and the long primary transcript is processed into a library of short CRISPR-derived RNAs (crRNAs) that contain a unique sequence complementary to a foreign nucleic-acid challenger7, 8, 9, 10, 11, 12. In Escherichia coli, crRNAs are incorporated into a multisubunit surveillance complex called Cascade (CRISPR-associated complex for antiviral defence), which is required for protection against bacteriophages13, 14. Here we use cryo-electron microscopy to determine the subnanometre structures of Cascade before and after binding to a target sequence. These structures reveal a sea-horse-shaped architecture in which the crRNA is displayed along a helical arrangement of protein subunits that protect the crRNA from degradation while maintaining its availability for base pairing. Cascade engages invading nucleic acids through high-affinity base-pairing interactions near the 5′ end of the crRNA. Base pairing extends along the crRNA, resulting in a series of short helical segments that trigger a concerted conformational change. This conformational rearrangement may serve as a signal that recruits a trans-acting nuclease (Cas3) for destruction of invading nucleic-acid sequences.

    Emphasis added, just to annoy our interlocutors. 🙂

    And here, on the pertinent Microbe Wiki page:

    https://microbewiki.kenyon.edu/index.php/The_CRISPR_Immune_System_in_Bacteria_and_Archaea

    you can find a good resolution image from that paper:

    https://microbewiki.kenyon.edu/images/e/e6/Cascade.PNG

  258. 258
    gpuccio says:

    Dionisio:

    From the Microbe Wiki page:

    History

    CRISPR sequences were first discovered in 1987 in Escherichia coli. They were observed in other bacterial species and in archaea in 2002. It was first suggested that CRISPR sequences are part of an immune system in 2005. This was due to the discovery of homology between spacer sequences and viral and plasmid DNA. Much has been learned about the function of cas proteins by disabling cas genes. For example, disabling the cas7 gene disrupts the cell’s ability to incorporate new spacers. Disabling the csn1-like gene causes a loss of resistance against phages, even if the relevant spacers are present. This shows that cas genes are necessary for immunity in addition to CRISPR sequences (Horvath and Barrangou. 2010).

    Irreducible complexity?

    And:

    Operation of the CRISPR/cas System

    Figure 2. Overview of the operation of the CRISPR/cas system. A schematic of CASCADE in E. coli is shown here. (Horvath and Barrangou. 2010) http://www.sciencemag.org/content/327/5962/167

    In general, operation of the CRISPR/cas system takes place in four steps:
    1. Spacers corresponding to fragments of DNA from a phage or another source are incorporated into CRISPR. Little is known about this process. However, it is believed to involve the Cas1 and Cas2 proteins. Also, new spacers are added at the leading end of the CRISPR sequence.
    2. CRISPR loci must be transcribed into pre-crRNA. A noncoding sequence at the leading end of CRISPR, rich in adenine and thymine, acts as a promoter for this purpose.
    3. Pre-crRNA must then be processed into crRNA. Each piece of crRNA consists of a single spacer between two half-repeats.
    4. After processing, the crRNA is used to neutralize foreign genetic material (Horvath and Barrangou. 2010).
    The CRISPR/cas system is similar in principle to the RNA interference used by eukaryotic cells; both use short RNA sequences to guide the destruction of foreign DNA by enzymes. However, these two systems employ entirely different sets of proteins. No homology has been found between CRISPR/cas and RNAi (Horvath and Barrangou. 2010), (Lintner et al., 2011).
    Although the alternating spacer repeat structure of CRISPR sequences is conserved across all species, the protein machinery which uses crRNA to destroy foreign genetic material is diverse. In some cases, highly intricate complexes composed of many different proteins are used to destroy foreign DNA (Wiedenheft et al., 2011). In other cases, a single protein with a guide RNA may be sufficient to cleave DNA (Cong et al., 2013). Three important examples of these protein mechanisms are CASCADE (Figure 2), the CMR complex, and Cas9. The CRISPR-associated complex for antiviral defense (cascade) degrades foreign DNA. The CMR complex uses crRNA to neutralize foreign RNA. Cas9 nuclease can accurately cleave DNA, and has great promise for genetic engineering.

    Procedures?

    OK, engineered or not, this has “great promise for genetic engineering”. Lucky us, poor intelligent designers, who can well learn from chance originated solutions (before anyone accuse me that I am saying that neo darwinism is only based on chance, I am using here the word in the ultra-wide meaning sponsored by DNA_Jock).

  259. 259
    gpuccio says:

    Zachriel:

    “One of the first steps was the ability of the organism to distinguish between food and itself or other like organisms. Amoebas have this basic ability, and macrophages often resemble amoebas in their behavior.”

    Sorry for you, but it seems that the concept of distinguishing between self and non self is quite older! (see the discussion about CRISPR).

  260. 260
    gpuccio says:

    To all:

    Just to remind what is obvious, the CRISPR system, although with differences in the specific solutions, is common to bacteria and archaea, so it is quite reasonable to believe that it originated in LUCA, that is 3.5 billion years ago or more.

    The Cas proteins are not extremely conserved between bacteria and archaea, but they have clear homology.

    So, the whole idea of memorizing in some form specific sequences of biological enemies and then using them for a specific, targeted defense, is very, very old.

  261. 261
    gpuccio says:

    Here is an example of a simple BLAST between the E. coli Cas A and Archaea. The best match is:

    CRISPR-associated protein Cse1 [Methanococcoides burtonii]:

    Identities: 122/533(23%)
    Positives: 212/533(39%)
    E = 8e-19

  262. 262
    Dionisio says:

    gpuccio

    Thank you for all that interesting information you have posted! Will take me some time to digest it well.

    Mio caro maestro GP, you may use and/or dispose of my posts as you please. I’m learning a lot from your insightful commentaries. Also enjoying reading the funny ones too. 🙂

    I’ve mostly just posted references to interesting papers written by dedicated researchers, highlighted some text within the abstracts and/or asked questions related to the papers. You’re much better prepared and more knowledgeable to review all that.

    BTW, you may want to check the last two posts (899 & 900) in the ‘third way’ thread.
    http://www.uncommondescent.com.....ent-547839

  263. 263
    Silver Asiatic says:

    Zac

    One of the first steps was the ability of the organism to distinguish between food and itself or other like organisms.

    Here’s the problem in an elementary form. The earliest life forms are merely chemical combinations (as it’s said). But as you point out, somehow these chemicals developed an ability to distinguish between itself and other like organisms.

    This sense of identity is unexplained and conflicts with what one should expect in the evolutionary process. It’s one thing to posit organisms as chemical combinations – but then to see a variety of organisms, each having a sense and preserving their own identity as those specific organisms doesn’t make sense at the chemical level.

    The organisms preserve their identity, but also have enough plasticity to evolve into new species of organisms.

    But any of these organisms are accidental chemical developments. There’s no need for them to preserve an identity or repel invaders.

    The idea that drives all of this is that these chemical assemblies we call ‘organisms’ have a need to ‘survive’ and to preserve themselves as those unique organisms.

    Those are teleological concepts. Chemicals want to survive and when they become organisms, they distinguish themselves from other organisms and want to preserve their identity.

  264. 264
    Silver Asiatic says:

    I’m willing to say, “I don’t know” and let people who understand immunology far better than I do figure it all out. They have a pretty impressive track record.

    That’s an honest reply, but it’s not very convincing, DNA_Jock. You’re defending The Theory. I look for a defense and a convincing explanation on, what appears to me and others as, a hugely difficult problem for evolution. But you just offered a statement of faith. Other people, supposedly, know how it all works. You come across as if evolutionary hypothesis are unquestionable, but clearly you can’t explain the origin of these cellular functions.

    Then, instead of researching your own theory and giving me an explanation, you tell me it’s my job.

    It’s like this — if I was trying to defend or promote my religious views, for example, and you presented a problem you have — what would you think if I said: “I can’t answer that difficulty regarding my own religion, but I just believe it. If you really have a problem with it, go research theology yourself.”

    It’s the people who wish to conclude design who must, according to the Isaac Newton of Information Theory, eliminate all possible chance hypotheses.

    As mentioned by gpuccio, it’s not reasonable to expect an elimination of all possible. The design inference, as with any abductive argument, arrives at a conclusion after a reasonable consideration of alternative views.

    You are going to have to learn a lot more biology…

    You’ve got a captive audience of people like me – non-specialists. I’m open to explanations.

    At the same time, it appears you’re saying ‘the answer is out there somewhere’.

  265. 265
    Zachriel says:

    Silver Asiatic: But as you point out, somehow these chemicals developed an ability to distinguish between itself and other like organisms.

    That’s correct, and the origin of the innate immune system is still obscure. It presumably originated very early in the evolution of life, long before the evolution of the adaptive immune system, which apparently co-opted various features of the innate immune system.

    Silver Asiatic: The organisms preserve their identity, but also have enough plasticity to evolve into new species of organisms.

    There’s no reason to suspect that lack of plasticity to be a significant problem for evolution over deep time.

    Silver Asiatic: But any of these organisms are accidental chemical developments. There’s no need for them to preserve an identity or repel invaders.

    The ones that don’t would be at a serious disadvantage to those that do.

    Silver Asiatic: The idea that drives all of this is that these chemical assemblies we call ‘organisms’ have a need to ‘survive’ and to preserve themselves as those unique organisms.

    They don’t “need” to survive. It’s just that those that do survive are those that have these capabilities.

  266. 266
    Silver Asiatic says:

    Curly Howard

    Silver, yes the pathogen will kill many organisms of that species as it has been for however many years, but it will not be able to kill this organism that has evolved this protein.

    As I posted elsewhere, the only reason a defense against the pathogen is needed is that there is some sort of ‘need for survival’ and ‘need to preserve the organism’. So that’s what should be explained.

    You’re not making any sense when you say “an immune system blocks the pathogen to preserve the organism. But this makes the organism resistant to evolving.”

    The evolutionary story requires that species of organisms become other species. As it happened, supposedly, they also become vastly more complex and diverse. ‘Preservation of the organism’ in a current state is obviously a barrier to ‘the organisms will change and become a new species’.
    Preserving current-state features is an obstacle to ‘evolving new, more sophisticated features’.

    Although different species change at different rates and to different degrees, depending on an infinite number of factors.

    I won’t take you too literally here, but if the number of factors causing evolutionary change is ‘infinite’ (and I believe it is), then there’s no way the theory could be predictive. This also points to the problem: an infinite number of factors supposedly causing a massive variety of unique organisms and features in biological life. But infinite factors and enormous capability for change, argues against the notion of self-identifying, self-preserving organisms and argues for a chaos of indistinguishable biological forms. It’s like trying to count how many rain drops in a cup of water – but there are no ‘drops’ as such. They’re merged together into one chemical fluid.

    No sh*t. That’s what we’ve been talking about, except for the fact that I’m arguing that one organism in this population develops a protein that has this most basic immune system function.

    I understand so far, but I wouldn’t call what you said to be convincing in the least.
    The pathogens kill the organism when there’s no immune system. However, one organism ‘develops’ (magically, for no reason) a protein that has the immune system function.
    We’ve seen, however the complexity of this system.

    This new protein can bind and block a pathogen. How is that not the evolution of an immune system (however basic) in one step?

    You’re attributing quite a lot to an accidental process.

  267. 267
    Axel says:

    Silver Fox, how can ‘chemicals want to survive’, before they become organisms? The will is a faculty of the soul, not of inanimate matter. I suspect it’s short-hand, on your part, though.

  268. 268
    Zachriel says:

    Silver Asiatic: ‘Preservation of the organism’ in a current state is obviously a barrier to ‘the organisms will change and become a new species’.

    Sure, but we can observe the process of variation, including the origin of novelty. We can measure its rate and compare it to historical rates of change.

    Silver Asiatic: I won’t take you too literally here, …

    ‘Infinite’, as in a very large number.

    Silver Asiatic: but if the number of factors causing evolutionary change is ‘infinite’ (and I believe it is), then there’s no way the theory could be predictive.

    Of course it can, as long as the number of trajectories is significantly less than the number of possibilities.

    Silver Asiatic: But infinite factors and enormous capability for change, argues against the notion of self-identifying, self-preserving organisms and argues for a chaos of indistinguishable biological forms.

    As evolution is largely incremental, that means it explores only a tiny portion of the conceivable space of adaptation.

    Silver Asiatic: The pathogens kill the organism when there’s no immune system.

    This was addressed. The innate immune system works by distinguishing between the organism and its kin and everything else. This can occur incrementally starting with a primitive system that absorbs everything, but then adapts to absorb with a degree of discrimination.

  269. 269
    Silver Asiatic says:

    how can ‘chemicals want to survive’, before they become organisms?

    Axel – yes, but when they become organisms they’re still ‘just chemicals’ – so how can they ‘want to survive’ as organisms? Why not just die and become inanimate matter again?

    The will is a faculty of the soul, not of inanimate matter. I suspect it’s short-hand, on your part, though.

    In the materialist view, there’s no real distinction between animate and inanimate matter in that regard. Living organisms are merely different chemical combinations.

    So, if inanimate matter does not want to survive, then living organisms should not want to survive either.

  270. 270
    Box says:

    Silver Asiatic: But any of these organisms are accidental chemical developments. There’s no need for them to preserve an identity or repel invaders.

    Zac: The ones that don’t would be at a serious disadvantage to those that do.

    Without the need or the intend to preserve a (non-existent) identity nothing will be preserved. So Zachriel’s “those that do” won’t exist. Materialism offers no explanation whatsoever for coherency; for an ‘organism’.

    Silver Asiatic: The idea that drives all of this is that these chemical assemblies we call ‘organisms’ have a need to ‘survive’ and to preserve themselves as those unique organisms.

    Indeed if chemical assemblies are all there is then in principle we cannot speak of ‘organisms’. ‘Organisms’ is a concept that materialism cannot accommodate. So under materialism there is nothing that needs to ‘survive’ and there is no self that needs to be preserved. So if materialism is true it follows that nothing will be preserved; IOW things will just fall apart, since there is no cause for binding.

    Zac: They don’t “need” to survive.

    There is no ‘they’ who do or don’t need anything.

    Zac: It’s just that those that do survive are those that have these capabilities.

    If there is no binding force that keeps things together, if there is ‘no one home’, things will inevitable just fall apart — as they do, in fact, at the moment of death. The question is: what power holds off that moment — precisely for a lifetime, and not a moment longer? One thing is certain: it’s a question that materialism cannot answer.

  271. 271
    Curly Howard says:

    Box, this is going nowhere fast. So let’s simplify it. If you can come up with one specific example that makes physiologic sense, of how my protein disrupts homeostasis, then I will concede.

  272. 272
    Curly Howard says:

    Silver,

    You are the only one here arguing that an immune system “preserves the organism in its current state.”

    What I am arguing is that the immune system (however basic) increases the survival of the organism and will spread within the population. This change in the population will have effects on the future of the species, including other changes. Changes build on each other, directly or indirectly. The immune system is not “preserving the organism” in a sense that it is “keeping the organism in its current state,” the immune system is “keeping the organism alive longer than other organisms of the population.”

    This whole “preserving current state thing” is nonsensical.

    Infinite number of factors means a huge number of factors that can act in an even larger number of combinations. Zachriel has explained your misunderstanding quite well.

    There is no “magic” involved.
    Change occurs in living things. In my example it is a simple change (the swapping of one exon for another) with a simple effect (the ability to bind a pathogen and block it). The system does not need to be complex to have an immune function. The complexity comes from millennia of evolution.

  273. 273
    Silver Asiatic says:

    Curly

    What I am arguing is that the immune system (however basic) increases the survival of the organism and will spread within the population.

    A lack of an immune system:

    – increases the survival of the pathogen, a ‘good’ evolutionary result
    – opens up a range of other options for the survival of the organism – mainly, the evolutionary development of entirely new features (thus species) where pathogens have no effect

    The immune system is not “preserving the organism” in a sense that it is “keeping the organism in its current state,” the immune system is “keeping the organism alive longer than other organisms of the population.”

    As above, a pathogen attacks the organism. With an immune system, the pathogen is blocked and the organism survives with its current features.

    However, with no immune system, the organism evolves (it’s just that easy, apparently) entirely new features and thus becomes a new species on the journey to becoming human beings.

    The system does not need to be complex to have an immune function. The complexity comes from millennia of evolution.

    This suggests that the complexity we read about on this thread is unnecessary. That sounds to me like you’re skipping over the entire problem and claiming that, given millennia of time, sophisticated systems emerge.

    But the problem of building an immune system that collects a repertoire of possible conditions and then uses intelligent selection to refine memory cells does not go away just by citing lots of time. A much better explanation is needed, in my view.

  274. 274
    Silver Asiatic says:

    Box 271

    That post really explains the problem very nicely and I have not seen a convincing response to that.

  275. 275
    Curly Howard says:

    What Silver? Are you really this lost? I don’t know how long I’m going to be able to continue this conversation if you are truly this confused.

    First, we are not talking about the survival or evolution of the pathogen. We are ignoring that.

    An immune system means the pathogen is blocked and the organism survives. Period.

    There is absolutely no need for the phrase “with its current features,” at the end of that sentence. Obviously that organism is going to survive with its current features and pass on this basic immune system, but to think the organism an it’s offspring are not open to any other changes is completely asinine. As I said, change is constantly occurring in living things. Just because survival has been increased for whatever reason, does not mean that the organism and it’s offspring isn’t going to undergo slight changes in any of its other characteristics. Whether an immune system is developed or not, every organism is going to undergo changes which can alter survival and lead to evolution.

    I really can’t believe I have to spell all this out. Wow.
    I guess I understand a lot more biology than I give myself credit for.

    Anyways, someone already pointed out that you are confusing the ideas of evolution at the organismal level and at the species level. But you seem to continue making the same mistake.

    The complexity is necessary when we take into account that pathogens have been evolving just as we have. Essentially multicellular organisms and pathogens have constantly been waging a molecular “arms race.” Our very complex system of dealing with pathogens today has stemmed from a much simpler system that has changed along with pathogens and has been constantly refined.

    I’m not about to launch into a discussion of the evolution of the entire immune system as it is today in us and other species. I am just trying to show how the first step in the evolution of an immune system might be possible. Box apparently thinks this first step would “disrupt homeostasis,” and you think it would “stop evolution,” both ideas couldn’t be more wrong.

  276. 276
    Box says:

    Silver Asiatic #275,

    Thank you. Actually I haven’t seen any response to this problem. Darwinian just-so-stories have only some meaning if an organism is assumed – as some sort of emergent *poofery*. Whenever one points out that this assumption is particularly groundless under materialism one is being ignored.

  277. 277
    Zachriel says:

    Box: Materialism offers no explanation whatsoever for coherency; for an ‘organism’.

    Way out there. Materialists can observe the cell membrane and other structures of the cell just like anyone else.

    Box: Indeed if chemical assemblies are all there is then in principle we cannot speak of ‘organisms’. ‘Organisms’ is a concept that materialism cannot accommodate.

    You seem to be conflating materialism with Zen Buddhism or something. Materialists generally have little difficulty in making distinctions.

  278. 278
    Box says:

    // follow up to #277//

    Or they (darwinists) pretend (?) not to understand what you are talking about – see e.g. Zachriel #278.

  279. 279
    Joe says:

    Unguided evolution cannot account for any immune system for the simple fact that unguided evolution cannot account for any organisms that have an immune system.

    BTW “evolution” is NOT being debated. What is being debated is whether or not it occurs via differing accumulations of genetic accidents, errors and mistakes OR is it being directed by its intelligent design?

  280. 280
    Dionisio says:

    gpuccio

    This discussion thread is past 280 posts, but still no one else, except you, has dared to answer the questions in post #157.

    Any idea why?

    🙂

  281. 281
    Box says:

    Gpuccio,

    Great OP. What makes it irreducible complex is that each step is meaningless without the next step. For instance, what good is a (extremely) complex system of measurement (step 5) without a (extremely) complex selecting system that can weed out the bad and preserve the good (step 6 & 7)?

    So no one has come up with a step-wise just-so-story of the ‘evolution’ of this system. Why am I not surprised?

  282. 282
    Silver Asiatic says:

    Box 279 & 282

    True

    We observe a massively complex and interactive, finely-tuned biological system. The description of the system alone (saying nothing about its supposed evolutionary origin) is extensive. As stated, there is a repertoire of potential conditions from which the cell selects and refines. Multiple processes work together – each being useless without the other. That’s irreducible complexity. But our opponents disagree. There is, apparently, some step-by-step evolutionary story about the origin of the system. But what is it?

    DNA_Jock was the most honest and direct so far. At least he has the good sense to recognize the problem, and the modesty to admit that he “doesn’t know”. His solution to the problem? “let people who understand immunology far better than I do figure it all out”. I commented on this – it’s a pretty weak defense. But I’ll agree with what it implies – even the people who understand immunology don’t have an answer. Maybe they’ll figure it out sometime.

    Brent reverted to what was described as: “…they (darwinists) pretend (?) not to understand what you are talking about…”
    He repeated several times that a protein will simply evolve an immune system and it will spread through the population – thus the problem is solved. This is not irreducible because it can all be done in one step, apparently.

    Zachriel followed with some one-liners: We note that chemical combinations form ‘organisms’ that self-identify and defend themselves with complex immune responses. How do we explain this? He makes it simple: “Materialists can observe the cell membrane …”

  283. 283
    gpuccio says:

    Box and Silver:

    Good thoughts!

    I am really amazed at the particular form of complexity that we observe in the immune system.

    Both the procedures that I have tried to briefly describe in the OP are wonderful examples of processes that reflect a designed purpose.

    The basic repertoire has no immediate utility, if not as a network of receptors for possible future encounters. The realization of such a network is a wonderful and extremely complex play of variation, starting from the repertoire of genes and going through the many ways that those genes are recombined and additionally modified, to the negative selection of self reacting configurations. And, obviously, the repertoire of receptors must be carefully available at the various body sites, and must be connected to the working of antigen presenting cells and T helper cells, and must be able to trigger an useful response through the soluble effectors (antibodies). And so on.

    The antibody affinity maturation is even more remarkable: selection and variation in cycles, realized by the cooperation of different cell types in different parts of the lymph node. Positive and negative selection at the cellular level, just to adjust the primary response for the future of the organism. Astonishing precision in targeting the right genetic regions, limiting as much as possible any damage to the rest of the genome.

    These proteins which effect variation, both in the first and the second scenario, are true lethal weapons, as shown by their role in many neoplasms. They must be used, and are used, with the highest control and attention to the details.

    The CRISPR system in prokaryotes is equally astonishing, given the much older context where it is found. Here, too, recognition of specific form is the key. Recognition, and memory, and re-recognition, and triggered reaction, the components of the cognitive algorithm are there, almost 4 billion years ago. The game of life is a game of intelligence just from the beginning.

  284. 284
    Box says:

    GPuccio: These proteins which effect variation, both in the first and the second scenario, are true lethal weapons, as shown by their role in many neoplasms. They must be used, and are used, with the highest control and attention to the details.

    Even Darwinians – like Curly Howard – will understand that such proteins cannot do without regulation. IOW how did it evolve? Given the unlikely event that the code for the protein is found by random changes, what is the probability that the regulation for the “lethal-weapon-protein” is already in place?

  285. 285
    Silver Asiatic says:

    @283 I meant Curly Howard, not Brent. Sorry!

  286. 286
    Curly Howard says:

    Box, I’m still waiting for a single example (that makes physiologic sense) of how my protein would disrupt homeostasis. If you can’t come up with one, then I’ll understand.

  287. 287
    Curly Howard says:

    Silver, I don’t “pretend to not understand.” The simple fact is that neither of your arguments make any sense from a biological perspective. It may make sense in your heads, but anyone who has an above average biology IQ would laugh at the things the two of you are saying.
    Since you have not responded to my last post, I will assume this conversation is over. Cheers.

  288. 288
    Silver Asiatic says:

    Curly

    I’m not about to launch into a discussion of the evolution of the entire immune system as it is today in us and other species. I am just trying to show how the first step in the evolution of an immune system might be possible.

    I didn’t respond because as I said, you explained nothing. The problem offered in the OP is massive. You presented an ad hoc story and wisely described that it “might be possible”.

    Ok, if it might be possible, then it also might not be possible at all. You’ve offered nothing to distinguish between the two options.

    If biologists would laugh at that simple, logical conclusion then it’s no wonder they have to pretend that they don’t understand the problem.

  289. 289
    Silver Asiatic says:

    A little research on homoestasis helps (from Wiki):

    In order to maintain protein homeostasis post-translationally, the cell makes use of molecular chaperones and/or chaperonins, which aid in the assembly or disassembly of proteins.[7] They recognize exposed segments of hydrophobic amino acids in the nascent peptide chain and then work to promote the proper formation of noncovalent interactions that lead to the desired folded state.[7] Chaperones begin to assist in protein folding as soon as a nascent chain longer than 60 amino acids emerges from the ribosome exit channel.[8] One of the most studied ribosome binding chaperones is trigger factor. Trigger Factor works to stabilize the peptide, promotes its folding, prevents aggregation, and promotes refolding of denatured model substrates.[9] Trigger factor not only directly works to properly fold the protein but also recruits other chaperones to the ribosome, such as Hsp70. Hsp70 surrounds an unfolded peptide chain, thereby preventing aggregation and promoting folding.

    As a very small beginning – just observe the teleological language used to describe that.

    A blind, unintelligent, accidental cause and what it produces. This sentence is brilliant:

    “[Chaperones] recognize exposed segments of hydrophobic amino acids in the nascent peptide chain and then work to promote the proper formation of noncovalent interactions that lead to the desired folded state.”

    http://en.wikipedia.org/wiki/Proteostasis

    Chaperones certainly sound very intelligent and friendly!
    They “recognize” issues and then “work to promote the proper formation” so that everything will arrive at “the desired state”. It’s nice that other chaperones are “recruited” because a lot of help is needed to maintain the organism. Evolution makes sure everything works out great because if not, then it would be very bad indeed!

    🙂

    I think it takes a very high IQ in biology to be blind to the problem here.

  290. 290
    Curly Howard says:

    Silver, your first post amounts to “our current immune system is massively complex, you have to explain every step of its evolution in order to have a conversation with me.”
    As I said, I was simply giving an example of how an immune system/response could evolve in a single simple step based on knowledge of known proteins and occurrences within the cell. If “it might not be possible” then you should be able to come up with a counter argument of why my system wouldn’t work.
    Calling it a “just-so story” and brushing it off shows how closed your mind is. You aren’t even willing to have a hypothetical conversation on the topic. It’s likely because you lack the knowledge to do so.

    Your second post amounts to “here read about chaperones.” You’re not helping box out at all. I am looking for something like “the protein will disrupt the osmotic pressure” or “the pH” and a concise explanation how it would do so.
    The presence of chaperones would actually play a role in blunting any disruption of homeostasis that a protein might have. They maintain protein functionality, so thank you for that.

    If this conversation requires a high biology IQ, I’d suggest you see yourself out.

  291. 291
    Zachriel says:

    Box: Zachriel #278

    You made this claim:

    Box: ‘Organisms’ is a concept that materialism cannot accommodate.

    As materialists do accommodate the concept of organism, then your statement is simply wrong.

    Silver Asiatic: We note that chemical combinations form ‘organisms’ that self-identify and defend themselves with complex immune responses. How do we explain this? He makes it simple: “Materialists can observe the cell membrane …”

    You somewhat mangled our statements.

    The first comment concerned how the complex immune systems evolved. The answer is it evolved from a simpler immune system, starting with the innate immune system, in particular, with the ability of an organism to recognize itself or its close relatives.

    The second question concerned Box’s strange claim that materialists can’t recognize the coherency (united as or forming a whole) of an organism. You might start with skin.

  292. 292
    Dionisio says:

    Silver Asiatic

    You shouldn’t worry about any IQ. Mine is lower than my age and it seems to change in the opposite direction. However, kf and gpuccio still let me participate in their discussion threads. Well, until the day they can’t stand anymore my annoying self-congratulatory comments full of trivially dumb questions. 🙂

    We should be open-minded, think out of the box, ask questions like children do, put everything to test.

    […]
    For it is written,

    “I will destroy the wisdom of the wise,
    and the discernment of the discerning I will thwart.”

    Where is the one who is wise? Where is the scribe? Where is the debater of this age?
    […]
    [1 Corinthians 1:18-31]

  293. 293
    Curly Howard says:

    Yeah, don’t worry about only having a basic understanding of biology. It shouldn’t stop you from having a conversation about complex topics and the most recent research in the field, right?
    Of course. That’s why they teach things like enzyme kinetics, binding affinity, and signal transduction pathways in a general biology course!

  294. 294
    Silver Asiatic says:

    Curly

    Silver, your first post amounts to “our current immune system is massively complex, you have to explain every step of its evolution in order to have a conversation with me.”

    I think GPuccio is looking for a much deeper engagement on what is actually proposed as the origin of the system. The question regards the irreducible complexity of what we see. You disagree with that. But I don’t think it’s sufficient, therefore, to merely speak about one step. But the floor is yours. You can explain as much or as little as you’d like. I’m merely saying that it seems like you’re offering very little – and the challenge is very great.

    As I said, I was simply giving an example of how an immune system/response could evolve in a single simple step based on knowledge of known proteins and occurrences within the cell. If “it might not be possible” then you should be able to come up with a counter argument of why my system wouldn’t work.

    Ok, understood. But when you say something “might be possible”, then I’d like to know what that means? How likely is it? What is the probability that it actually is impossible? The problem is that we’re just dealing with imaginary scenarios – certain lucky mutations could do just about anything in the cell, if we want to put it that way.

    Your second post amounts to “here read about chaperones.” You’re not helping box out at all. I am looking for something like “the protein will disrupt the osmotic pressure” or “the pH” and a concise explanation how it would do so.

    I can’t speak for Box but I’m looking for an explanation for the origin of chaperones. They contributed to homoestasis – providing stability. Why? This brings us to the nature of the organism. Why would chemical combinations create organisms that preserve themselves and find some kind of “desired state” of equilibrium? Why do blind mutations develop a system that “works towards the proper formation of interactions”?

    Evolution is not directed to a desired end. But here we have elements of the cell collaborating towards a balance within the cell.

    The presence of chaperones would actually play a role in blunting any disruption of homeostasis that a protein might have. They maintain protein functionality, so thank you for that.

    You’re restating the problem here, not solving it.

    The cell had to evolve chaperones to blunt disruptions to homoestasis. How and why did that happened on a step-by-step basis?

  295. 295
    Dionisio says:

    Silver Asiatic and Box

    The high IQ doesn’t seem to help your interlocutors to answer questions like the ones posted @157.

    Is that why they seem so disappointed, annoyed, frustrated?

    🙂

  296. 296
    Joe says:

    Again, the question is NOT “did/ could the immune system evolve?”. The question is can unguided evolution, ie accumulations of genetic accidents, errors and mistakes, produce an immune system and the organisms that have one? And how can we test such a claim?

  297. 297
    Dionisio says:

    AFAIK, in no biology course they teach (in a comprehensive and logically coherent manner) how they could get the biological systems researchers observe and study today.
    Most serious scientists are quite busy trying to figure out how those systems function and what they do. No much time left for OOL issues.

  298. 298
    Curly Howard says:

    Silver, I’m not sure what gpuccio’s looking for because he went all elementary school-tantrum on me a while back.
    Anyways, if you and Box were able to converse about biology at this level, maybe we’d be able to make it past this first step. Unfortunately, you two are unable to make any sense of things in the context of biology. How can I try to “offer more” when you can’t even understand my simple example?

    As far as possibility of my example goes, that is what we we are trying to hash out right now. I say it’s possible and give a brief outline, and you’re supposed to come up with something that might limit the possibility of an immune system arising in this way. Then I try to rebut. That’s how things work, no? So far the two of you have come up with homeostasis and the evolution “show-stopper” argument. Both, in my understanding, are nonsensical and have already been addressed.

    And now you want an explanation for the origin of chaperones?
    Move the goalposts much?
    You’ve bounced from my original hypothetical to an explanation of the whole immune system, and now to an explanation of the evolution of chaperones and homeostasis. It’s like talking to a child with ADD. Please stay on topic.

  299. 299
    Dionisio says:

    Silver Asiatic and Box

    Could it be that your interlocutors seem so disappointed, annoyed, frustrated, because they realize that, as more research is done, more light is shed on the elaborate cellular and molecular choreographies orchestrated as interwoven mechanisms operating within amazingly complex biological systems?

    Their comments may reveal their embarrassment. But maybe we can sympathize with them. Can you imagine not being able to respond the questions raised by someone with much lower IQ?

  300. 300
    Silver Asiatic says:

    Curly

    As far as possibility of my example goes, that is what we we are trying to hash out right now. I say it’s possible and give a brief outline, and you’re supposed to come up with something that might limit the possibility of an immune system arising in this way. Then I try to rebut. That’s how things work, no?

    You said it might be possible. I asked how probable it is. I can’t rebut anything until I know that. One in 10^18 is still ‘possible’. You can just provide some probability calculations.

    to an explanation of the evolution of chaperones and homeostasis

    As stated before, you act like you don't understand. Box was talking about the evolution of homeostasis from the beginning. You said nothing about it.

  301. 301
    Dionisio says:

    gpuccio

    This discussion, following your insightful OP, has 300+ posted comments, but still no one else, except you, has dared to answer the questions in post #157.

    Any idea why?

    🙂

  302. 302
    Curly Howard says:

    Silver, you don’t need a precise calculation of probability to be able to talk about the possibility of something occurring. We know quite a bit about how things work at the molecular, cellular and organismal levels and this allows us to talk about simplified, hypothetical examples like the one I gave. If you actually knew what you were talking about you’d either be able to rebut my argument or at the very least advance the conversation further. You do neither.

    Also Box was not talking about the evolution of homeostasis as far as I know. He was talking about my protein disrupting it. Again, feel free to prove me wrong.

  303. 303
    Silver Asiatic says:

    Curly

    Silver, you don’t need a precise calculation of probability to be able to talk about the possibility of something occurring.

    I’ve never seen science done like that before – by merely saying something is possible and offering no range of probabilities. But ok, it’s possible that God created the immune system out of nothing.

  304. 304
    Curly Howard says:

    Oh well excuse me. I didn’t realize we were “doing science” right now. I thought we were just having a conversation about biological systems and their potential evolutionary pathways.

    What if I told you the probability was 1 in a billion. What would that allow you to do?

  305. 305
    Silver Asiatic says:

    Curly

    What if I told you the probability was 1 in a billion. What would that allow you to do?

    Question how you arrived at that number.

  306. 306
    Curly Howard says:

    Yeah. I figured. How would you go about calculating the probability of my hypothetical proto-immune system arising in the way I have described?

  307. 307
    Curly Howard says:

    By the way silver, trying to calculate the probability of something arising through the course of evolution is a pretty awful way of “doing science.” Almost as bad as saying “god created the immune system out of nothing.”

    Why do you think god created such a variety of immune systems? Was he using the good ol’ trial and error method as he put his creatures together?
    Why not build an immune system for us that allows us to fight off all the pathogens? That would e nice wouldn’t it? Then we wouldn’t have to give ourselves those “autism-causing vaccines” and get our flu shots every year.
    Food for thought.

  308. 308
    Dionisio says:

    Silver Asiatic

    You may put the probabilities aside for a moment and ask your interlocutors to respond the questions in post #157, if they have the guts and humility to do so.

  309. 309
    Me_Think says:

    Wow, this thread has grown in the few days I and my group were off to build our autonomous ATV for an Arduino competition – which we lost 🙁 . I wish an ID agent was available to fly in and fix the GPS module which malfunctioned. Unfortunately, we don’t know what is an ID agent, so it’s tough to search for an agent. Let me know when you find one.

  310. 310
    Dionisio says:

    One can tell the other interlocutors are in panic mood when they send their ‘strong’ AI ’emotional’ robot brigade to try to put off the fire. If only those high IQ folks could try to answer the questions in post #157, they could improve their embarrassingly discredited image. But nah, they won’t. What else is new? 🙂

  311. 311
    Me_Think says:

    Dionisio @ 311

    One can tell the other interlocutors are in panic mood when they send their ‘strong’ AI ‘emotional’ robot brigade to try to put off the fire

    Dionisio has still not understood that we were in agreement about Arduino AI ! How embarrassing.
    About Questions in #157, Google might help, if not, you may have to wait for scientists to get interested enough to research and answer your questions. In any case, don’t expect answers from the cutting edge ID scientists brigade.

  312. 312
    Dionisio says:

    #312 Me_Think

    You’re embarrassingly wrong again, buddy.

    Oh, well, what else is new?

    There’s no need to Google anything or wait for anyone.

    If you would have read this thread more carefully, you should have noticed that gpuccio was the only person who dared to answer all those questions, and he did it correctly.

    None of your party comrades dared to even attempt to present counterarguments in response to gpuccio’s insightful comments on that subject.

    Keep busy working on your Arduino entertainment.

    BTW, the young son of a friend of mine built an interesting Arduino-based machine, which he sells online very well, as a side hobby/business. That’s not his main business.

  313. 313
    Me_Think says:

    Dionisio @ 313

    BTW, the young son of a friend of mine built an interesting Arduino-based machine, which he sells online very well, as a side hobby/business. That’s not his main business.

    Please keep away from him ! Let him grow with real scientific acumen.

  314. 314
    Joe says:

    Curly Howard:

    By the way silver, trying to calculate the probability of something arising through the course of evolution is a pretty awful way of “doing science.”

    You don’t have anything else, Curly. You don’t have any evidence. You don’t have a model and you don’t have any testable entailments.

    THAT is a very awful way of doing science.

    Why not build an immune system for us that allows us to fight off all the pathogens? That would e nice wouldn’t it?

    Not in a world designed for scientific discovery.

  315. 315
    Dionisio says:

    #314 Me_Think

    Unlike you, that young man doesn’t believe in the ‘strong’ AI hogwash that you defend so blindly. He knows how to think by himself, hence he won’t accept your senseless ’emotional robots’ fairy tales.

  316. 316
    Silver Asiatic says:

    Curly

    Why do you think god created such a variety of immune systems? Was he using the good ol’ trial and error method as he put his creatures together?
    Why not build an immune system for us that allows us to fight off all the pathogens? That would e nice wouldn’t it? Then we wouldn’t have to give ourselves those “autism-causing vaccines” and get our flu shots every year.
    Food for thought.

    Yes, food for thought and interesting questions. I have a lot of answers to “why would God …” questions but that kind of discussion is theological and it requires first, a belief that God exists. After that, I’d need to know what you think about God – the nature of God, etc.

    In this case, you’re thinking that an immune system that fights off all pathogens would be better. Or, no organisms that were ever vulnerable to any pathgens at all and would never require immune systems. Or there could be no evil or suffering in the world. Or, organisms could live on earth forever – no need for reproduction. God could populate the earth and leave it at that — there are lots of possibilities. But you have to start with God and what you know about God to be able to discover answers.

    Evolution has similar problems. We have to recognize that most of it is driven by chance. That’s why we look at probabilities.

    You’d need to estimate how many mutations it would require to achieve the new function (in your example the new protein co-opted the pre-existing regulatory system so that’s not the most difficult challenge), and how long it would take to evolve that number of coordinated mutations to arise in a population. Some empirical studies have been done on this (Gauger & Axe, 2012) and they concluded that it takes a minimum of 7 or more mutations to change the function of a protein. The waiting time for that is 10^27 years (the universe is 10^10 years old).

    But more than that, someone could estimate how many coordinated mutations, in total, were required (factoring in the effect of negative mutations) to construct the entire immune system we saw illustrated in the OP.

    Each step requires X mutations. How many changes in the process have to occur simultaneously? If any, that speaks to irreducible complexity because it’s unreasonable to assume that mutations will occur in a coordinated pattern.

    Eventually, you come up with some kind of probability that the process is the result of an unintelligent, unguided process.

    In the end, you can still say “it might have happened” – but some events are so incredibly improbable that it has to rely on the lucky of luckiest coincidences and it’s more reasonable to conclude that “it’s impossible”.

  317. 317
    Curly Howard says:

    Silver, how would an immune system that fights off all pathogens, not be better?

    Anyways, as I said, calculating probability of something occurring through evolution is an awful way to go about science. There are simply too many unknown factors to look at protein evolution in the way that gauged does in that paper. Sure you can look at the differences in two proteins that exist today and is the central idea of that paper. But evolution does not say that the second protein evolved from the first protein, it says that both proteins evolved from a common ancestor. So right off the bat, the core of the paper is based on falsehood. Also, the paper doesn’t take into account the variety of mechanisms of mutation, instead it just assumes that mutations always occur one nucleotide at a time and that nothing effects their frequency. Returning to my example we can also look at it from the other side; there’s also the possibility that the pathogen evolved to be killed by what was formerly a host species. This may seem counter-intuitive at first but you have to remember that the pathogen is evolving just as the host is. A change in the pathogen may be beneficial for its survival in another host or in the environment but allows for host recognition in the original host species. Here we have an increase in survival of both species along with the arrival of a very basic immune response that can undergo changes and refinement itself.

    As you can see, there is an almost infinite number of factors that would go into calculating the probability of a mechanism evolving through the course of evolution. Especially one that occurred hundreds of thousands of years ago in a species that no longer exists, but only has descendants who themselves have been evolving for hundreds of thousands of years.

    I don’t think we’re even close to being able to accurately calculate the probability of something arising through evolution. We simply don’t know enough.

  318. 318
    Joe says:

    What does that mean, Curly? What does “something arising through evolution” mean in a debate about whether or not evolution is telic or blind and unguided?

    Blind and unguided evolution can neither be modeled nor tested.

    And if we “simply don’t know enough” then that is what needs to be told to students as opposed to stifling inquiry and baldly declaring it wasn’t via intentional design.

  319. 319
    Silver Asiatic says:

    Curly

    As you can see, there is an almost infinite number of factors that would go into calculating the probability of a mechanism evolving through the course of evolution.

    Agreed.

    I don’t think we’re even close to being able to accurately calculate the probability of something arising through evolution.

    That’s an honest reply. At present we can’t calculate it and we’re not even close.

    I’ll just echo what Joe said above – this fact you point out here should be part of the teaching on evolutionary theory.

  320. 320
    Curly Howard says:

    So are you agreeing that the conclusion of the gauger paper (that they can calculate a specific “waiting time” and have also shown the impossibility of evolving protein 2 from protein 1 through probability) is completely unsupported?

    I mean if we’re being honest here, the paper is a joke.

    Anyways, that we “know so little about something” is a fact of every scientific field of inquiry. Should they also make sure to tell students in every other science class about how little we actually know? I mean just learning the stuff is usually frustrating enough, nevermind telling the students that some of the details they’re learning might not even be correct. Let’s be realistic here.

    We might be missing a significant amount of information, some of the latest research conclusions may even be wrong, but it’s quite obvious that the core of evolutionary biology is correct. It is the best explanation for the diversity of life that we see today.
    If I were to try to draw a parallel, it’s like you are trying to say that our current understanding of cellular processes are all wrong because we don’t know the functions of many proteins, we don’t know how lipid rafts work and aren’t even completely sure they exist, etc. The list goes on for miles, but we aren’t questioning cell biology or claiming its teachers should make sure to tell students that there is a lot we don’t know. Why is that?

    Have you run out of nonsensical thoughts about my hypothetical first immune system? I guess someone with little knowledge of the topic being discussed should shy away from talking about it. Better to keep your mouth shut and let people think you’re a fool, then open it and remove all doubt, right? Box apparently took those words to heart a while ago.

  321. 321
    Joe says:

    We might be missing a significant amount of information, some of the latest research conclusions may even be wrong, but it’s quite obvious that the core of evolutionary biology is correct. It is the best explanation for the diversity of life that we see today.

    Evolutionary biology can’t get beyond populations of prokaryotes given starting populations of prokaryotes. Not very good if you need to explain anything beyond prokaryotes.

  322. 322
    Dionisio says:

    Integrin-dependent interactions between T cells and antigen-presenting cells are vital for proper T cell activation, effector function, and memory.

    http://www.uncommondescent.com.....ent-548268

  323. 323
    Dionisio says:

    how the adhesion and signaling activities of active LFA-1 promote T cell priming?

    how mechanical forces at the IS affect T cell functions in vivo?

    http://www.uncommondescent.com.....ent-548271

  324. 324
    Dionisio says:

    Integrity of the dendritic cell (DC) actin cytoskeleton is essential for T cell priming, but the underlying mechanisms are poorly understood.

    http://www.uncommondescent.com.....ent-548273

  325. 325
    gpuccio says:

    Dionisio:

    Wonderful links. The concept of immunological synapse is specially intriguing, reminding the strong similarities between the immune system and the nervous system.

    Here is a link:

    http://www.nature.com/nri/jour.....44_F3.html

    to a figure which very “simply” sums up the interactions (or at least, part of them) between Antigen presenting cell, T helper cell, B cell and dendritic cell in the lymph node at the time of the primary response, when the responsive B cell is selected and expanded.

    Now, I would like to ask our interlocutors: here is a selection, without any doubt. What is “natural” in it? Isn’t it obvious that the selection happens because an extremely complex, irreducibly complex system, with a very specific configuration which is in no way “natural”, is already present, ready to work as soon as a foreign antigen (the environmental information) enters the system?

    In this figure only, I count 4 different cell types and 7 different cell states, and about 15 different complex molecules implied in the interactions. And this is certainly a gross simplification.

    This is the very simple meaning of what I call “Intelligent Selection”: a selection which takes place because there is a very complex and specific system, explicitly configured for the function of effecting the selection itself.

  326. 326
    gpuccio says:

    Dionisio:

    From this paper:

    http://www.nature.com/nri/jour.....ri3801.pdf

    an interesting summary:

    B cell and T cell lineages are ancient

    Although our appreciation of the B cell and T cell pathways of lymphocyte development is fairly recent, this organizational scheme has proven to be a fundamental principle of the adaptive immune system in all vertebrates. All jawed vertebrates, including sharks and other cartilaginous fish, have genes encoding the B cell receptor (BCR), ?? and ?? T cell receptors (TCRs), MHC class I and II proteins, and recombination-activating gene 1 protein (RAG1) and RAG2 (REF. 78). An alternative adaptive immune system has been defined in the extant jawless vertebrates, lamprey and hagfish, which have none of the above cardinal elements used by jawed vertebrates to generate clonally diverse receptors for B cells and T cells79. Instead of the immunoglobulin-based components that are used by lymphocytes in jawed vertebrates to construct the BCR and the TCR, lymphocytes in the jawless vertebrates use leucine-rich repeat (LRR) sequences to construct variable lymphocyte receptors (VLRs) for antigen recognition (reviewed in REF. 80). Three lamprey VLR loci — VLRA, VLRB and VLRC — each contain an
    incomplete germline gene that is flanked by hundreds of different LRR-encoding sequences. During their development in a thymus-equivalent or haematopoietic region, lymphocytes use the flanking LRR sequences as templates to assemble mature VLR genes in a stepwise manner.
    The different VLR types are expressed in a clonally diverse manner by separate lymphocyte lineages. The lamprey VLRA+ and VLRC+ lymphocytes resemble thymus-derived ?? and ?? T cells, respectively, and VLRB+ lymphocytes closely resemble mammalian B cells and give rise to plasma cells that secrete VLRB antibodies81. The remarkable parallels between these lymphocyte lineages in jawless and jawed vertebrates suggest that the genetic programmes for the major lymphocyte differentiation pathways evolved in a common ancestor before the convergent evolution of the different types of antigen receptors in jawless and jawed vertebrates.

    Emphasis added.

  327. 327
    Curly Howard says:

    “Yeah guys, come look at how complex all this biology is that I’ve copy/pasted! That’s definitely irreducibly complex! Right?”

    -Typical IDer “doing science”

  328. 328
    gpuccio says:

    “Yeah guys, come look at how complex all this biology is that I’ve copy/pasted! That’s definitely irreducibly complex! Right?”

    -Typical IDer “doing science”

    Typical mock/scorn for lack of any dignified argument.

  329. 329
    Curly Howard says:

    I’ve already made my argument. You pooped your pants and ran home after I gave you a little attitude. Have you found the irreducible core of anything yet?

  330. 330
    gpuccio says:

    Just for general knowledge: I rarely decide that I will no more discuss with someone, but if I do, I stick to it.

  331. 331
    Silver Asiatic says:

    Typical mock/scorn …

    A solid indicator that the person has nothing to offer.

  332. 332
    Curly Howard says:

    I’m sorry to hear that pucci, but I guess I understand why you guys don’t want to talk in-depth about biology.
    Same goes for you silver.
    You guys copy/paste some complicated biology, declare irreducible complexity, and trade high-fives. But when anybody tries to debate your claims, you are forced to demonstrate your lack of biological knowledge until ultimately you back off (if you’re smart enough).

    Good chat guys, it’s been fun.

  333. 333
    Piotr says:

    #331 Gpuccio,

    That looks a pretty evasive manoeuvre to an observer. Curly Howard may not mince words, but he hasn’t been actually rude to you, and he has raised a number of valid points you’ve left unaddressed.

  334. 334
    gpuccio says:

    Piotr:

    IMO, he has been worse than rude. I am a strange person, I am more susceptible to what people say, rather than to how they say it. Dishonest people disturb me more than insults (which, in a sense, can be fun 🙂 ).

    You are an interlocutor that I respect deeply. If you have any points that you want to discuss with me, even borrowed from others, I will be happy to discuss them with you in depth, as we have done so many times. You should know that I never try to evade discussion, just to evade unpleasant people.

  335. 335
    gpuccio says:

    Piotr:

    I quote myself:

    “Now, I would like to ask our interlocutors: here is a selection, without any doubt. What is “natural” in it? Isn’t it obvious that the selection happens because an extremely complex, irreducibly complex system, with a very specific configuration which is in no way “natural”, is already present, ready to work as soon as a foreign antigen (the environmental information) enters the system?

    In this figure only, I count 4 different cell types and 7 different cell states, and about 15 different complex molecules implied in the interactions. And this is certainly a gross simplification.

    This is the very simple meaning of what I call “Intelligent Selection”: a selection which takes place because there is a very complex and specific system, explicitly configured for the function of effecting the selection itself.”

    I suppose this is an argument. Right or wrong, it is an argument. You are free to comment and discuss.

  336. 336
    Curly Howard says:

    If I had actually been rude, I assure you I would have been banned already. The threshold for banning is quite low here, I would know.
    You being “more susceptible to what people say, rather than how they say it” hasn’t proven true in our conversation.

  337. 337
    Dionisio says:

    gpuccio

    This discussion, following your insightful OP, has 337 posted comments and has been visited 954 times, so far, but still no one else, except you, has dared to answer the questions in post #157.

    All your ‘nice’ and ‘polite’ interlocutors have done so far is whine and bark up the wrong trees. Poor things. They appear frustrated by the recent avalanche of research reports that are shedding more light on the elaborate cellular/molecular choreographies orchestrated within biological systems. We should feel sympathy for their uncomfortable situation, which will only worsen, as dedicated scientists continue to work hard trying to figure out how the biological interwoven mechanisms function.

  338. 338
    Dionisio says:

    gpuccio

    Thank you for your insightful comments #326, 327. I’m looking into those papers you referenced.

  339. 339
    gpuccio says:

    Dionisio,

    Thank you for the comments. You know, I would never ban anyone from a discussion, but I still believe that any sentient person has a right to decide whom it is worthwhile to discuss with.

    I really hope that Piotr may join the discussion about the “number of valid points” I’ve “left unaddressed”.

  340. 340
    Dionisio says:

    gpuccio

    I really hope that Piotr may join the discussion about the “number of valid points” I’ve “left unaddressed”.

    What ‘valid points’? In which thread or posts?

    Can’t they just point to the posts and quote the text that contains those ‘unaddressed valid points’?

    What about the questions in post #157 which no one else, except you, has dared to answer?

    If I were in your ‘moderator’ position, I would have removed the unnecessary comments posted by certain interlocutors. They don’t add any value to the discussion and are only unnecessary distractions. Time is too precious to be squandered in senseless discussions.

    However, I respect your patience/tolerance, which I have publicly praised in more than one occasion in this blog, even though I don’t agree with. I definitely lack those virtues.

    There are general discussions threads in this same blog where they could practice their mocking/scorning abilities if they want to. But they should stay out of serious biological discussions like this, where comments should stick to the topic of the OP (in this case the antibody affinity maturation or closely related issues).

    BTW, a while back someone wrote an intriguing comment raising the possibility that some of the whining interlocutors could be paid agents working for this blog, in order to entertain the onlookers/lurkers, to test our patience, to increase the traffic, or for some other unknown to me reasons. However, I don’t find that intriguing suggestion easy to accept as real. But who knows? 🙂

  341. 341
    Me_Think says:

    Dionisio @ 316

    Unlike you, that young man doesn’t believe in the ‘strong’ AI hogwash that you defend so blindly.

    I admire your persistence in denying that we are in agreement when it comes to ‘strong’ AI, but do you realize you come across as a dolt ?

  342. 342
  343. 343
    Me_Think says:

    gpuccio
    Interesting paper:

    The Evolution of Adaptive Immune Systems
    , although it doesn’t answer all questions.

  344. 344
    Dionisio says:

    #342 Me_Think

    ty umnitsa! prosto molodyets!

    You know that ‘strong’ AI is hogwash, a figment in your and your comrades’ imagination, wishful thinking.

    Hopefully someday you’ll wake up from that daydreaming state and realize how wrong you were.

  345. 345
    Dionisio says:

    #344 Me_Think

    That’s a serious way to engage in this discussion. Thank you!

    The paper was published almost 9 years ago, but still it’s worth reviewing it. However, keep in mind that it’s possible that the whole ‘picture’ now looks much more complex than it did then.

    Let’s see what gpuccio has to say about it.

  346. 346
    Dionisio says:

    #346 addendum

    From the referenced paper:

    Speculation on Why and When the Two Recombinatorial Immune Systems Evolved
    […]
    The resource material needed to trace the most informative roots of our V(D)J recombinatorial immune system may have been lost with the extinction of agnathans other than lampreys and hagfish around 400 million years ago.
    […]
    In this highly speculative scenario,…
    […]
    Many challenging issues clearly remain unresolved about how and why very different components of the innate immune system were co-opted for use in the evolutionary construction of two distinctive recombinatorial immune systems.

  347. 347
    Dionisio says:

    #347 follow-up

    Does the referenced paper pass the “where’s the beef?” test?

  348. 348
    Dionisio says:

    #348 follow-up

    From the paper referenced by gpuccio @327:

    The remarkable parallels between these lymphocyte lineages in jawless and jawed vertebrates suggest that the genetic programmes for the major lymphocyte differentiation pathways evolved in a common ancestor before the convergent evolution of the different types of antigen receptors in jawless and jawed vertebrates.

  349. 349
  350. 350
    Dionisio says:

    #346 addendum

    Does the referenced paper cover all the details mentioned @326 & @327?

  351. 351
    sparc says:

    333
    Curly HowardFebruary 15, 2015 at 2:32 pm

    I’m sorry to hear that pucci, but I guess I understand why you guys don’t want to talk in-depth about biology.
    Same goes for you silver.
    You guys copy/paste some complicated biology, declare irreducible complexity, and trade high-fives. But when anybody tries to debate your claims, you are forced to demonstrate your lack of biological knowledge until ultimately you back off (if you’re smart enough).

    Good chat guys, it’s been fun.

    Predicting that this thread will evolve exactly in this direction was not really difficult because GP braught up the very same “intelligent selection” BS back in 2008.

  352. 352
    Me_Think says:

    Dionisio @ 351

    Does the referenced paper cover all the details mentioned @326 & @327?

    I have clearly stated:

    …, although it doesn’t answer all questions.

    I am not really interested in how things evolved because I never ever believe some ID agent guides cellular processes.If you need specific answers, you need to search. I came across some paywalled papers on evolution of immune system. May be if you pay, you will get to know more.
    I know a single cell, when combined with chemical and pressure taxis, can do complex things like solve maze, take ‘decision’ and optimize paths (Yes I am talking of single cell , no brain Slime Mold- Physarum polycephalum) , so I am not surprised that Nature can evolve complex immune system without an ID agent guiding the process.

  353. 353
    Dionisio says:

    #352 sparc

    Predicting that this thread will evolve exactly in this direction was not really difficult because GP braught up the very same “intelligent selection” BS back in 2008.

    This time the arguments supporting gpuccio’s proposition are much better than they were back in 2008. The research done since then has produced more information that strengthens gpuccio’s position.

    As more research is being done at an accelerated pace these days, one may easily predict that in the near future gpuccio’s proposition will be even stronger than today.

    BTW, did you mean ‘brought’ ?

  354. 354
    Dionisio says:

    #353 Me_Think

    Did you notice that @346 I thanked you for providing the reference to that paper in your post #344?

    However, this time your whole comment @353 is worth much less than ‘guano’ (Spanish) because ‘guano’ can be used as fertilizer, but your comment @353 is completely useless.

    After you posted #344, I hoped you were finally trying to engage in this discussion seriously, but now I see that you are insisting in writing the same ‘wanu’ (Quechua) you’ve been writing before. No improvement. What a disappointment.

    The news coming from the biology research front are not encouraging to you and your party comrades these days. It ain’t gonna get better for y’all. Better think about this carefully.

    🙂

  355. 355
    Dionisio says:

    #352 sparc

    You’re participation in this discussion has been worse than poor so far.

    Can you do better?

    Would you dare to answer the questions in post #157?

    Are they too difficult for you? Note that you may simply provide references to papers that could answer the questions. C’mon, give it a try. 🙂

    BTW, don’t count on the 2009 paper referenced in post #344, because it may not answer those questions either. Better get more recent papers.

    PS. Your party comrades have done as embarrassingly bad as you in this discussion too. Poor things. It ain’t gonna get better for y’all in the future. More research is being done. Fasten your seatbelts.

  356. 356
    Dionisio says:

    #353 Me_Think

    Did you read post #347?

  357. 357
    Dionisio says:

    #356 correction

    #352 sparc

    You’re participation in this discussion has been worse than poor so far.

    Can you do better?

    Would you dare to answer the questions in post #157?

    Are they too difficult for you? Note that you may simply provide references to papers that could answer the questions. C’mon, give it a try. 🙂

    BTW, don’t count on the 2009 2006 paper referenced in post #344, because it may not answer those questions either. Better get more recent papers.

    PS. Your party comrades have done as embarrassingly bad as you in this discussion too. Poor things. It ain’t gonna get better for y’all in the future. More research is being done. Fasten your seatbelts.

    I mistakenly wrote 2009 instead of 2006. The paper referenced @344 is 9 years old.

  358. 358
    Dionisio says:

    #352 sparc

    FYI – Post #358 corrects a mistake in post #356.

    This last decade has been very prolific in research papers on the discussed subject. The 9-year old paper referenced @344 is old in some important aspects.

    BTW, at least Me_Think gave it a try and provided an old reference, to no avail, but you have not even tried. Why? Lack of arguments? That’s fine, just admit it. Lack of humility to admit it? Well, join your comrades’ club! 🙂

  359. 359
    Dionisio says:

    gpuccio

    It seems like post #344 is the most serious attempt to discuss our ‘nice’ interlocutors have made so far.

    Does that 9-year old document answer the most important outstanding questions raised in more recent papers?

  360. 360
    Box says:

    Curly Howard,

    CH: Box, I’m still waiting for a single example (that makes physiologic sense) of how my protein would disrupt homeostasis.

    I’m not sure what you ask me to do. My simple claim is that all proteins need regulation in order to preserve homestasis – concentration and right place needs to be controllable. Of course regulated proteins is exactly what we see in organisms. I drew attention to the obvious problem that this poses to an evolutionary concept of introducing new proteins – they too need regulation and the idea that regulation is already in place before the introduction of new protein seems ludicrous. So IMHO this boils down to a chicken egg problem – irreducible complexity.

    Unregulated proteins cause a host of problems. Would you like me to cite some examples? Here we have an example of a protein (MYH11) that can become unregulated by sperm germ-line mutation. In the Zebrafish unregulated MYH11 is thought to be responsible for “zebrafish meltdown phenotype” and in humans there is a correlation with cancer.

    All mutations resulted in unregulated molecules displaying constitutive motor activity, similar to the mutant myosin underlying mlt. Thus, MYH11 mutations appear to contribute also to human intestinal neoplasia. Unregulated MYH11 may affect the cellular energy balance or disturb cell lineage decisions in tumor progenitor cells.

    Maybe you can provide some references to newly evolved proteins that – for some mysterious reason – don’t need regulation?

    BTW I have noticed that you ignored my question in #285 about the evolution of the “lethal-weapon-protein”. Why not give it a go?

  361. 361
    gpuccio says:

    Dionisio:

    “It seems like post #344 is the most serious attempt to discuss our ‘nice’ interlocutors have made so far.

    Does that 9-year old document answer the most important outstanding questions raised in more recent papers?”

    No. But it fully supports the points I emphasized in post #327. 🙂

  362. 362
    gpuccio says:

    sparc:

    “Predicting that this thread will evolve exactly in this direction was not really difficult because GP braught up the very same “intelligent selection” BS back in 2008.”

    Wow! I have devoted fans here!

    Thank you, I am impressed. I think I have debated the concept of IS against NS for years, many times, in many contexts. But I am glad that you keep track of the oldest examples.

  363. 363
    gpuccio says:

    Dionisio:

    In brief, we have a rather sudden appearance of an adaptive immune system in agnathians, and then the rather sudden appearance of a new, different adaptive immune system in gnathostomes. About 500 million years ago.

    Interesting. But why should the neo darwinists try to explain those things? It’s enough to say “evolved” instead of “appeared”, and to throw in “convergent evolution” and “cooption” here and there. Problem solved.

  364. 364
    Dionisio says:

    gpuccio

    Agree. Thank you.

    BTW, I see you have loyal fans keeping track of your posts for years. That’s nice, isn’t it? 🙂

  365. 365
    Dionisio says:

    gpuccio

    Interesting. But why should the neo darwinists try to explain those things? It’s enough to say “evolved” instead of “appeared”, and to throw in “convergent evolution” and “cooption” here and there. Problem solved.

    My boss at work would not have let me get away with such a tricky way of solving our engineering design software development problems. They would have fired me right away.

  366. 366
    Silver Asiatic says:

    In brief, we have a rather sudden appearance of an adaptive immune system in agnathians, and then the rather sudden appearance of a new, different adaptive immune system in gnathostomes. About 500 million years ago.

    Interesting. But why should the neo darwinists try to explain those things? It’s enough to say “evolved” instead of “appeared”, and to throw in “convergent evolution” and “cooption” here and there. Problem solved.

    It’s interesting and amazingly deceptive how the whole thing works. I find myself buying-into it and overlooking the enormous flaws in the attempted explanation.

    The first and most essential part of the ‘explanation’ is to start with something that is unexplained, but already works.

    In this case, start with a ‘complex innate immune system’ which is found in single-cell organisms. It provides ‘generic’ responses. (The paper is talking about the adaptive immune system so it can skip the origin of the precursor).

    Once you have that in place, replication, insertions, cooption and recombination of signal sequences can be speculated quite easily. A new adaptive system evolves – then, convergently, another similar one evolves.

    But a step-by-step process?

  367. 367
    Dionisio says:

    gpuccio

    Your interlocutors should read your posts #326 & 327 to see if they can finally understand the real situation you keep explaining here in this discussion.

  368. 368
    Dionisio says:

    #367 Silver Asiatic

    The first and most essential part of the ‘explanation’ is to start with something that is unexplained, but already works.

    That’s not a serious approach to explain things, but apparently they manage to get away with that trick.

  369. 369
    Curly Howard says:

    Oh my, Box. Oh. My.

    You’re not sure what I’m asking you to do because you have no idea what you are talking about, which I will prove in just a moment.

    I have repeated numerous times that all proteins that are expressed, new or old, will have some form of regulation. If you knew the basics of gene expression, you would understand this. Some proteins are under much more regulation than others. Think about tissue specific genes versus “house-keeping genes.” There is a spectrum to everything that occurs in biology.
    My protein does not need much in the way of regulation, as I have already explained.

    Now, I’ll show you how this next part is going to go:

    We are talking about expression of a protein, right? So changes to non-coding regions?
    -Yes.

    In your example, how is the protein becoming unregulated?
    -By alterations within the coding regions.

    The protein expression is not changing. The amino acid sequence of the protein is changing and it results in what is called a constitutively active protein. Do you know what this means?
    -No.

    It means that the protein’s function is not regulated, it is always active. The expression levels have not changed. Likely if memory serves me correctly, myosin’s ability to auto-inhibit has been shut down.
    -Ok.

    So when they say “Unregulated MYH11 may affect the cellular energy balance or disturb cell lineage decisions in tumor progenitor cells,” this is because the function of the protein has been altered, it is not because the expression level has changed. Your example has nothing to do with what we are talking about. Do you have any idea what you are talking about, Box?
    -No.

    When I said to Silver back in 321, “Better to keep your mouth shut and let people think you’re a fool, then open it and remove all doubt, right,” you really should have listened.

    As for the “lethal-weapon-protein,” they are seen in highly specialized processes that have been developed and refined through evolution. They are under tight control because of their downstream effects. However, many proteins can be expressed at a wide range of levels with no effect on the cell; my protein is one of those. Obviously any changes that occur in the genome that are significantly detrimental to the organism will result in their deletion from the population.

    I suggest you go back to keeping your mouth shut.

    But then, who would I have to talk with. Or should I say, talk “at.”

    =)

  370. 370
    Dionisio says:

    #367 Silver Asiatic

    Once you have that in place, replication, insertions, cooption and recombination of signal sequences can be speculated quite easily. A new adaptive system evolves – then, convergently, another similar one evolves.

    At my work, the director of development would not have let anyone be so vague when explaining any development procedures.
    They would have kicked out anyone who would dare to explain things in such vague terms.

    But apparently our ‘brilliant’ interlocutors can get away with such tricks. Definitely this world is more tolerant of nonsense.

  371. 371
    gpuccio says:

    Piotr?

    “That looks a pretty evasive manoeuvre to an observer… he has raised a number of valid points you’ve left unaddressed” (post #334)

    “If you have any points that you want to discuss with me, even borrowed from others, I will be happy to discuss them with you in depth, as we have done so many times.” (post #335)

    Evasive?

  372. 372
    Box says:

    Curly Howard #370,

    Your posts remain entirely unresponsive. I’ll try to explain the issue one more time:

    C.H: I have repeated numerous times that all proteins that are expressed, new or old, will have some form of regulation.

    How will a new protein have some form of regulation? Is regulation in place before the introduction of the new protein?

    C.H: My protein does not need much in the way of regulation, as I have already explained.

    You did no such thing. You merely stated it. But even so, let’s assume it needs little regulation, how do we explain that this ‘little regulation’ is in place at the moment the new protein is introduced?

    C.H: It means that the protein’s function is not regulated, it is always active. The expression levels have not changed.

    So? How does it help your position that the protein is only partly unregulated? I offered this example to show how destabilizing unregulated (or partly unregulated) proteins are.

    C.H: As for the “lethal-weapon-protein,” they are seen in highly specialized processes that have been developed and refined through evolution. They are under tight control because of their downstream effects.

    Yes of course, however this doesn’t answer the question how the “lethal-weapon-protein” can be introduced without a tight regulation system already in place.

  373. 373
    Piotr says:

    #372 Gpuccio,

    Sorry, I’m not taking part in this discussion. Truth to tell, I shouldn’t be posting at all — I have students who won’t grade themselves — but I have to look at something else that Excel spreadsheets from time to time. Anyway, I don’t know enough about the immune system to be much use as a discussant, whether with my own points or borrowed ones. I was only hoping for the thread to develop so that I could learn something from lurking. But if you and Curly Howard can’t get along well, so be it.

  374. 374
    Silver Asiatic says:

    Dionisio

    At my work, the director of development would not have let anyone be so vague when explaining any development procedures.
    They would have kicked out anyone who would dare to explain things in such vague terms.

    But apparently our ‘brilliant’ interlocutors can get away with such tricks. Definitely this world is more tolerant of nonsense.

    Good points. In the world of engineering or software, you have to be very specific in describing how one event causes the next in sequence, and precisely what kind of logic is used to select one outcome versus another.

    Evolutionary biology, however, has a few advantages that make it much easier to offer vague explanations – and this allows it to have a lot of tolerance for imaginary situations.

    First, it’s talking about events that supposedly occurred in the deep past. The evolutionary story is protected by this buffer of time. Over 10 million years? The simplistic evolutionary mechanisms can achieve anything.

    Secondly, the evolution-story begins with its protagonist already in place. It’s the invisible, unintelligent, blind-but-brilliantly-genius, guiding-agent that does all these things. It’s the uber-mechanism – no longer just natural selection, because that doesn’t work. It’s the ‘thing’ that does all the selecting, refining, strategizing, optimizing, switching, inserting, protecting, defending, enhancing and enabling that needs to happen. It’s an agent of “good things for every organism”. Once you accept that this invisible agent-mechanism exists, then it’s very easy to accept that DNA is spliced, combined, inserted and rejoined to create an adaptive immune system.

    Third, the reason the blind-genius agent is accepted so easily (aside from the atheistic bias at work) is because we already have self-replicating living beings that are being affected by the invisible-evo-agent. Evolution benefits from this, where software and engineering cannot, because we’re talking about Living Organisms. And no matter what biologists or materialists may claim we all know there is a mystery to life. We’re all part of that mystery and we know it.

    So, when someone says, “the adaptive immune system emerged 500 million years ago”, it sounds perfectly ok. We have a huge amount of time, things ’emerge’ and we’re talking about life which is mysterious. Life is so mysterious that it has this invisible agent walking along with it, enabling and strategizing for the important task of survival.

    Now, no matter what happened or not, it was all for survival.

    The organisms that didn’t have an immune system? Well, they didn’t survive, of course. That’s the beauty of the immune system. It ’emerged’ and therefore species that have it survived.

    Convergent evolution? The invisible-agent is capable of creating almost exactly the same solutions in non-ancestral species because … whatever. It doesn’t matter. The most absurdly improbable occurrences (in technology for example) are easily accepted in biology.

  375. 375
    Curly Howard says:

    Unresponsive? So showing exactly how clueless you are about the topic at hand is “unresponsive?”

    Your example wasn’t even in the same ballpark as our conversation. Dysregulation of protein function is completely different from expression of the protein.

    “How will a new protein have some form of regulation? Is regulation in place before the introduction of the new protein?”

    Like I said, if you knew the details of how gene expression works, you would already have your answer to this question.

    In my example, the protein co-opts the regulatory mechanisms of the protein it evolved from. This is because my protein is the product of alternative splicing in a way similar to that of Dscam in drosophila. My protein does not need excessive levels of regulation; it just needs to be present to a certain degree within the organism. It sits around waiting to interact with its pathogen binding-partner.

    “So?” Like I said, regulation of function and regulation of expression = apples and oranges, mate.

    “doesn’t answer the question how the “lethal-weapon-protein” can be introduced without a tight regulation system already in place.” You are making the mistake of assuming that when the protein appeared, it was a “lethal-weapon-protein.” This is laughable. These lethal weapon proteins originally evolved with a new beneficial function to the cell, it was over millennia that they evolved precise regulatory mechanisms according to their downstream effects, becoming what they are today. Of course interruption of these precise regulatory mechanisms in certain proteins today will have a “lethal-weapon” effect.

    Have you come up with a way that my protein disrupts homeostasis yet?

    I gave you some hints even; homeostasis is the maintenance of pH, osmolarity, temperature, etc.

    Would my protein disrupt any of these to a degree that would have an effect on the organism (make sure it makes physiologic sense!)?

    Maybe you can get silver to help. Or has he realized that he is not equipped to talk about biology at this level?

  376. 376
    Box says:

    Curly Howard #376,

    C.H.: Dysregulation of protein function is completely different from expression of the protein.

    You seem to think that it is my claim that they are identical. Maybe you have misunderstood that the point I raised about regulation is by no means limited to the expression of the protein.

    Box:“How will a new protein have some form of regulation? Is regulation in place before the introduction of the new protein?”

    C.H.: Like I said, if you knew the details of how gene expression works, you would already have your answer to this question.

    Nope, again my question is in no way limited to the expression of genes. It’s about the entire regulation: the production of protein at the right time, maintenance of the required amount, being chaperoned to the right location and so forth.

    C.H.: Like I said, regulation of function and regulation of expression = apples and oranges, mate.

    You are the one who compartmentalized regulation. I’ve been meaning to discuss regulation in its entirety from the beginning of our little discussion.

    C.H.: These lethal weapon proteins originally evolved with a new beneficial function to the cell, it was over millennia that they evolved precise regulatory mechanisms according to their downstream effects, becoming what they are today.

    Sure that is your belief, but describe step-by-step how this happened. “It took a lot of time” isn’t exactly an explanation, now is it?

    C.H.: In my example, the protein co-opts the regulatory mechanisms of the protein it evolved from.

    So new proteins are regulated by (second-hand) regulation systems already in place; so only the introduction of the very first protein is a problem for your position? In my understanding of the precision of the goings on in the cell such an explanation seems highly unlikely. Can you reference a new protein that fits the regulatory mechanisms of another protein?

    C.H.: Would my protein disrupt any of these to a degree that would have an effect on the organism (make sure it makes physiologic sense!)?

    Is your protein incapable of disrupting anything? Can it be in the wrong place? Wrong amount perhaps?

  377. 377
    Silver Asiatic says:

    Box

    Sure that is your belief, but describe step-by-step how this happened. “It took a lot of time” isn’t exactly an explanation, now is it?

    As the story goes: “A long time ago it emerged because it offered a survival-benefit. Then it changed over millennia to become what it is today”.

    Is your protein incapable of disrupting anything? Can it be in the wrong place? Wrong amount perhaps?

    That’s the great thing about an imaginary protein.

  378. 378
    Curly Howard says:

    Right Box, so in a conversation about the effects of varying protein expression, you bring up an example of altering protein functionality. Sure, makes sense.

    Gene expression covers the timing of protein production, amounts, and just about everything else. No chaperone transport needed for my protein. Gene expression probably covers close to 99% of the regulatory control over proteins.

    I “compartmentalized” regulation to the control of gene expression because that is what we are talking about. “Does expression of the protein need to be highly regulated?” is the question we’ve been dealing with.

    The answer is no, in fact both its expression and function do not need to be highly regulated. As I said, my protein only needs to be present in relatively low amounts, and it does not need to be activated or inhibited. Remember, it is not an enzyme with a specific catalytic function.

    Ah, yes. The good ol’ ID “you have to explain every single step” argument. If that is your argument then we have nothing to talk about.

    “So new proteins are regulated by…” I am in no way claiming all new proteins do this. This is one possible mechanism and the mechanism that my protein used. But in general, sure I would guess that the evolution of most proteins at first uses “second-hand” regulation. You should bear in mind that the regulation of gene expression is nowhere near as clear cut as the diagrams your biology pop-up book shows you. It’s a mess. Anyways, speculation about the regulation of the first protein is a bit beyond me, but I would argue that at that point, regulation wouldn’t really be needed or at least that simple mass action would keep expression levels high enough, but not too high.

    All proteins that are produced by alternative splicing fit two or more proteins to the same regulatory mechanisms. I don’t know ages of protein lineages, but I’m sure that if you wanted to, you’d be able to find alternative spliced proteins that have arisen recently. Of course that depends on your definition of recent, which I dare ask.

    If my protein disrupted anything critical, it would immediately be deleted from the population. Seeing as how most of the protein shares the same exons of another protein, the chances of that happening are slim. The new exon that confers the ability to bind the pathogen is specific to an extramembrane domain of a pathogen protein, so no, it will not likely bind something of the host organism, but sure the chance is always there however slim. If the protein is transported to the mitochondria then it probably won’t function. And as long as the protein is present at relatively low levels at least, it will confer a basic immune response.

  379. 379
    Cross says:

    Curly Howard @ 379

    “Ah, yes. The good ol’ ID “you have to explain every single step” argument. If that is your argument then we have nothing to talk about.”

    Translation, I can’t explain it, time = magic.

    Cheers

  380. 380
    gpuccio says:

    Piotr:

    Thank you for answering. I hope your students will grade well.

    I certainly can’t get along well with Curly Howard, as much as I certainly can get along well with you. I think that threads and discussions can develop just the same, in full respect of our likes and dislikes, which are often a very private value.

    And I hope that, in your free moments, you can enjoy your lurking. 🙂

  381. 381
    gpuccio says:

    Cross:

    It’s strange how those who cannot explain one single step complain so often that we ask them to explain every single step.

    If I discuss with someone who explains 999 steps, and I insist that the 1000th is remaining unexplained, then maybe I am being fastidious.

    But if I discuss with someone who can explain nothing, absolutely nothing, and then he complains that I am requiring that he explain every single step, it’s not exactly the same thing…

  382. 382
    Cross says:

    gpuccio @ 382

    Indeed, you are asking them to explain “the magic of time”.

    Cheers

  383. 383
    Box says:

    Curly Howard,

    C.H.: But in general, sure I would guess that the evolution of most proteins at first uses “second-hand” regulation. You should bear in mind that the regulation of gene expression is nowhere near as clear cut as the diagrams your biology pop-up book shows you. It’s a mess.

    Okay, so this is your explanation of how newly evolved proteins can be regulated. Again, this is at odds with my understanding of the necessary precision of the going ons in organisms. Moreover, to rehash my original point, it seems at odds with the delicate balancing act an organism performs (homeostasis) – especially from a materialistic viewpoint. How such a balancing act can be performed – how equilibrium can be maintained – while things are “a mess”, as you state, is beyond me.

  384. 384
    Dionisio says:

    #382 gpuccio

    But if I discuss with someone who can explain nothing, absolutely nothing, and then he complains that I am requiring that he explain every single step, it’s not exactly the same thing…

    Perhaps it is because the embarrassment for not being able to explain anything is magnified proportionally to the number of steps they are asked to explain?

    That’s very frustrating. But it gets worse than that. Because instead of explaining it themselves, they could at least provide references to papers that explain the discussed subject, indicating the page numbers where the requested explanations are written in.
    But they don’t do even that.

  385. 385
    Dionisio says:

    #375 Silver Asiatic

    Yes, it’s simply pathetic.

  386. 386
    Me_Think says:

    Cross @ 383

    Indeed, you are asking them to explain “the magic of time”.

    Dionisio @ 386

    Yes, it’s simply pathetic.

    Yes, it’s simply pathetic. Give me a high five. I don’t know why scientists don’t spend more time explaining how ID agent helped in immune system design and development using Bio C++ version 2.0. At least the ID scientists could try to explain in some colleagues reviewed ID journal.

  387. 387
    Dionisio says:

    #387 Me_Think

    You’ve got it all wrong again. What else is new?

    Most biology researchers are busy trying to figure out how the amazingly complex biological systems function, hence they don’t have time to squander on senseless OOL debates.
    OOL is a wonderful mystery that no one can understand.

  388. 388
    Me_Think says:

    Dionisio @ 388

    Most biology researchers are busy trying to figure out how the amazingly complex biological systems function, hence they don’t have time to squander on senseless OOL debates.

    Right. That’s also my position. So why don’t ‘ID scientists’ spend some time on it, since they do nothing else?

  389. 389
    Curly Howard says:

    Unfortunately box, when you start looking at cell biology in detail, a lot of things are going to be at odds with your understanding.

    If we were to look just at the initiation of transcription, you’d find that not only does it occur at the typical start site within the promoter in one direction, but it also occurs at nearby positions going in the opposite direction, it occurs at enhancers, and in both directions there too. These are unstable transcripts that are immediately degraded, and we have been hard-pressed to find a function for any of them. Also, the typical recruitment of general transcription factors, and subsequently RNA polymerase, are often found to be significantly different from the sequential steps shown in textbooks. I’m sorry to break it to you, but the linearity shown in textbooks is far from what is really going in in the cell.

    The “delicate balancing act” a cell performs is the product of the complex checks and balances system that has evolved. In my opinion you are twisting the definition of “homeostasis” but it is actually quite malleable, so I’ll let it slide. In the end, to disrupt homeostasis it either takes a large amount of a small disruption, or it takes a small amount of a very specific disruption. Varying expression levels of a protein, or expression of a new protein are not likely to have much effect on homeostasis. The only way it would happen is if homeostasis is very sensitive to that single protein’s expression levels (which is rare) or if the new protein had a very specific, detrimental function (which is also rare).

  390. 390
    Curly Howard says:

    Cross, I haven’t even been able to make it past the first step with your biologically challenged friends. Do you have anything intelligent to say?

  391. 391
    Curly Howard says:

    Oh yeah silver, you never responded to my question about the gauger biocomplexity paper.
    From you saying “at present we can’t calculate it [probability of the protein evolving] and we’re not even close.” I assume you would agree that a paper that actually tries to calculate this probability is completely unsupported, no?

  392. 392
    Querius says:

    Heh. Considering the abuse CH is exhibiting in 391 towards Cross, it seems like CH has conceded the argument.

    And the quotes in bornagain77’s post @ 84 bear repeating:

    The Humpty-Dumpty Effect: A Revolutionary Paper with Far-Reaching Implications – Paul Nelson – October 23, 2012
    Excerpt: Anyone who has studied the protein folding problem will have met the famous Levinthal paradox, formulated in 1969 by the molecular biologist Cyrus Levinthal. Put simply, the Levinthal paradox states that when one calculates the number of possible topological (rotational) configurations for the amino acids in even a small (say, 100 residue) unfolded protein, random search could never find the final folded conformation of that same protein during the lifetime of the physical universe. Therefore, concluded Levinthal, given that proteins obviously do fold, they are doing so, not by random search, but by following favored pathways. The challenge of the protein folding problem is to learn what those pathways are.
    http://www.evolutionnews.org/2…..65521.html

    Confronting Science’s Logical Limits – John L. Casti – 1996
    Excerpt: It has been estimated that a supercomputer applying plausible rules for protein folding would need 10^127 years to find the final folded form for even a very short sequence consisting of just 100 amino acids. (The universe is 13.7 x 10^9 years old). In fact, in 1993 Aviezri S. Fraenkel of the University of Pennsylvania showed that the mathematical formulation of the protein-folding problem is computationally “hard” in the same way that the traveling-salesman problem is hard.
    http://www.cs.virginia.edu/~ro…..Limits.pdf

    BA77 continues: That no one really has a firm clue how proteins are finding their final folded form is made clear by the immense time (a few weeks) it takes for a few hundred thousand computers, which are linked together, to find the final folded form of a single protein:

    A Few Hundred Thousand Computers vs. (The Folding Of) A Single Protein Molecule – video
    https://www.youtube.com/watch?v=lHqi3ih0GrI

    The reason why finding the final form of a folded protein is so hard for supercomputers is that it is, as with DNA, like the ‘traveling salesman’ puzzle, which are ‘Just about the meanest problems you can set a computer (on) ‘.

    DNA computer helps traveling salesman – Philip Ball – 2000
    Excerpt: Just about the meanest problems you can set a computer belong to the class called ‘NP-complete’. The number of possible answers to these conundrums, and so the time required to find the correct solution, increases exponentially as the problem is scaled up in size. A famous example is the ‘travelling salesman’ puzzle, which involves finding the shortest route connecting all of a certain number of cities.,,,
    Solving the traveling-salesman problem is a little like finding the most stable folded shape of a protein’s chain-like molecular structure — in which the number of ‘cities’ can run to hundreds or even thousands.
    http://www.nature.com/news/200…..13-10.html

    Thank you, bornagain77. The bottom line is that there simply aren’t enough billions of years on earth to turn miracles into the mundane.

    -Q

  393. 393
    gpuccio says:

    I will restate here a few points which are interesting. To do that, I quote again from the paper referenced in my post #327 (with my emphasis):

    “B cell and T cell lineages are ancient

    The remarkable parallels between these lymphocyte lineages in jawless and jawed vertebrates suggest that the genetic programmes for the major lymphocyte differentiation pathways evolved in a common ancestor before the convergent evolution of the different types of antigen receptors in jawless and jawed vertebrates.”

    So, my points are:

    a) There is a general programme which is at the foundation of the two different implementations of adaptive immune system. Very simply, it is based on the idea of recognizing specific forms of specific parts of the aggressor, memorizing them, and setting a response programme which will allow a better defense in future encounters. IOWs, the whole recognition – memory -response pattern.

    b) If we include also the CRISPR system in prokaryotes, we have three very different implementations of those ideas.

    c) In particular, the system in jawless fish and the system in jawed vertebrates are deeply different, even if they use similar general concepts.

    d) The two different implementations require extremely complex coordination of molecular and cellular resources. Defining them “irreducibly complex” is probably an understatement.

    e) The only “explanation” offered seems to be that they are an example of “convergent evolution”. Beautiful!

    Like flight in insects, birds and mammals, I suppose…

  394. 394
    Dionisio says:

    #389 Me_Think

    You keep getting it wrong all the time. Where’s your reading comprehension?

    Here’s what I wrote @388:

    “Most biology researchers are busy trying to figure out how the amazingly complex biological systems function, hence they don’t have time to squander on senseless OOL debates.
    OOL is a wonderful mystery that no one can understand.

    However, most official biology-related textbooks indicate that OOL is not a mystery, but a known fact. Isn’t that a lie? Why are lies allowed to poison students’ minds?

    Humility to admit the unknown is a rare virtue in the human condition, but it’s necessary for science to be reliable and truthful.

    Do you agree that OOL is a wonderful mystery that no one can understand.?

    Yes, no, maybe?

    Please, try not to bark up the wrong tree again. Think.

  395. 395
    Me_Think says:

    Dionisio @ 395
    Where is your reading comprehension ?
    This is what I posted:

    Dionisio @ 388

    Dio: Most biology researchers are busy trying to figure out how the amazingly complex biological systems function, hence they don’t have time to squander on senseless OOL debates.

    MT: Right. That’s also my position. So why don’t ‘ID scientists’ spend some time on it, since they do nothing else?

    As for your question:

    Do you agree that OOL is a wonderful mystery that no one can understand.?
    Yes, no, maybe?

    It is a mystery. I don’t know if it’s wonderful ! For me the fact that the GPS module in a Chinese mobile phone works better than the more expensive Arduino GPS module is a wonderful mystery 🙂

  396. 396
    Dionisio says:

    Can someone read carefully the OP, posts 326, 327, 394, and then present a comprehensive, logically coherent counterargument?

  397. 397
    Me_Think says:

    Dionisio @ 397
    Do you think microbiologists are swarming UD ? It is either you who has to search for answers or ask ID Scientists at Bio complexity to do cutting edge research for you.

  398. 398
    gpuccio says:

    Me_Think:

    This is a blog, where some issues are routinely debated. Many people come here from both sides.

    The thing works this way: one presents arguments, others, if they don’t agree, present counter-arguments, if they have them.

    All those who read can judge for themselves the quality of the arguments, or the quality or absence of the counterarguments.

    If your argument is that microbiologists are too busy to offer counterarguments to the arguments presented here, well, anyone can judge the relevance and quality of your statement.

  399. 399
    Dionisio says:

    #396 Me_Think

    That “GPS module in a Chinese mobile phone” that impressed you so much, was designed by very smart engineers. Each of those engineers was at some point just a single cell (a.k.a. zygote).

    Now, that’s a real wonderful mystery.

    Regardless of anyone’s opinion.

    That’s as close to absolute reality as we can perceive.

    I challenge anyone and their cousins to present a comprehensive, logically coherent counterargument.

    But they will have to be extremely well prepared to withstand a blitzkrieg interrogation on cell fate specification, determination, differentiation, migration mechanisms at the deepest level of molecular details.

    Did you get it right this time?

    Let’s hope so. 🙂

  400. 400
    Me_Think says:

    Dionisio @ 400

    Each of those engineers was at some point just a single cell (a.k.a. zygote).

    Now, that’s a real wonderful mystery.

    Regardless of anyone’s opinion.

    I disagree. Every cell can be further shown to be just combination of fermions. BTW zygote is not a single cell, it is made of 2 gamete cells.

  401. 401
    Me_Think says:

    GP @399

    The thing works this way: one presents arguments, others, if they don’t agree, present counter-arguments, if they have them.
    All those who read can judge for themselves the quality of the arguments, or the quality or absence of the counterarguments.

    I agree. However evolution of a system which has not been studied (search throws up very few papers, some paywalled) widely can be answered by specialists only, and there aren’t any visiting UD.

  402. 402
    Dionisio says:

    #398 Me_Think

    You keep getting it all wrong, buddy.

    The research papers published in several peer-review journals are generally the main source of information for my current biology learning, in preparation for my work on an educational software development project. Obviously, with the caveat that sometimes those peer-reviewed papers could be fraudulent.

  403. 403
    Me_Think says:

    Dionisio @ 403

    You keep getting it all wrong, buddy.
    The research papers published in several peer-review journals are generally the main source of information for my current biology learning, in preparation for my work on an educational software

    Did I get ferminons are fundamental wrong? or that zygotes are not single cell wrong?
    Hmmm. I hope the educational software that says zygote is a single cell is never published.

  404. 404
    Dionisio says:

    #401 Me_Think

    What you wrote is very inaccurate, to say it euphemistically. 🙂

    The zygote is the most powerful stem cell in the whole developmental process.

    It is a complete single cell, containing the genetic information from two haploid cells.

    The mechanisms behind its formation and behind the development process that follows are amazing.

    The origin of all that is part of the wonderful mystery that many call OOL.

  405. 405
    Me_Think says:

    Dionisio,

    Me_Think @ 401 :

    zygote is not a single cell, it is made of 2 gamete cells

    Dionisio @ 405

    It is a complete single cell, containing the genetic information from two haploid cells.

    Well? Is your claim now that gametes are not haploid cell?! I fervently hope that educational software you were talking about is stopped!

  406. 406
    gpuccio says:

    Me_Think:

    “zygote is not a single cell, it is made of 2 gamete cells”

    I am not sure what you mean. The zygote is certainly a single cell. And it is certainly derived from the union of two gametes (each with half of the genetic information in the zygote).

    Regarding fermions, cells are certainly made of fermions, like all material objects, but what makes a cell a cell, and not a stone, is the special configuration and properties of its material components. I suppose you understand that well enough.

  407. 407
    Dionisio says:

    Someone suggested, a while back in another discussion, that some atheist interlocutors who appeared stubbornly confused and misinformed, are just paid agents working for this blog, in order to provoke heated debates and thus increase the number of visitors.
    I could not believe that, but lately I’ve started to suspect that perhaps it’s possible that idea is not too far off reality? 🙂
    Just look at the latest posts by some interlocutors here. Unless they are undercover agents, pretending to be so confused in order to make the atheists look embarrassingly arrogant, their comments make little sense, if any at all.
    However, how can we know their real motives? Should we ask the admin of this blog to reveal it? 🙂

  408. 408
    Me_Think says:

    GP @ 407
    Oh God. Why is your timing so bad? Dionisio and me were just starting to have fun.
    Dio @ 408,
    You haven’t answered this:
    Well? Is your claim now that gametes are not haploid cell?! I fervently hope that educational software you were talking about is stopped!
    P.S: Flash software- right?

  409. 409
    Dionisio says:

    #409 Me_Think

    Please, quote the exact text where I wrote whatever you claim that I wrote. Can you try better next time you write something here?

  410. 410
    Me_Think says:

    Dionisio @ 410
    Dionisio style answer:
    Read comment # 406

    You have still not answered comment # 409 :-
    Flash software- right?

  411. 411
    Silver Asiatic says:

    ch

    I assume you would agree that a paper that actually tries to calculate this probability is completely unsupported, no?

    Not completely unsupported. It’s the best attempt that has been made yet and by doing it we learn more about the challenge.

  412. 412
    Joe says:

    MT:

    Every cell can be further shown to be just combination of fermions. BTW zygote is not a single cell, it is made of 2 gamete cells.

    A zygote is a diploid cell. Also I don’t think it is OK to call a gamete a cell- even though it is called a cell- because they cannot reproduce. They seem to more akin to formed elements than to cells.

  413. 413
    Dionisio says:

    #401 Me_Think

    I disagree. Every cell can be further shown to be just combination of fermions. BTW zygote is not a single cell, it is made of 2 gamete cells.

    Do you still stand publicly by your statement affirming that a zygote is not a single cell?

    Or do you prefer to humbly admit your mistake and accept the correction written by gpuccio @407?

    The term ‘single’ in this context indicates that it is one cell. This term is commonly used in biological research in order to emphasize the distinction from grouped cells.
    The same term could be used in reference to other diploid cells.

  414. 414
    gpuccio says:

    Aurelio Smith:

    And half wrong. But he is probably only kidding, and it is not really the case of “defending” him. 🙂

    He should have said: the zygote is a single cell, derived from the union of two haploid gametes.

    The important point is that the zygote is a single, individual cell, from the moment it is born to the moment it divides. Its origin is in a way special.

    But it could be interesting to remember that there may be zygotes derived from the genetic information of one cell (and the epigenetic information of another one), like in cloning.

  415. 415
    Dionisio says:

    #415 Aurelio Smith

    Me_Think is therefore half-right in saying

    No, he’s wrong in stating that the zygote is not one cell. That’s a fundamental biology concept, very basic.

    The majority of the cells in our bodies are diploid. That term generally is related to the number of chromosomes in each cell nucleus.

    BTW, why did he need one of his party comrades to come to his rescue and admit he’s at least half-wrong?

    Couldn’t he admit it himself?

    The original statement he was trying to criticize was that each of us at some point started as a single cell. His failed attempt to criticize that simple statement has backfired.

    Why did he have to get into this kind of unnecessary embarrassment in order to criticize such a simple statement?

    Was there something in that statement that bothered him so much?

    Can any of his party comrades explain that behavior for him?

    Unless he will dare to do it himself this time?

    PS. This side discussion, unnecessarily provoked by Me_Think, is off topic in this thread, therefore it could be moved out to another thread.

  416. 416
    gpuccio says:

    Silver Asiatic:

    I think that the Gauger paper is very good, and it is an example of a very realistic and empirical way of approaching a very difficult issue (the topology of the protein functional space), which is crucial to the ID – neodarwinism debate.

    Some of our interlocutors complain that ID scientists do no research, and then are quite ready to throw “mock and scorn” on any ID research as soon as they see it, on no reasonable basis at all. Anyone is free to judge their behaviour.

  417. 417
    Curly Howard says:

    Yes, I have conceded because cross has provided such an intelligent refutation and the other two geniuses are bringing up such well-educated posts…not.

    And calling the gauger paper the “best attempt” is quite a twist. They come to the conclusion that one current protein couldn’t have evolved from another current protein (which isn’t what evolution even says happened) based on single amino acids changes while looking for a very specific function (assuming evolution occurred in this way is asinine).They knew what the results were going to be before they even started writing, in fact i didn’t even see any original research when I skimmed the paper, where is their supplemental data?
    The paper is a joke and yet I it’s totes here as “very good.”

  418. 418
    Silver Asiatic says:

    gpuccio

    I think that the Gauger paper is very good, and it is an example of a very realistic and empirical way of approaching a very difficult issue (the topology of the protein functional space), which is crucial to the ID – neodarwinism debate.

    Some of our interlocutors complain that ID scientists do no research, and then are quite ready to throw “mock and scorn” on any ID research as soon as they see it, on no reasonable basis at all. Anyone is free to judge their behaviour.

    Great points. I thought the Gauger paper was excellent for it’s clarity. Then it’s as you say – she is criticized for doing the work. But do any of the critics improve on the work that was done? No – they just sit back and condemn it.

    I think it’s quite right to see what is happening and make a judgement about the behavior.

  419. 419
    Curly Howard says:

    “Excellent for its clarity”
    Is code for “the content was crap.”
    I mean the only real experimental results are in the last figure, and it appears that the plates shown are only the controls. Not to mention it’s also the only figure that doesn’t even have a legend, just a link that leads to nowhere for me.

    Guess I shouldn’t really be surprised.

  420. 420
    Dionisio says:

    Curly Howard

    Can you read carefully the OP, posts 326, 327, 394, and then provide at least one reference to any paper that presents a serious, comprehensive, logically coherent counterargument?

  421. 421
    gpuccio says:

    Silver Asiatic:

    By the way, here is the abstract of the Gauger paper:

    Enzymes group naturally into families according to similarity of sequence, structure, and underlying mechanism. Enzymes belonging to the same family are considered to be homologs–the products of evolutionary divergence, whereby the first family member provided a starting point for conversions to new but related functions. In fact, despite their similarities, these families can include remarkable functional diversity. Here we focus not on minor functional variations within families, but rather on innovations–transitions to genuinely new catalytic functions. Prior experimental attempts to reproduce such transitions have typically found that many mutational changes are needed to achieve even weak functional conversion, which raises the question of their evolutionary feasibility. To further investigate this, we examined the members of a large enzyme superfamily, the PLP-dependent transferases, to find a pair with distinct reaction chemistries and high structural similarity. We then set out to convert one of these enzymes, 2-amino-3-ketobutyrate CoA ligase (Kbl2), to perform the metabolic function of the other, 8-amino-7-oxononanoate synthase (BioF2). After identifying and testing 29 amino acid changes, we found three groups of active-site positions and one single position where Kbl2 side chains are incompatible with BioF2 function. Converting these side chains in Kbl2 makes the residues in the active-site cavity identical to those of BioF2, but nonetheless fails to produce detectable BioF2-like function in vivo. We infer from the mutants examined that successful functional conversion would in this case require seven or more nucleotide substitutions. But evolutionary innovations requiring that many changes would be extraordinarily rare, becoming probable only on timescales much longer than the age of life on earth. Considering that Kbl2 and BioF2 are judged to be close homologs by the usual similarity measures, this result and others like it challenge the conventional practice of inferring from similarity alone that transitions to new functions occurred by Darwinian evolution.

    The objection that evolution would not go from one current protein to another current protein, but rather from a common progenitor to the two current proteins is really silly.

    First of all, we have not the hypothesized “common progenitor”, and the only sensible way to explore the topology of the functional space is by comparing real proteins, and not fairy tales. That’s how science works.

    Second, the paper is not dealing with the emergence of new protein families, but with the much “lesser” hypothesis of the derivation of one protein from another one inside a definite protein family. Indeed, the hypothesis tested is the possible transition between two proteins which have been chosen because they are extremely similar, especially at structure level. Even so, the paper shows that a transition between the two forms is much more difficult than usually thought.

    Now, let’s try to imagine how easy it would be to find the specific sequences of hundreds of AAs that are necessary for the working of complex proteins, like ATP synthase, which have emerged practically “from nothing” in the oldest time of OOL.

    The importance of the paper is that it documents, for the first time, the huge barriers that exist in the topological space of protein function, not only for the emergence of new structures, like new domains or superfamilies, but even for the “simple” transition in an already existing family, where usually microevolutionary events are supposed to be able to tweak an existing structure from one function to a slightly different one.

    Moreover, critics can well check or falsify these results by showing how easy it can be to derive new functional proteins from similar, existing proteins, by a random quantifiable process of mutations.

  422. 422
    Dionisio says:

    #423 gpuccio

    The hurdles described in your comments and in the referred paper seem numerous and difficult. But let’s think abstractly and assume for a moment that all those challenges are ‘somehow’ (borrowing a term commonly seen in some ‘scientific’ literature these days) overcome and that all the required proteins can be ‘somehow’ produced, through genetic expression or another way.
    Does that get us the amazingly complex interwoven mechanisms that researchers see in the biological systems? IOW, the protein availability is a necessary condition, but is it sufficient, in order to have those elaborate cellular and molecular choreographies orchestrated within the biological systems? Are there other factors to consider?

  423. 423
    Dionisio says:

    gpuccio

    Anything related to this discussion in the following link?

    http://www.uncommondescent.com.....ent-548888

  424. 424
    Me_Think says:

    Aurelio Smith @ 415

    Me_Think is therefore half-right in saying:..

    Thank you, but as I said in comment # 409

    Dionisio and me were just starting to have fun.

    Dionisio @ 417

    Unless he will dare to do it himself this time?

    PS. This side discussion, unnecessarily provoked by Me_Think, is off topic in this thread, therefore it could be moved out to another thread.

    You brought up Zygote- not me. I have no problem if these comments are deleted, but you still haven’t answered( Dionisio insistent style):

    You have still not answered comment # 409 :-
    Flash software- right?

  425. 425
    Me_Think says:

    gpuccio @ 423

    The importance of the paper is that it documents, for the first time, the huge barriers that exist in the topological space of protein function, not only for the emergence of new structures, like new domains or superfamilies, but even for the “simple” transition in an already existing family, where usually microevolutionary events are supposed to be able to tweak an existing structure from one function to a slightly different one

    This all boils down to impossibility of search landscape ( Axe et al.).I have discussed this in various threads.These are the quotes from the threads. HTH:

    Imagine a solution circle (the circle within which solution exists) of 10 cm inside a 100 cm square search space.

    The area which needs to be searched for solution is pi x 10 ^2 = 314.15
    The total Search area is 100 x 100 = 10000.
    The % area to be searched is (314.15/10000) x 100 = 3.14%

    In 3 dimensions,the search area will be 4/3 x pi x 10^3
    Area to search is now cube (because of 3 dimensions) = 100^3.
    Thus the % of area to be searched falls to just 4188.79/100^3 = 0.41 % only.

    Hypervolume of sphere with dimension d and radius r is:
    (Pi^d/2 x r^d)/r(d/2+1)

    HyperVolume of Cube = r^d
    At 10 dimensions, the volume to search reduces to just: 0.000015608 %
    But in nature, the actual search area is incredibly small. As wagner points out in Chapter six,

    In the number of dimensions where our circuit library exists—get ready for this—the sphere contains neither 0.1 percent, 0.01 percent, nor 0.001 percent. It contains less than one 10^ -100th of the library
    ====

    A ball (representing the search volume) with constant radius occupies ever-decreasing fractions of a cube’s volume as dimensions increases.
    I will quote Wagner himself:

    This volume decreases not just for my example of a 15 percent ratio of volumes, but for any ratio, even one as high as 75 percent, where the volume drops to 49 percent in three dimensions, to 28 percent in four, to 14.7 percent in five, and so on, to ever-smaller fractions.

    What this means:
    In a network of N nodes and N-1 neighbors, if in 1 dimension, 10 steps are required to to discover new genotype/procedure, in higher dimension, this 10 steps reduces drastically to fraction of 1 step !

    ======
    Imagine your Facebook network. Your immediate friends will have interest similar to yours. As you venture out in your network and traverse your friend’s friend network, or further on to friend’s friend’s friend network, you will encounter someone with totally different interest (akin to new function – this may or may not help in generating a new phenotype).
    Now imagine this Facebook network of yours balled up.It took many steps to reach the node where the person with a totally different interest exist on a 2d network. In your balled network, you have to travel maximum half of the steps to reach the same person. Now imagine this in higher and higher dimensions (perhaps like crushing the balled Facebook further). You will find you have to travel not even a fraction of 1 step to reach the person, and you will find a huge number of persons with dissimilar interests (akin to new functions – many of it helping to build a new phenotype or at-least help this generation survive better to start the search all over again with the advantage of the new phenotype) in just that fraction of 1 step, and that’s the reason improbabilities of ID don’t matter.

  426. 426
    Joe says:

    Me Think- The “improbabilities of ID” are all your position has. If you had something else we could discuss that.

  427. 427
    Dionisio says:

    #426 Me_Think

    No, these comments won’t be deleted, because the ID folks want the onlookers/lurkers to read them too. After all, some commenters here have them all in mind when they write their comments.

    Are you an undercover agent working for this blog?

    Is that why you seem always so confused? Are you just pretending it, as per your contract with the blog admin?

    Does your contract allow you to reveal it publicly?

    🙂

  428. 428
    Me_Think says:

    Dionisio @ 429
    Again (Dionisio insistence style:)

    You have still not answered comment # 409 :-
    Flash software- right?

  429. 429
    Dionisio says:

    #430 Me_Think

    You’re wrong again, buddy.

    My post #410 graciously answered your post #409.

    Did you miss it?

    Read it carefully. My message was very clear to anyone who is willing to understand it.

    Don’t forget that you made a gross conceptual mistake when you stated that the zygote is not a single cell. Too late now, everybody has seen how you have avoided admitting to your error. Even one of your party comrades had to come to your rescue, but it was too little, too late. Unless y’all are undercover agents working for this blog, trying to make the atheists look foolish. If that’s the case, then you’re doing a great job and they should give you a bonus. 🙂

    PS. By now the onlookers/lurkers may be very concerned about your constant failure to stay seriously focused in on the main subject of this discussion.

  430. 430
    gpuccio says:

    Me_Think:

    I really think that Wagner and you don’t know what you are talking about.

    I have tried to understand what you mean, and I think that in the end you are just saying that in “many dimensions” (whatever that means in biology) it is easier to go out of some functional space.

    We certainly agree that it is easy to go out of a functional space. That’s exactly what happens when a single nucleotide substitution generates a mutation which inactivates a protein which is essential: you know, that’s what genetic mendelian diseases incompatible with life are.

    The problem is not how easy it is to go out of a functional territory. The problem is how likely it is to land in another functional territory.

    In particular, in biology, “another functional territory” means a new configuration which has to have three properties:

    a) It must be functional

    b) It must be naturally selectable (IOWs it must confer a reproductive advantage and expand and be fixed). Otherwise, no probabilistic advantage is reached.

    c) It must be a step towards some future new complex configuration which is both functional and selectable (otherwise, all we have is a microevolutionary event which is not a step towards a macroevolutionary result, and that is exactly what we observe in all known microevolutionary events).

    The simple problem is not that it is difficult to leave the functional island, but that the functional island is surrounded by oceans of non functional, non selectable configurations, and almost all of them are unrelated to possible highly complex functional and selectable configurations, like the specific configuration of ATP synthase, just to give an old example.

    That’s why “improbabilities of ID” do matter. They are not “improbabilities of ID”. They are improbabilities of reality. And you don’t know what you are talking about.

  431. 431
    Me_Think says:

    Dionisio @ 431

    My post #410 graciously answered your post #409

    Thanks for your graciousness.

    Don’t forget that you made a gross conceptual mistake when you stated that the zygote is not a single cell. Too late now,

    Ha, cutting off half the sentence is not gracioius. Please be gracious again and quote full sentences.

    PS. By now the onlookers/lurkers may be very concerned about your constant failure to stay seriously focused in on the main subject of this discussion.

    Hmm…May be you will understand comment # 427 and find some relevance ?

    BTW,

    You have still not answered comment # 409 :-
    Flash software- right?

  432. 432
    Me_Think says:

    gpuccio @ 432

    really think that Wagner and you don’t know what you are talking about.

    Really ?

    Publications (Peer Reviewed)

    2014
    160. Payne, J.L., Wagner, A. (2014) The robustness and evolvability of transcription factor binding sites. Science 343, 875-877.[link]

    159. Wagner, A. (2014) A genotype network reveals homoplastic cycles of convergent evolution in influenza A (H3N2) evolution. Proceedings of the Royal Society B: Biological Sciences 281, 20132763. [reprint request]

    158. Szovenyi, P., Devos, N., Weston, D.J., Yang, X., Hock, Z., Shaw, J.A., Shimizu, K.K., McDaniel, S., Wagner, A. Efficient purging of deleterious mutations in plants with
    haploid selfing. Genome Biology and Evolution 6, 1238-1252. [reprint request]

    157. Wagner, A., Rosen, W. (2014) Spaces of the possible: universal Darwinism and the wall between technological and biological innovation. Journal of the Royal Society Interface 11, 20131190. [reprint request]

    156. Payne, J.L., Wagner, A. Latent phenotypes pervade gene regulatory circuits. BMC Systems Biology 8 (1), 64. [reprint request]

    155. Dhar, R., Bergmiller, T., Wagner, A. (2014) Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes. Evolution 68, 1775-1791. [reprint request]

    154. Hayden, E., Bratulic, S., Konig, I., Ferrada, E., Wagner, A. (2014) The effects of stabilizing and directional selection on phenotypic and genotypic variation in a population of RNA enzymes. Journal of Molecular Evolution 78, 101-108. [reprint request]

    153. Barve, A., Hosseini, S.-R., Martin, O.C., Wagner, A. Historical contingency and the gradual evolution of metabolic properties in central carbon and genome-scale metabolisms. BMC Systems Biology 2014, 8:48. [reprint request]

    152. Wagner, A. (2014) Mutational robustness accelerates the origin of novel RNA phenotypes through phenotypic plasticity. Biophysical Journal 106, 955-965. [reprint request]

    151. Sunnaker, M., Zamora-Sillero, E., Garcia de Lomana, A.L., Rudroff, F., Sauer, U., Stelling, J., Wagner, A. (2014) Topological augmentation to infer hidden processes in biological systems. Bioinformatics 30, 221-227. [reprint request]

    150. Wagner, A., Andriasyan, V., Barve, A. (2014) The organization of metabolic genotype space facilitates adaptive evolution in nitrogen metabolism. Journal of Molecular Biochemistry 3: 2-13. [reprint request]

    149. Payne, J.L., Moore, J.H., Wagner, A. (2014) Robustness, evolvability, and the
    logic of genetic regulation. Artificial Life 20, 111-126. [reprint request]

    2013

    148. Barve, A., Wagner, A. (2013) A latent capacity for evolutionary innovation through exaptation in metabolic systems. Nature 500, 203-206. [reprint request]

    147. Sunnaker, M., Zamora-Sillero, E., Dechant, R., Ludwig, C., Busetto, A.G., Wagner, A., Stelling, J. (2013) Automatic generation of predictive dynamic models reveals nuclear phosphorylation as the key Msn2 control mechanism. Science Signaling 6, ra41. [reprint request]

    146. Szovenyi, P., Ricca, M., Hock, Z., Shaw, J.A., Shimizu, K.K., Wagner, A. (2013) Selection is no more efficient in haploid than in diploid life stages of an angiosperm and a moss. Molecular Biology and Evolution 30: 1929-1939. [reprint request]

    145. Payne, J.A., Wagner, A. (2013) Constraint and contingency in multifunctional gene regulatory circuits. PLoS Computational Biology 9 (6), e1003071. [reprint request]

    144. Dhar, R., Saegesser, R., Weikert, C., Wagner, A. (2013) Yeast adapts to a changing stressful environment by evolving cross-protection and anticipatory gene regulation. Molecular Biology and Evolution 30, 573-588. [reprint request]

    143. Sabath, N., Ferrada, E., Barve, A., Wagner, A., (2013) Growth temperature and genome size in bacteria are negatively correlated, suggesting genomic streamlining during thermal adaptation. Genome Biology and Evolution 5, 966-977. [reprint request] .

    142. Bilgin, T., Kurnaz, I.A., Wagner, A. (2013) Selection shapes the robustness of ligand-binding amino acids. Journal of Molecular Evolution 76, 343-349. [reprint request] .

    141. Bichsel, M., Barbour, A.D., Wagner, A. (2013) Estimating the fitness effect of insertion sequences. Journal of Mathematical Biology 66, 95-114. [reprint request]

    140. Wagner, A. (2013) Genotype networks and evolutionary innovations in biological systems. In Handbook of Systems Biology. Eds: Walhout, A.J.M., Vidal, M., Dekker, J., Academic Press, London, p 251-264. [reprint request]

    139. Wagner, A. (2013) Metabolic networks and their evolution. In Encyclopedia of Systems Biology; p 1256-1259; Dubitzky, W., Wolkenhauer, O., Yokota, H., Cho, K.-H. (eds) Springer, New York.

    2012

    138. Barve, A., Rodrigues, J.F.M., Wagner, A. (2012) Superessential reactions in metabolic networks. Proceedings of the National Academy of Sciences of the U.S.A. 109 (18), E1121-E1130. [reprint request]

    137. Wagner, A. (2012) The role of robustness in phenotypic adaptation and innovation. Proceedings of the Royal Society B: Biological Sciences 279, 1249-1258.[reprint request]

    136. Hayden, E.J., Wagner, A. (2012) Environmental change exposes beneficial epistatic interactions in a catalytic RNA. Proceedings of the Royal Society B: Biological Sciences 279, 3418-3425.   Â

    135. Chen, B., Wagner, A. (2012) Hsp90 is important for fecundity, longevity, and buffering of cryptic deleterious variation in wild fly populations. BMC Evolutionary Biology 12, 25. [reprint request]

    134. Wagner, A. (2012) The role of randomness in Darwinian evolution. Philosophy of Science 79, 95-119. [reprint request]

    133. Sabath, N., Wagner, A., Karlin, D. (2012) Evolution of viral proteins originated de novo by overprinting. Molecular Biology and Evoluion 29, 3767-3780.

    132. Guo, B., Zuo, M., Wagner, A. (2012) Pervasive indels and their evolutionary dynamics after the fish-specific genome duplication. Molecular Biology and Evolution. doi: 10.1093/molbev/mss108. [reprint request]

    131. Bragg, J.G., Quigg, A., Raven, J.A., Wagner, A. (2012) Protein elemental sparing and codon usage bias are correlated among bacteria. Molecular Ecology 21, 2480–248. [reprint request]

    130. Ferrada, E., Wagner, A. (2012) A comparison of genotype-phenotype maps for RNA and proteins. Biophysical Journal 102, 1916-1925. [reprint request]

    129. Matias Rodrigues, J.F., Rankin, D., Rossetti, V., Wagner, A., Bagheri, H.C. (2012) Differences in cell division rates drive the evolution of terminal and differentiation in microbes. PLoS Computational Biology 8 (4), e1002468. [reprint request]

    128. De la Chaux, N., Tsuchimatsu, T., Shimizu, K.K., Wagner, A. (2012) The predominantly selfing plant Arabidopsis thaliana experienced a recent reduction in transposable element abundance compared to its outcrossing relative Arabidopsis lyrata. Mobile DNA 3, 2. [reprint request]

    127. Bilgin, T., Wagner, A. (2012) Design constraints on a synthetic metabolism. PLoS ONE 7(6): e39903. [reprint request]

    126. Wagner, A. (2012) Metabolic networks and their evolution. Evolutionary Systems Biology/Advances in Experimental Medicine and Biology 751: 29-52. [reprint request]

    125. Wagner, A. (2012) High dimensional adaptive landscapes facilitate evolutionary innovation p271-282 in Svensson, E.I., Calsbeek, R. (eds) The adaptive landscape in evolutionary biology. Oxford University Press, Oxford, UK. [reprint request]

    124. Wagner, A., Weikert, C. (2012) Phenotypic constraints and phenotypic hitchhiking in a promiscuous enzyme. The Open Evolution Journal 6, 14-28. [reprint request]

    123. Hayden, E., Wagner, A. (2012) Directional selection causes decanalization in a catalytic RNA. PLoS ONE 7(9), e45351. [reprint request]

    2011

    122. Hayden, E.J., Ferrada, E., Wagner, A. (2011) Cryptic genetic variation promotes rapid evolutionary adaptation in an RNA enzyme. Nature 474, 92-95.[reprint request]

    121. Wagner, A. (2011) The molecular origins of evolutionary innovations. Trends in Genetics 27, 397-410. [reprint request]

    120. Wagner, A. (2011) Genotype networks shed light on evolutionary constraints. Trends in Ecology and Evolution 26, 577-584. [reprint request]

    119. Dhar, R., Sägesser, R., Weikert, C., Yuan, J., Wagner, A. (2011) Adaptation of Saccharomyces cerevisiae to saline stress through laboratory evolution. Journal of Evolutionary Biology 5, 1135-1153. [reprint request]

    118. Wagner, A. (2011) The low cost of recombination in creating novel phenotypes. Bioessays 33, 636-646. [reprint request]

    117. Zamora-Sillero, E. Hafner, M., Ibig, A., Stelling, J., Wagner, A. (2011) Efficient characterization of high-dimensional parameter spaces for systems biology. BMC Systems Biology 5, 142. [reprint request]

    116. Samal, A., Wagner, A., Martin, O.C. (2011) Environmental versatility promotes modularity in large scale metabolic networks. BMC Systems Biology 5,135.[reprint request]

    115. Espinosa-Soto, C. Martin, O.C., Wagner, A. (2011) Phenotypic plasticity can facilitate adaptive evolution in gene regulatory circuits. BMC Evolutionary Biology 11:5, doi:10.1186/1471-2148-11-5. [reprint request]

    114. Rodrigues, J.F.M., Wagner, A. (2011) Genotype networks, innovation, and robustness in sulfur metabolism. BMC Systems Biology 5:39. [reprint request]

    113. Raman, K., Wagner, A. (2011) The evolvability of programmable hardware. Journal of the Royal Society Interface 8: 269-281. [reprint request]

    112. Raman, K., Wagner, A. (2011) Evolvability and robustness in a complex signaling circuit. Molecular BioSystems 7, 1081-1092. [reprint request]

    111. De la Chaux, N., Wagner, A. (2011) BEL/Pao retrotransposons in metazoan genomes. BMC Evolutionary Biology 11 :154. [reprint request]

    110. Wright, J., Bellissimi, E., de Hulster, E., Wagner, A., Pronk, J.T., van Maris, A.J.A. (2011) Batch and continuous culture-based selection strategies for acetic acid tolerance in xylose-fermenting Saccharomyces cerevisiae. FEMS Yeast Research 11,299–306. [reprint request]

    109. Espinosa-Soto, C., Martin, O.C., Wagner, A. (2011) Phenotypic plasticity can increase phenotypic variability after non-genetic perturbations in gene regulatory circuits. Journal of Evolutionary Biology 24, 1284-1297. [reprint request]

    108. Guo, B., Wagner, A., He, S. (2011) Duplicated gene evolution following whole-genome duplication in teleost fish. pp. 27-36. In: Friedberg, F. (ed.), Gene duplication. InTech, Rijeka, Croatia. [reprint request]

    2010

    107. Espinosa-Soto, C., Wagner, A. (2010) Specialization can drive the evolution of modularity. PloS Computational Biology 6: e1000719. [reprint request]

    106. Samal, A., Matias Rodrigues, J.F.., Jost, J., Martin, O.C., Wagner, A. (2010) Genotype networks in metabolic reaction spaces. BMC Systems Biology 4:30. [reprint request]

    105. Rankin, D.J., Bichsel, M. Wagner, A. (2010) Mobile DNA can drive lineage extinction in bacterial populations. Journal of Evolutionary Biology 23, 2422-2431. [reprint request]

    104. Raman, K., Wagner, A. (2010) The evolvability of programmable hardware. Journal of the Royal Society, Interface. June 9, doi: 10.1098/rsif.2010.0212. [reprint request]

    103. Ferrada, E., Wagner, A. (2010) Evolutionary innovations and the organization of protein functions in genotype space. PLoS ONE 5(11): e14172. doi:10.1371/journal.pone.0014172. [reprint request]

    102. Bichsel, M., Barbour, A.D., Wagner, A. (2010) The early phase of an insertion sequence infection. Theoretical Population Biology 78, 278-288. [reprint request]

    101. Sulc, P., Wagner, A., Martin, O.C. (2010) Quantifying slow evolutionary dynamics in RNA fitness landscapes. Journal of Bioinformatics and Computational Biology 8, 1027-1040. [reprint request]

    100. Wagner, A. (2010) On the energy and material cost of gene duplication. In: Dittmar, K., Liberles, D. Evolution after gene duplication. Wiley-Blackwell, Hoboken, NJ, p 207-214. [reprint request]

    99. Bragg, JG, Wagner, A. (2010) The evolution of protein material costs. In: Evolutionary genomics and systems biology, Caetano-Anolles, G., Ed., Wiley, NY, pp. 203-211. [reprint request]

    2009

    98. Bragg, J.G., Wagner, A. (2009) Protein material costs: single atoms can make an evolutionary difference. Trends in Genetics 25, 5-8. [reprint request]

    97. Martin, O.C.M., Wagner, A. (2009) Effects of recombination on complex regulatory circuits. Genetics 183, 673-684. [reprint request]

    96. Wagner, A. (2009) Evolutionary constraints permeate large metabolic networks. BMC Evolutionary Biology 9:231 [reprint request]

    95. Rodrigues, J., Wagner, A. (2009) Evolutionary plasticity and innovations in complex metabolic reaction networks. PloS Computational Biology 5(12): e1000613. [reprint request]

    94. Hafner, M., Koeppl, H., Hasler, M., Wagner, A. (2009) “Glocal” robustness analysis and model discrimination for circadian oscillators. PloS Computational Biology 5(10): e1000534. [reprint request]

    93. de la Chaux, N., Wagner, A. (2009) Evolutionary dynamics of the LTR retrotransposon roo inferred from twelve complete Drosophila genomes. BMC Evolutionary Biology 9:205. [reprint request]

    92. Wagner, A. (2009) Transposable elements as genomic diseases. Molecular Biosystems, 5 32. [reprint request]

    91. Wagner, A. (2009) Networks in molecular evolution. In: Meyers, R.A. (ed.) Encyclopedia of Complexity and System Science. Springer, Heidelberg. [reprint request]

    90. Hafner, M., Koeppl, H., Wagner, A. (2009) Evolution of feedback loops in oscillatory systems. Proceedings of the Third International Conference on Foundations of Systems Biology in Engineering (FOSBE 2009), Denver, CO, August 9-12, 2009. [reprint request] Hafner et al. 2009

    2008

    89. Wagner, A. (2008) Neutralism and selectionism: A network-based reconciliation. Nature Reviews Genetics 9, 965-974. [reprint request]

    88. Wagner, A. (2008) Robustness and evolvability: A paradox resolved. Proc. Roy. Soc. London Series. B 275, 91-100. [reprint request]

    87. Ferrada, E., Wagner, A. (2008) Protein robustness promotes evolutionary innovations on large evolutionary time scales Proc. Roy. Soc. London Series. B 275:1595-602.
    [reprint request]

    86. Wright, J., Wagner, A. (2008) The systems biology research tool: Evolvable open-source software. BMC Systems Biology 2:55. [request reprint]

    85. Martin, OC, Wagner, A. (2008) Multifunctionality and robustness tradeoffs in model genetic circuits. Biophysical Journal 94, 2927-2937. [request reprint]

    84. Wagner, A. (2008) Gene duplications, robustness, and evolutionary innovations. Bioessays 30, 367-373. [reprint request]

    83. Felix, M-A, Wagner, A. (2008) Robustness and evolution: concepts, insights, and challenges from a developmental model system. Heredity 100, 132-140. [reprint request]

    82. Jörg, T., Martin, OC, Wagner, A. (2008) Neutral network sizes of biological RNA molecules can be computed and are atypically large. BMC Bioinformatics 9:464. [reprint request]

    81. Wagner, A., de la Chaux, N. (2008) Distant horizontal gene transfer is rare for mobile prokaryotic DNA. Molecular Genetics and Genomics 280, 397-408. [reprint request]

    80. Wright, J., Wagner, A. (2008) Exhaustive identification of steady state cycles in large stoichiometric networks. BMC Systems Biology, 2:61. [reprint request]

    79. Fuller, M., Wagner, A. , Enquist, J. (2008) Using network analysis to characterize forest structure. Natural Resources Modeling 21, 225-247. [reprint request]

    2007

    78. Ciliberti, S., Martin, OC, Wagner, A. (2007) Innovation and robustness in complex regulatory gene networks. Proc. Natl. Acad. Sci. U.S.A. 104, 13591-13596. [reprint request]

    77. Ciliberti, S, Martin, OC, Wagner, A. (2007) Robustness can evolve gradually in complex regulatory networks with varying topology. PLoS Computational Biology 3(2): e15. [reprint request]

    76. Wagner, A., Lewis, C., Bichsel, M. (2007) A survey of transposable elements using IScan. Nucleic Acids Research 35, 5284-5293. [reprint request]

    75. Wagner, A. (2007) Rapid detection of positive selection in genes and genomes through variation clusters. Genetics 176: 2451–2463. [reprint request]

    74. Bragg, JG, Wagner, A. (2007) Protein carbon content evolves in response to carbon availability and may influence the fate of duplicated genes. Proc. Roy. Soc. London Series. B 274, 1063-1070. [reprint request]

    73. Wagner, A. (2007) From bit to it: The transformation of information into living matter by metabolic networks. BMC Systems Biology 1: 33. [reprint request]

    72. Wagner, A. (2007) Energy costs constrain the evolution of gene expression. Journal of Experimental Zoology (Molecular and Developmental Evolution) 308B:322–324 [reprint request]

    71. Wagner, A., Wright, J. (2007) Alternative routes and mutational robustness in complex
    regulatory networks. Biosystems 88, 163-172. [reprint request]

    70. Wagner, A. (2007) Gene networks and natural selection: Is there a network biology? In Pagel, M. Pomiankowski, A. (eds.) Evolutionary Genomics and Proteomics, Sinauer Associates, Sunderland, MA, USA. [Abstract]

    69. Sumedha, Martin, OC, Wagner, A. (2007) New structural variation in evolutionary searches of RNA neutral networks. Biosystems 90: 475-485.

    More here
    Just because he hasn’t published in vanity ID journals doesn’t mean he doesn’t know what he is talking about 🙂

  433. 433
    gpuccio says:

    Me_Think:

    A list of publications is not an argument, and is not guarantee of being right on a particular point. Do you believe differently?

    However, I was referring to your personal argument as offered by you quoting Wagner. I am not interested in people, but in arguments.

    We could simply say that the argument you offered is silly. Is that more clear?

    Now, please don’t answer that with a list of your publications.

  434. 434
    gpuccio says:

    Dionisio:

    “Does that get us the amazingly complex interwoven mechanisms that researchers see in the biological systems? IOW, the protein availability is a necessary condition, but is it sufficient, in order to have those elaborate cellular and molecular choreographies orchestrated within the biological systems? Are there other factors to consider?”

    No, it doesn’t. No, it is not. And yes, there are.

    Let’s say that we are in front of an amazing multilayered irreducible complexity. 🙂

  435. 435
    Me_Think says:

    gpuccio @ 432

    We could simply say that the argument you offered is silly. Is that more clear?
    The simple problem is not that it is difficult to leave the functional island, but that the functional island is surrounded by oceans of non functional, non selectable configurations, and almost all of them are unrelated to possible highly complex functional and selectable configurations

    You argued that

    Wagner and you [Me_Think] don’t know what you are talking about.

    By flaunting a long list of publications (which ID Scientists can’t match),I showed he knows what he is talking about.What he researched and published in his book is what I have offered as an argument for landscape search.
    You , Axe etal. are essentially claiming that evolution is a white noise landscape. Wagner shows that by using network search in hyper-dimensional (which is nothing but the structural dimensions) search space, the improbabilities of searching vanishes .
    A more appropriate argument would be if you claim network search cannot be equated to landscape search and so volume search doesn’t apply -only surface area of the search sphere should be used. May be I would be stumped ,or not – I would have to work that out.

  436. 436
    gpuccio says:

    Me_Think:

    Maybe Wagner knows what he is talking about when he talks of his personal ideas. He can well publish thousands of publications about his personal ideas. That does not imply that his ideas are true.

    Frankly, I don’t know his ideas in detail, and I cannot care less about them for what I have heard until now. As far as your argument goes, as you have expressed it, apparently based, correctly or not, on hi, ideas, I can only repeat: it is silly, if you intend it as an argument applied to proteins and biology (as you seem to intend it).

    If you believe that what you said has any relevance to the points I highlighted in post #432, please express your ideas. I will be happy to hear them.

    And if you need time to “work it out”, please take all the time you need. I am not CH, and as I have said, I am interested in arguments, not in individual persons (or numbers of publications).

  437. 437
    Me_Think says:

    gpuccio @ 438

    Frankly, I don’t know his ideas in detail, and I cannot care less about them for what I have heard until now.

    Well if you don’t care about an Evolutionary Biologist’s peer reviewed papers and how networked hyper dimension space demolishes silly Axe and Dembski’s search algorithm and landscape arguments, what is the point of arguing at all ?!!!

    And if you need time to “work it out”, please take all the time you need.

    Since it involves taking derivative of hyperspace function and possibly Poly Gamma to see if a certain dimension will give maximum search area, it will take time, but I am not sure it is worth it. In any case I will work it out , may be to use in some other thread

  438. 438
    Dionisio says:

    Ok, too much digression.

    Let’s go back to the main topic of this discussion:

    Can Me_Think, Wagner or anybody else provide at least one reference to any paper that presents a serious, comprehensive, logically coherent counterargument for what gpuccio wrote in the OP, and later in posts 326, 327, 394, 436?

    Can Me_Think, Wagner or anybody else provide at least one reference to any paper that can seriously answer the questions in post #157?

  439. 439
    Box says:

    Wagner terms DNA an “hyperastronomical library”.

    Wagner: The deepest secrets of nature’s creativity reside in libraries just like this: all-encompassing and hyperastronomically large. Only instead of being written in human language, the texts in these libraries are written in the genetic alphabet of DNA and the molecular functions that DNA encodes. The library’s chemical language can express life itself—all of it.

    The problem is how to find anything in this huge library.

    Wagner: The problem is much worse in a hyperastronomical library. The universal library might well contain the secret to immortality—or at least the perfect recipe for turkey stuffing—yet the library is so large that we would never find it unless we knew where to look.

    The solution: assume that the library is a 5000-dimensional space and everything can be found in a few steps.

    Wagner: In other words, we can arrange the library’s metabolic texts on the corners of a hypercube in a 5,000-dimensional space. This is why off-the-shelf shelving would not work. You cannot cram the metabolic library into three puny dimensions. It needs thousands of dimensions to breathe.
    (…) And what holds for one corner of the cube holds for any other corner: It has three neighbors. Likewise, in a 5,000-dimensional cube, each and every metabolism has as many neighbors as there are dimensions, five thousand in all. You can walk from each metabolic text in five thousand different directions, to find one of its five thousand neighbors in a single step. (…)
    Evolving organisms are like visitors to the metabolic library. Gene deletions and gene transfer allow them to walk through the library, to step from one metabolic text to another, often an immediate neighbor. (…)
    Evolution can reach them in a few small steps, minor edits in a genotype.

  440. 440
    Dionisio says:

    #441 Box

    Within the main topic of this thread:

    Can you, Wagner or anybody else provide at least one reference to any paper that presents a serious, comprehensive, logically coherent counterargument for what gpuccio wrote in the OP, and later in posts 326, 327, 394, 436?

    Can you, Wagner or anybody else provide at least one reference to any paper that can seriously answer the questions in post #157?

  441. 441
    gpuccio says:

    Box:

    I still find Wagner’s ideas irrelevant. Maybe Me-Think will convince me of the opposite.

    Moreover, he goes on discussing metabolisms, as though they were existing building stones. What about the complex proteins which make those metabolisms possible? Maybe if we arrange them in a 10000-dimensional icosahedron, it will be easy to find new functional proteins for all necessities.

    We should alert protein engineers of that intriguing possibility.

  442. 442
    Box says:

    Dionisio #442,

    I have a hard time reading Wagner and keep a straight face. This guy not only assumes that DNA and metabolic texts (the “hyperastronomical library”) is somehow organized in a 5,000-dimensional space, but also assumes the existence of “genotype networks”. Why do they exist? For the same reason that 5000-dimensional space exists: otherwise things don’t work.

    Wagner: Viewed from afar, the library’s explorers, from bacteria to blue whales, might appear like giant clouds of dust grains—dwarfed by the library itself—drifting this way and that, from one stack to the next, endlessly meandering swirls of living things that try new combinations of chemical reactions over and over and over again. Some die. Others survive, and pass innovative combinations on to subsequent generations. This churning mass of life is evolution in action.
    That action would vanish if genotype networks did not exist.

    Is there a (scientific) way to detect “genotype networks” in 5,000-dimensional space? I guess not, but Wagner doesn’t seem worried about those details.
    Where does the information in the “hyperastronomical library” and the “genotype networks” come from? As far as I can tell Wagner doesn’t offer any explanation.


    edit: Gpuccio,
    Wagner comes across as a guy who never parted with the crazy ideas of the hippie movement.

  443. 443
    gpuccio says:

    Me_Think:

    This is from one of the most recent papers by Wagner:

    The points of correspondence between biology and technology we discussed are far from complete [32,67,122]. However, they already insinuate that highly successful biological and technological systems share a property that is independent of both biology and technology. This property, one might call it innovability, emerges from the organization of a space of possible innovations, designs or genotypes [6]. Because such spaces are mathematical concepts, one could easily dismiss them and their organization as figments of our imagination, were it not for what Nobel laureate Eugene Wigner called the ‘unreasonable effectiveness of mathematics’ in explaining the natural world [123]. It suggests that such spaces and the innovations therein have an existence beyond our limited minds. And while concepts such as this, for more than two millennia, were the subject of non-experimental disciplines such as mathematics and philosophy, they have now become accessible to experimental science. For example, recent technological advances in biology permit the synthesis of arbitrary new protein genotypes. In doing so, they also permit the exploration of a genotypes space through experiment and computation [124–126]. Technological systems are not far behind, as explorations of digital circuit spaces testify [119,127]. Efforts such as this will undoubtedly accelerate the demolition of the conceptual wall separating biological and technological innovation.

    And he is perfectly right. There is no conceptual wall separating biological and technological innovation: both are examples of design.

  444. 444
    Silver Asiatic says:

    In other words, we can arrange the library’s metabolic texts on the corners of a hypercube in a 5,000-dimensional space. This is why off-the-shelf shelving would not work. You cannot cram the metabolic library into three puny dimensions. It needs thousands of dimensions to breathe.

    I think it would be a lot better if we arranged the library into a 50,000 dimension space. That way each ‘metabolic text’ would have ten times more opportunities only one step away.

  445. 445
    gpuccio says:

    Box:

    Wagner’s reasoning, in a nutshell, as I see it:

    Biological objects and human artifacts both have similar properties.

    They both seem designed.

    But, as we cannot accept that biological objects are designed, we could propose that human artifacts are, after all, the result of universal darwinism.

  446. 446
    gpuccio says:

    I will say it again: Borges was a great poet, and his vision of the Library of Babel has more beauty and sincere desperation in itself than all the arrogant pseudo-scientific constructions of multiverses and multidimensional hypercubes.

  447. 447
    gpuccio says:

    Box:

    “I have a hard time reading Wagner and keep a straight face.”

    There is no need to keep a straight face. I hope we are still allowed to laugh, in this world. It’s a precious part of our libertarian free will.

  448. 448
    Dionisio says:

    gpuccio

    Your OP has been visited 1166 times so far. There are 450 follow-up comments. However, not a single counterargument for the challenge described @440.

    It seems like your ‘nice’ interlocutors lack serious arguments to post here.

    Oh, well… there’s not much we can do about it. 🙂

  449. 449
    Me_Think says:

    ID ers,
    Sigh.There are 5,500 metabolic pathways. You can explore all the pathways at biocyc
    These are represented by the hypothetical library (Just like landscapes in Dembski, Axe papers).If you ever feel like looking up Wagner’s papers, data and software, you will understand that structural dimensions run into millions! You can get software, research data at: Wagner’s Zurich univ page Get into the habit of reading something other than Marvel comics if you need to understand anything useful.

  450. 450
    Joe says:

    Me Think- what is your point? Your position doesn’t have a mechanism capable of producing metabolism.

  451. 451
    Box says:

    Okay, how do genotype networks come into existence? Well, according to Wagner, by “self-organization” in the “timeless eternal realm of nature’s libraries”. Makes perfect sense, right? This is great stuff.

    Wagner: Genotype networks are yet another example of the pervasive self-organization we first encountered in chapter 2—the same phenomenon that pervades both the living and nonliving worlds, from the formation of galaxies to the assembly of membranes. But they are a peculiar example of self-organization. Unlike galaxies, which self-assemble through the gravitational attraction of cosmic matter, or biological membranes, which self-organize through the love-hate relationship of lipid molecules with water, genotype networks DO NOT EMERGE OVER TIME. They exist in the timeless eternal realm of nature’s libraries. [FAR OUT MAN!] But they certainly have a form of organization—so complex that we are just beginning to understand it—and this organization arises all by itself [Of course! That goes without saying. SURE THING] And as with galaxies and membranes, the principle behind their self-organization is simple: Life is robust. This robustness is both necessary for genotype networks—otherwise synonymous texts would be isolated from one another—and it is sufficient.17 Wherever metabolisms, proteins, and regulatory circuits are robust, genotype networks emerge.

    [My emphasis]

  452. 452
    Silver Asiatic says:

    genotype networks DO NOT EMERGE OVER TIME. They exist in the timeless eternal realm of nature’s libraries.

    That’s great science. There’s a timeless and eternal realm where genotype networks exist. And libraries arise all by themselves. That’s a pretty important part of the story of origins, I’d think.

  453. 453
    Me_Think says:

    Box,
    Keep reading. The book is for general audience. It gets into hypercubes and network search only later. Why don’t you start reading chapter 6 to see how search space reduces, and as quoted by you earlier: Evolution can reach them in a few small steps, minor edits in a genotype.

  454. 454
    Box says:

    Me_Think #455: Why don’t you start reading chapter 6 (..)?

    That’s a weird request, since the quote I provided in post #453 is from CHAPTER SIX, “The Hidden Architecture”.

  455. 455
    Me_Think says:

    Right Just read further along to here:

    A ball with constant radius occupies ever-decreasing and ever-tinier fractions of a cube’s volume.32 (This volume decreases not just for my example of a 15 percent ratio of volumes, but for any ratio, even one as high as 75 percent, where the volume drops to 49 percent in three dimensions, to 28 percent in four, to 14.7 percent in five, and so on, to ever-smaller fractions.)33
    The same counterintuitive phenomenon holds in other libraries of innovation: The more dimensions they have—the larger their collection of metabolisms or molecules—the smaller the distance to find specific innovations. A browser who starts with a metabolism that can survive on some foods and then blindly searches for one that can thrive on others needs to change only a few reactions and explore a tiny fraction—too small to imagine—of the metabolic library before stumbling upon the right text. The same holds true for RNA. Starting from an existing RNA molecule, a nearby molecule with a new shape—any new shape you choose—will be found after changing only a few of the molecule’s nucleotide building blocks and having explored a tiny fraction of the library.34
    The astonishing fact that evolution needs to explore one 10-100th of a library to secure the arrival of the fittest goes a long way to explain how blind search produces life’s immense diversity. Evolution does not have to search the entire haystack, because the haystack contains more than one needle. In fact, thanks to robustness, and the genotypic disorder it permits, the haystack contains too many needles to count, and they are organized into sprawling but navigable networks.

    Funny, how it negates the oft repeated ‘Needle in Haystack’ ID position.

  456. 456
    Joe says:

    Me Think- your position still doesn’t have a mechanism capable of producing biological reproducers

  457. 457
    Silver Asiatic says:

    genotype networks DO NOT EMERGE OVER TIME

    That negates Darwinism and any step-by-step story of origins.

  458. 458
    Me_Think says:

    …And here’s the bit on robustness. Combined with hyperdimension, the search network reduces probability of finding new functions to almost nil- unlike ID’s ‘improbable search landscape’. Now ID can’t claim search is improbable.

    Robustness isn’t limited to metabolism and whole genomes. It is just as pervasive in individual proteins like lysozyme. This protein kills bacteria by destroying their wall of protective molecules. It appears not only in human saliva, tears, and even mother’s milk, but in a large number of other animals, and even in viruses that attack bacteria.13 When scientists want to find out how a protein like this works, they do something akin to knocking out genes in a genome, but on a smaller scale—they change individual letters in the protein’s amino acid string and observe the effects of each change. When they engineered more than two thousand lysozyme variants, each one with a single altered amino acid, they found that some sixteen hundred variants—more than 80 percent—could still kill bacteria. Proteins like lysozyme, and there are many, are as robust as metabolisms. And the same holds for regulation circuits—we already heard about a circuit in the bacterium Escherichia coli that can be rewired in the laboratory without ill effects (chapter 5).
    The most obvious benefit of such robustness is that it keeps organisms alive. Its importance goes back all the way to the first self-replicating RNA molecules and the fatal error catastrophe, in which small errors compound over time until replication becomes impossible (chapter 2). That was a true catch-22: RNA molecules have to self-replicate with few errors to acquire the ability to self-replicate with few errors. But only a bit of the obustness in today’s RNA could lower the bar for this problem to a manageable height: Because a few replication errors in a robust molecule do not erode its ability to self-replicate, robustness provides a stay of execution by error catastrophe, perhaps long enough to stumble upon better replicators.14
    But the importance of robustness goes far beyond that. It explains the mystery of genotype networks and of innovability.

  459. 459
    Joe says:

    Yes Me Think, it was intelligently designed to be robust. That robustness allows for alternative splicing, overlapping genes and RNA splicing and editing.

    And it remains that your doesn’t have a mechanism capable of producing living organisms, let alone the genetic, regulatory and metabolic networks.

  460. 460
    Me_Think says:

    …and anyone interest in further research can download the Matlab package here:
    A matlab package to sample high-dimensional parameter spaces
    A matlab toolbox to determine the robustness

  461. 461
    Dionisio says:

    gpuccio

    Your OP has been visited 1170 times so far. There are 460+ follow-up comments. However, not a single counterargument for the challenge referenced in post #440.

    Even sparc has let us down, after triggering your OP. Does that mean that your ‘nice’ interlocutors lack serious arguments to post here?

    Oh, well… there’s not much we can do about it. 🙂

  462. 462
    Silver Asiatic says:

    And the same holds for regulation circuits—we already heard about a circuit in the bacterium Escherichia coli that can be rewired in the laboratory without ill effects (chapter 5).

    Regulatory circuits that can be re-wired without ill effects are far more evidence for design than of an unguided process. Robustness is a quality for the preservation of life – or survival, as the author says. But this apparent need for survival is also unexplained in a blind, chemical process. What it says, instead, is that life is something entirely different than chemical combinations alone. Robustness, preservation, stability, regulation and defense of the organism, self-organizing networks and the centrality of survival — all point to life as something important, or intended.

  463. 463
    Box says:

    As far as I understand Wagner he holds that the old RM+NS is incompetent as a search. IOW his book confirms the ID critique on Neo-Darwinism. How does he ‘solve’ the search problem? By hypothesizing things like hyperastronomical libraries in multidimensional space, genotype networks and other undetectable fantasy stuff.
    Okay admittedly that would speed up the search. However the law of conservation of information teaches us that you cannot beat a blind search. So where does the information in the libraries and the networks come from? This question Wagner attempts to answer by “self-organization”.

  464. 464
    Me_Think says:

    SA and Box,
    If you understand Axe’s landscape search with minima and maxima hills and landscapes, you should have no problem understanding Wagner’s hyper-dimension search Both Axe and Dembski’s search is a white noise landscape search. When you take biological structural dimension into account, the search space reduces. As commented earlier in this thread:

    Imagine a solution circle (the circle within which solution exists) of 10 cm inside a 100 cm square search space.

    The area which needs to be searched for solution is pi x 10 ^2 = 314.15
    The total Search area is 100 x 100 = 10000.
    The % area to be searched is (314.15/10000) x 100 = 3.14%

    In 3 dimensions,the search area will be 4/3 x pi x 10^3
    Area to search is now cube (because of 3 dimensions) = 100^3.
    Thus the % of area to be searched falls to just 4188.79/100^3 = 0.41 % only.

    Hypervolume of sphere with dimension d and radius r is:
    (Pi^d/2 x r^d)/r*(d/2+1) r* = Gamma function – when will UD enable LaTeX ?

    HyperVolume of Cube = r^d
    At 10 dimensions, the volume to search reduces to just: 0.000015608 %
    In the number of dimensions where our circuit library exists—get ready for this—the sphere contains neither 0.1 percent, 0.01 percent, nor 0.001 percent. It contains less than one 10^ -100th of the library

  465. 465
    Me_Think says:

    ….continued from comment #437

    A more appropriate argument would be if you claim network search cannot be equated to landscape search and so volume search doesn’t apply -only surface area of the search sphere should be used. May be I would be stumped ,or not – I would have to work that out

    Ok. the math works out as below:

    The surface area of the network over the search sphere can be given by 2 Pi^(d/2)/ Gamma (d/2)
    Derivative with respect to d gives
    Pi^d/2 [Log(Pi)- Ploy Gamma (0, d/2)]/ Gamma (d/2)
    Solving for d and Finding root gives the Maximum surface Area at dimension 7.26, so the maximum surface area is reached at 7th structural dimension. Since bio-structures are all above 7 dimension we can safely say even if we take search space as a surface area and not volume, above 7 dimensions, the area will keep decreasing. As an Example for a unit sphere and dimensions from 1 to 10 will give :

    2, 2 (Pi), 4 (Pi), 2 (Pi)^2, (8 (Pi)^2)/3, (Pi)^3,
    (16 /(Pi)^3)/15, (Pi)^4/3,(32 (Pi)^4)/105, (Pi)^5/12

    which gives:

    2, 6.28319, 12.5664, 19.7392, 26.3189, 31.0063, 33.0734, 32.4697, 29.6866, 25.5016

    Note that area falls off after dimension 7. At 100th dimension, the value is just Pi^50/304140932017133780436126081660647688443776415689605120000000000 = 2.3682*10^-38

  466. 466
    Box says:

    Me_think #466,
    You seem to suggest that Wagner’s reduction of search space has to do with known biologic structures.

    Me_Think: When you take biological structural dimension into account, the search space reduces.

    This is not the case at all – it’s all fantasy stuff. Wagner hypothesizes a huge (hyperastronomical) “metabolic library” and then looks for an environment / organization that solves the search problem that follows from such a huge library. He comes up with follow-up hypothesis: 5,000-dimensional space. Search problem solved, since the hypothesized multidimensional space connects everything in the hypothesized library by just a few steps.
    IOW this is all just pure fantasy stuff and there is no connection whatsoever with biological structures as we know them.

    But although it is hopeless to imagine higher-dimensional spaces, they follow the same laws as our three-dimensional space: The edges of a hypercube are equally long, adjacent edges are at right angles to one another, and each corner corresponds to a possible metabolism. And such cubes in high-dimensional space turn out to have curious properties well suited to house the metabolic library.
    The number of corners in a square is four, in a cube it doubles to eight, and in a four-dimensional hypercube it doubles again to sixteen. With every added dimension, it doubles, and by the time you have reached 5,000 dimensions, this number has become the hyperastronomical 2^5000, the size of the metabolic library. In other words, we can arrange the library’s metabolic texts on the corners of a hypercube in a 5,000-dimensional space. This is why off-the-shelf shelving would not work. You cannot cram the metabolic library into three puny dimensions. It needs thousands of dimensions to breathe.

    [Wagner, Chapter 3]

  467. 467
    Me_Think says:

    Box,
    5000 is the metabolic pathways number – it is not a fantasy. The library is hypothetical in the same sense that landscape in search landscape is (Axe, Dembski et al). Wagner shows how searching the genotype network at hyper dimension (which is structural dimension) reduces search space. I think if you read the book for comprehension instead of for scoring points, you would understand.

  468. 468
    Box says:

    Me_Think,
    I’m not talking about metabolic pathways. I’m talking about the hypothesized “hyperastronomical metabolic library” and multidimensional space. Are you saying that these are empirical facts?

  469. 469
    gpuccio says:

    Aurelio Smith:

    No need to shout. Everybody knows that.

    And most needles are so small, that the probability of finding one of those needles is so low that it will never happen.

    Shout that, if you like.

  470. 470
    gpuccio says:

    Me_Think:

    Yous arguments still look silly.

    First of all, define what you mean by “dimensions”. OK, there are a number of metabolisms. And a number of functional proteins. But those are not dimensions. They are occurrences.

    The search space is the combinatorial space of sequences. There is no other search space, because random variation is random variation of nucleotide sequences.

    The only correct question is: how many of the possible combinatorial sequences are functional? How many are selectable?

    What is the sequence relationship between functional islands? (That we know well: none, at the superfamily level).

    These are the questions. The rest is (how was it, DNA_Jock?): bafflegab.

  471. 471
    Joe says:

    Aurelio Smith:

    You could say the environment is the designer of evolutionary change.

    You can say anything, however you still need the evidence to support it.

  472. 472
    gpuccio says:

    Aurelio Smith:

    That is a discussion I have had many times, probably even with you. No reason to repeat all the details here. My simple point is that nobody has ever said that there is only one needle. The number and probability of needles is an integral part of ID theory.

    That’s why I am really amazed that Wagner and you are so excited by the idea that there is more than one needle. That’s all.

  473. 473
    Box says:

    Aurelio Smith: It’s an analogy for the multi-dimensional nature of the niche environment.

    Reference please. I have Wagner’s book in front of me. A search for “niche” produces just one unrelated hit: ‘But because waters of all temperature mix around a vent, a suitable temperature niche exists for any one of proto-life’s chemical transformations’

  474. 474
    Dionisio says:

    gpuccio

    Several new references to recent papers on very important subjects (posts #288-291) in this thread:

    http://www.uncommondescent.com.....ent-549082

  475. 475
    Dionisio says:

    finding the needles in the haystacks won’t resolve the problems:

    #436 gpuccio

    let’s think abstractly and assume for a moment that all those challenges are ‘somehow’ (borrowing a term commonly seen in some ‘scientific’ literature these days) overcome and that all the required proteins can be ‘somehow’ produced, through genetic expression or another way.

    Does that get us the amazingly complex interwoven mechanisms that researchers see in the biological systems?

    No, it doesn’t.

    IOW, the protein availability is a necessary condition, but is it sufficient, in order to have those elaborate cellular and molecular choreographies orchestrated within the biological systems?

    No, it is not.

    Are there other factors to consider?

    yes, there are.

    Let’s say that we are in front of an amazing multilayered irreducible complexity. 🙂

  476. 476
    Box says:

    Aurelio #482,

    Thank you. I gather now that your posting #474 was in fact not responsive to what I said – “hyperastronomical metabolic library” and “multidimensional space” are terms used by Wagner and are not equal to RM and NS.

  477. 477
    Dionisio says:

    #480 addendum
    Perhaps a more practical approach, instead of trying to resolve abstract probability problems, would be to try to describe in details how our best scientists and engineers would have built the known biological systems, but in a way that could have also occurred ‘naturally’ without their intervention?
    Maybe that has been done already? Is it documented somewhere?
    However, most probably the majority of the researchers are busy trying to figure out how the biological systems function, hence they don’t have time to squander on senseless OOL research.
    🙂

  478. 478
    gpuccio says:

    Aurelio Smith:

    “We should not confuse maps and territories.”

    Absolutely! That’s one of my strongest principles. (Have you ever read about NLP?) 🙂

  479. 479
    gpuccio says:

    Dionisio:

    You ask:

    “Maybe that has been done already? Is it documented somewhere?”

    I will answer quoting Me_Think’s words (hardly an accomplice of mine):

    “However evolution of a system which has not been studied (search throws up very few papers, some paywalled) widely can be answered by specialists only, and there aren’t any visiting UD.”

    The simple answer is: it has not been done; it is not documented anywhere.

    Like many other things…

  480. 480
    gpuccio says:

    Dionisio:

    Great stuff on Nature from the NIH Roadmap Epigenomics Consortium!

    Now, let’s absorb this new avalanche of data. 🙂

  481. 481
    Dionisio says:

    gpuccio

    Great stuff on Nature from the NIH Roadmap Epigenomics Consortium!
    Now, let’s absorb this new avalanche of data. 🙂

    Yes, that’s exactly right!

  482. 482
    Me_Think says:

    Box @ 471

    I’m not talking about metabolic pathways. I’m talking about the hypothesized “hyperastronomical metabolic library” and multidimensional space. Are you saying that these are empirical facts?

    Of course it is based on facts. Why don’t you read the book?:

    thanks to twentieth-century biochemistry and to the technological revolutions of the early twenty-first century. They gave us access to a mountain of metabolic information on more than two thousand different organisms, stored in giant online repositories, such as the Kyoto Encyclopedia of Genes and Genomes, or the BioCyc database, and accessible in split seconds from any computer with an Internet connection.2
    Figure 4 shows how we can organize this information. The left side of the figure stands for a list of five thousand reactions—written as chemical equations. To avoid clutter I wrote out the molecules in only one of them—the sucrose-splitting reaction—but simplified all others to a single letter. Let’s consider one organism, such as E. coli or a human, and mark a “1” next to a reaction if our organism can catalyze this reaction—it has a gene making an enzyme for it. Otherwise we’ll mark a “0.” The result is a long list of ones and zeroes like that in the figure, a compact way to specify a metabolism.
    Bacteria such as E. coli can make all twenty amino acids in proteins, whereas metabolic cripples like us humans can make only twelve of them. We lack the necessary enzymes and reactions for the remaining eight. The figure’s shorthand way of describing a metabolism is ideal for expressing differences like this: Because we lack some reactions, our list of reactions contains some zeroes where that of E. coli contains ones.
    A list like this is also an extremely compact way to write an organism’s metabolic genotype—the part of the genome encoding its metabolism—because an organism’s list of reactions is ultimately encoded in its DNA. You can also think of the list as a text written in an alphabet with only two letters, and without spaces or punctuation marks, like this: “1001 . . . 0110 . . . 0010.” The first letter in such a text might correspond to the sucrose-splitting reaction, which is present (“1”) in this example, whereas the second reaction might be one of those needed to synthesize an essential amino acid—it is absent (“0”) in this example text but could be present (“1”) in another organism’s genotype—and so on.
    It is a text in a library vast beyond imagination, the library of all possible metabolisms.
    The number of texts in that library can be calculated with the same arithmetic that computed the size of the universal library of books. Because each reaction in the known universe of reactions can be either present or absent in a metabolism, there are two possibilities (present or absent) for the first reaction, two for the second reaction, and so on, for each reaction in the universe. To calculate the total number of texts, we multiply the number 2 by itself as many times as there are reactions in our universe. For a universe of 5,000 reactions, there are 2^5000 possible metabolisms, 2^5000 texts written in the alphabet of zero and one, each of them standing for a different metabolism. This number is greater than 10^1500,( MT: actually it’s 1.4 x10^1505. If we take 5,500 as lsited in BioCyc, we have a ‘library’ of 4.62×10^1655) or a 1 with 1,500 trailing zeroes. While not quite as large as the number of texts in the universal library of human books, it is still much larger than the number of hydrogen atoms in the universe. The metabolic library is also hyperastronomical.

    Similarly, for proteins of say 150 amino acids, each genotype will have 150 x 19 (20-1) = 2850 neighbors in the genotype network.
    He even gives the reason for the library analogy (in Chapter Three Notes)

    This analogy is inspired by a famous short story of the Argentine author Jorge Luis Borges entitled “The Library of Babel” (Spanish original: “La biblioteca de Babel”), published in English translation in Borges (1962). The idea behind this short story, however, predates Borges. It has been used by many other authors, including Umberto Eco and Daniel Dennett

  483. 483
    gpuccio says:

    Me_Think:

    And so? After we have discovered that 2^5000 is a big number, and that one can do a silly thing like representing complex biochemical sets of reactions with a 0 or a 1, how does the argument go on?

    Just for curiosity.

    And where are the “5000 dimensions”? Up to now, we have only defined a very abstract set of 5000 “metabolic reactions”, and then the set of all their possible combinations, considering each reaction as binary (present or absent). The first set has cardinality 5000. The second set has cardinality 2^5000.

    OK, that is rather trivial. How does the argument go on? Please, explain.

  484. 484
    gpuccio says:

    Me_Think:

    By the way, I have dealt with a scenario strongly related to the Library of Babel issue in this OP:

    “An attempt at computing dFSCI for English language”

    http://www.uncommondescent.com.....-language/

    You may have a look at it, if you like.

    Combinatorial search spaces are the essence of ID theory.

  485. 485
    Dionisio says:

    gpuccio

    Do you consider the subjects of these two recent references (@293-294) interesting too?

    http://www.uncommondescent.com.....ent-549122

  486. 486
    Dionisio says:

    gpuccio

    Recent references starting @295 here:

    http://www.uncommondescent.com.....ent-549208

  487. 487
    Dionisio says:

    gpuccio

    Your expresion “new avalanche of data” @487 is very accurate.

    I’ve been selectively looking at what has appeared about very specific topics just recently and it’s simply overwhelming.

    Without the zotero tools I’d be completely disoriented. But even with those tools it’s very difficult for me to keep up with what’s coming out of research. Even considering that papers have to go through peer-review ‘delay’ before they get published.

    How can they analyze all that information accurately?

    It’s beyond fascinating.

    🙂

  488. 488
    Box says:

    Gpuccio,

    GP: And so? After we have discovered that 2^5000 is a big number, and that one can do a silly thing like representing complex biochemical sets of reactions with a 0 or a 1, how does the argument go on?

    Excellent question. I think I have uncovered some of Wagner’s line of thought. One can say a lot about Wagner as a writer, but one cannot say that his writing style is crisp …

    Starting from the quote provided by Me_Think in #489 Wagner focusses on bacteria, because multicellular animals cannot effectively “explore the metabolic library”.

    Wagner: the real geniuses of innovation are the smallest organisms on the planet: bacteria.

    He goes on listing reasons why: faster reproduction, horizontal gene transfer, absorption of DNA from other cells and so forth

    Wagner: (…) bacteria are masters of metabolic innovation. (…) the shelves of life’s universal library contain a virtually infinite number of masterpieces waiting to be found. (…) Everywhere on this planet, a relentless shuffling and mixing and recombining of genes takes place. Wherever microbial life occurs, in the depth of the oceans and on arid mountaintops, in scalding hot springs and on frigid glaciers, in fertile soils and desiccated deserts, inside and around our bodies, life is experimenting with every conceivable combination of new genes, rereading, editing, and rejuggling its metabolic texts without pause, yielding an enormous and still growing diversity of metabolisms.

    Here comes Wagner’s first big idea: Because of all this gene transfers between bacteria and other organisms the ENTIRE “library” of all possible metabolic texts is available to every bacterium.

    Wagner (commenting on his computer model of E.coli): New genes—acquired through gene transfer or otherwise—can change the genotype that brings forth this phenotype. If this change allows the mutant to metabolize ethanol, we replace the “0” next to ethanol with a “1.” Because every conceivable metabolic innovation can be written like this, by replacing a “0” with a “1” in a metabolic phenotype, there are about as many possible metabolic innovations as there are phenotypes.36

    After that Wagner goes on housing the library – which contains the metabolic information of more than two thousand different organisms – in 5,000-dimensional space thereby ‘solving’ the search problem – after he notices that the library is too big to find anything ; see Wagner post # 468. Let’s call this Wagner’s second big idea.

    Is Wagner restricted to explaining bacterial life – since they are the only ones with access to the ‘hyperastronomical’ library? Wagner himself doesn’t seem to think so and points to various connections between multicellular organisms and bacteria. He seems to hold that the innovations by bacteria explain the innovations of multicellular life:

    Wagner: We think of a phenotype as something we can see, and many metabolic phenotypes are plain as daylight. They include the melanins that protect our skin against radiation, that camouflage a lion’s fur, and that color the ink of an octopus. All of them are molecules synthesized by metabolism. And so are the various pigments that dye tree leaves, lobsters, flowers, and chameleons, whether for defense, courtship, or sometimes for no good reason at all.31 But metabolic phenotypes do not end at this visible surface. They extend to depths that are hidden from our eyes yet visible to chemical instruments—and to natural selection. Their most important role is to ensure viability itself, which boils down to the ability to synthesize sixty-odd molecules very different from those pretty pigments—they are the essential biomass molecules I mentioned in chapter 2.

    // Summing up: there seems to be some grounding in reality for the availability of the entire library to bacteria – the gene transfer stuff. However I have still no clue what could possibly ground 5,000-dimensional space. //

  489. 489
    gpuccio says:

    Box:

    Thank you for trying to help. I must say that I am not any nearer to understand, but certainly it’s not your fault. 🙂

    What I would like to know is: what is Wagner’s “big idea” which explains how extremely unlikely things can be found by random search?

    Maybe Me_Think can help. After all, he is a fan of the guy. 🙂

  490. 490
    Box says:

    Gpuccio,

    Reading Wagner is like wading through a swamp of complete confusion.
    About your question, the hypothetical 5,000-dimensional space connects everything in a few steps. So that ‘solves’ the search problem.

    Wagner: You can walk from each metabolic text in five thousand different directions, to find one of its five thousand neighbors in a single step. (…)
    Evolving organisms are like visitors to the metabolic library. Gene deletions and gene transfer allow them to walk through the library, to step from one metabolic text to another, often an immediate neighbor. (…)
    Evolution can reach them in a few small steps, minor edits in a genotype.

    Yes … it is indeed very “imaginative”.

    edit: come to think of it…. “a few small steps” sounds good, however in this hypothetical 5,000-dimensional space there are so many small steps that one wonders if the search is indeed reduced.

  491. 491
    Zachriel says:

    Box: come to think of it…. “a few small steps” sounds good, however in this hypothetical 5,000-dimensional space there are so many small steps that one wonders if the search is indeed reduced.

    What it means is that the probability of disconnected islands is vanishingly small. It also means there are many dimensional directions that can lead to increased fitness, many ‘ways’ to climb.

  492. 492
    Box says:

    Zachriel: What it means is that the probability of disconnected islands is vanishingly small. It also means there are many dimensional directions that can lead to increased fitness, many ‘ways’ to climb.

    Yes, indeed. So bacteria are able to find a flagellum in a few steps. However one has to believe in Wagner’s hyperastronomical library in 5,000-dimensional space in order to find such a scenario feasible.

    Are Wagner’s ideas gaining ground in mainstream biology?

  493. 493
    Zachriel says:

    Box: So bacteria are able to find a flagellum in a few steps.

    That depends on the starting point, of course.

    Box: Are Wagner’s ideas gaining ground in mainstream biology?

    We’re not familiar with Wagner’s ideas, however, we are familiar with multidimensional search spaces.

  494. 494
    Dionisio says:

    Ok, I admit that this off topic discussion on multidimensional search spaces is very high above my pay grade. However, since now the number of hypothetical steps has been reduced so drastically, can someone provide reference to serious peer-reviewed scientific paper(s) containing comprehensive, logically coherent, step-by-step explanations of how the bacteria could have appeared and how the first multicellular organisms could have appeared? Please, provide links and corresponding page numbers to locate the text.
    Thanks.

  495. 495
    Dionisio says:

    gpuccio

    Who would have thought that your OP will reach over 500 follow-up posted comments, but not a single serious counterargument for the challenging references summarized in post #440?

    Your interlocutors have let us down. What a disappointment. They sounded more knowledgeable and capable before you started this OP. At least that was the wrong perception I got when I read sparc’s challenging comments that triggered your OP.

    Oh well, what else is new?

  496. 496
    gpuccio says:

    Box and Zachriel:

    Excuse me, but apparently what I can understand of Wagner’s “argument” is the following:

    a) If we have a set of 5000 metabolic pathways

    b) If we describe each member of the set as “off” (0) or “on” (1)

    c) We have a set of 2^5000 states and

    d) We can go from one state to another one by turning on or off a single metabolic pathway.

    Is that all? Is it really that trivial? And what has that to do with the search for a functional state in a search space which is huge?

    A few simple questions:

    1) The set of 5000 metabolisms is a hugely complex dictionary. Where did it come from?

    2) Turning on or off a metabolic pathway can be a one bit operation, if the metabolic pathway is there and there is a one bit switch which can turn it on or off. That’s what happened with the citrate pathway in the Lenski experiment. But where did the metabolic pathway come from?

    3) Again, I cannot see the “multidimensional space”. We have a set of 2^5000 states. We imagine that we can change the bits of each state. That is similar to a search for a functional protein in the sequence space, but the sequence space is made of random aminoacid sequences, while this “space” is made of complex and functional metabolisms.

    4) That said, it remains to be seen how many of the 2^5000 combinations are functional, and naturally selectable. Frankly, I could not care less. The whole discourse is, up to now, utterly senseless.

    If anyone can make sense of it, please talk!

  497. 497
    Zachriel says:

    Dionisio: However, since now the number of hypothetical steps has been reduced so drastically, can someone provide reference to serious peer-reviewed scientific paper(s) containing comprehensive, logically coherent, step-by-step explanations of how the bacteria could have appeared

    You’re choosing very ancient transitions that have left little physical evidence. The origin of the first cells is obscure. You might check out the work of Jack Szostak’s Lab for some general ideas how it was thought to have occurred.
    http://molbio.mgh.harvard.edu/szostakweb/

    Dionisio: and how the first multicellular organisms could have appeared?

    This is also somewhat enigmatic; however, it is not as mysterious as the origin of the first cell. The basic history was adhesion then differentiation then apoptosis. See this review; Müller, The Origin of Metazoan Complexity: Porifera as Integrated Animals, Integrative and Comparative Biology 2003.

    The key is the stepwise increase in complexity.

  498. 498
    Dionisio says:

    #504 Zachriel

    Ok, will look into them. Thank you.

  499. 499
    Dionisio says:

    #504 Zachriel

    I did not find, in the sources you suggested*, any comprehensive, logically coherent, step-by-step explanations of how the bacteria or the first multicellular organisms could have appeared. Perhaps my ignorance didn’t allow me to see it clearly? Can someone else point to the page numbers (from-to) where those explanations are written in? Thanks.

    Besides, the more specific challenge summarized in post #440 remains undisputed.

    (*) suggested sources

    http://molbio.mgh.harvard.edu/szostakweb/

    http://www.jstor.org/discover/.....id=3739600

    http://icb.oxfordjournals.org/content/43/1/3.full

  500. 500
    gpuccio says:

    Dionisio:

    Zachriel is a master of language and clever expression, and that’s why I appreciate him so much.

    Look at this masterpiece:

    “You’re choosing very ancient transitions that have left little physical evidence.”

    Who could deny that?

    “The origin of the first cells is obscure.”

    The understatement of the century, but certainly true.

    “You might check out the work of Jack Szostak’s Lab for some general ideas how it was thought to have occurred.”

    You certainly might. Indeed, you did.

    And you certainly found “some general ideas how it was thought to have occurred”. You did. Very general, certainly, and not about what happened, but certainly about what “was thought to have occurred”.

    “This is also somewhat enigmatic; ”

    The second understatement of the century, but certainly true.

    “however, it is not as mysterious as the origin of the first cell.”

    Not sure, but it is probably true. Let’s say that we could reasonably agree.

    “The basic history was adhesion then differentiation then apoptosis.”

    Well, a reasonable list of complex processes which certainly have an important role. None of them explained. Just think of what “differentiation” implies, for example.

    “See this review; Müller, The Origin of Metazoan Complexity: Porifera as Integrated Animals, Integrative and Comparative Biology 2003.”

    Certainly a reasonable advice: looking at what has been said about an issue is certainly a reasonable step in making up our ideas.

    “The key is the stepwise increase in complexity.”

    This is masterful. Look at that word, “stepwise”. He did not say “gradual”, which is something I would have certainly agreed with, in general terms (who can deny that graduality is there, often together with sudden jumps?). And he did not say that “stepwise increase” was all that there is, only that it is the key to something.

    And what does “stepwise” mean? All and nothing. What is a “step”? One bit? The emergence of a new protein? Of a new pathway? Of a new species? And so on… Everything can be a “step”.

    OK, the final result is that Zachriel has said a few effective things, most of them undeniable, some of them vague, all of them essentially reasonable, all of them intelligent in their form, which give the idea that there are a lot of important things that you don’t know, and that you are not considering, and that, while you have your arguments, those arguments can be essentially addressed.

    A final consideration: I am not criticizing Zachriel at all. As I have said many times, I really like him, and there is no irony in this. He is intelligent, and generally respectful. This post of mine should be considered a tribute. 🙂

  501. 501
    Dionisio says:

    gpuccio

    I’m glad you’ve clarified this so well for me. I really appreciate it. Hopefully onlookers/lurkers will benefit from reading your comments too (your OP has been visited 1260 times so far).

    I wasn’t familiar with the suggested sources or their authors, hence I thought it was worth taking a look at them.

    I’m not a big fan of getting too involved in OOL debates. Personally I don’t know how or when it happened, but I believe it has a supernatural cause. Besides, OOL debate doesn’t seem to offer much value to my software development project. However, it’s an important part of the ongoing debate in this site and outside.

    To me, it’s much more important for science today to dedicate more time and resources to the research of the biological systems and their functioning. There are many outstanding questions to be answered in those areas. Medicine and health maintenance programs benefits much more from that research.

    Among your very insightful comments, you wrote:

    Just think of what “differentiation” implies, for example.

    Differentiation could be preceded by the highly complex mechanisms of specification and determination. All that together seems like a whole branch of the most advanced biology research these days. Just look at the numerous related references posted in the ‘third way’ and the ‘mystery’ threads in UD since last summer.

    That’s why words like ‘differentiation’ in Z’s post attracted my attention and made me look into the suggested sources. But all I found there was a combination of general ideas mixed with some specific references to a few fundamental properties that could be part of an explanation, but were not the explanations themselves.

    BTW, one of the suggested sources is around 12 years old, which seems like a very long time in light of the fast-paced biology research these days.

    I have seen more recent papers on the evolutionary topic, but they seem to lack the explanations requested in posts #440 and 501. However, my poor biological knowledge might have kept me from noticing the explanations. That’s why I insist that those who know more provide the references and indicate the page numbers where the requested explanation is to be found. Quoting some related text could help too. Apparently nothing that meets those requirements has been presented here so far.

    Again, thank you very much for your timely commentary.

  502. 502
    Dionisio says:

    #508 corrections

    Personally I don’t know exactly how or when it happened, but I believe in its supernatural cause.

    Medicine and health maintenance programs could benefit much more from that research.

    And it’s actually benefitting from it already. Unfortunately some delays might have been indirectly caused by misleading presuppositions based on unfounded worldview positions, which kept researchers from being open-minded and thinking out of the box. Thus for years scientists either expected too much from certain things or too little from others. Fortunately these days apparently some gross misconceptions are being clarified and research seems heading in the right direction, producing an overwhelming avalanche of data that must be carefully analyzed.
    These are fascinating times to watch what’s going on in biology research.

  503. 503
    Zachriel says:

    Dionisio: I did not find, in the sources you suggested*, any comprehensive, logically coherent, step-by-step explanations of how the bacteria or the first multicellular organisms could have appeared.

    Z: You’re choosing very ancient transitions that have left little physical evidence. The origin of the first cells is obscure.

    Did you not find the work at Szostak’s lab to be relevant?

    gpuccio: Well, a reasonable list of complex processes which certainly have an important role.

    Good, so we agree we have evidence of the broad historical outline.

    As for adhesion, we have some evidence of its evolutionary origin. See Abedin & King, Diverse evolutionary paths to cell adhesion, Trends in Cellular Biology 2010; or Miller et al., The evolutionary origin of epithelial cell-cell adhesion mechanisms, Current Topics in Membranes 2013.

    Dionisio: Medicine and health maintenance programs could benefit much more from that research.

    What research is that?

  504. 504
    Box says:

    Zachriel,

    Box: So bacteria are able to find a flagellum in a few steps.

    Zachriel: That depends on the starting point, of course.

    The starting point is pretty irrelevant in Wagner’s hyperastronomical library in 5,000-dimensional space, since about everything is interconnected – that’s the whole bizarre point.

  505. 505
    Box says:

    Zachriel,

    gpuccio: Well, a reasonable list of complex processes which certainly have an important role.

    Zachriel: Good, so we agree we have evidence of the broad historical outline.

    In post #507 Gpuccio calls you “a master of language and clever expression”, but this childish attempt is not a good example of your trickiness. What exactly do you think that you and GPuccio agree on? What “evidence”? What “historical outline”?

    Are you serious?

  506. 506
    Dionisio says:

    #510 Zachriel

    What research is that?

    Sorry, but I’m far from being “a master of language and clever expression” like you (according to gpuccio @507).

    Please, note that post #509 starts with the phrase: “#508 corrections”. Hence, the piece of text that was quoted and corrected in post #509 was originally within the comment posted @508, therefore it must be read within that original context:

    To me, it’s much more important for science today to dedicate more time and resources to the research of the biological systems and their functioning. There are many outstanding questions to be answered in those areas. Medicine and health maintenance programs could benefit much more from that research.

    The rest of the comment in post #509 is an addendum to the previously quoted text correction:

    And it’s actually benefitting from it already. Unfortunately some delays might have been indirectly caused by misleading presuppositions based on unfounded worldview positions, which kept researchers from being open-minded and thinking out of the box. Thus for years scientists either expected too much from certain things or too little from others. Fortunately these days apparently some gross misconceptions are being clarified and research seems heading in the right direction, producing an overwhelming avalanche of data that must be carefully analyzed.
    These are fascinating times to watch what’s going on in biology research.

  507. 507
    Silver Asiatic says:

    gpuccio

    OK, the final result is that Zachriel has said a few effective things, most of them undeniable, some of them vague, all of them essentially reasonable, all of them intelligent in their form, which give the idea that there are a lot of important things that you don’t know, and that you are not considering, and that, while you have your arguments, those arguments can be essentially addressed.

    You’re being very considerate and charitable – and that’s good. And yet I think you’re also saying that we could go on-and-on forever with discussions in this vein … brief, reasonable, ambiguous comments pointing out that we don’t know certain things and referencing other works which are equally ambiguous and speculative.

    When an expert says “it could have happened this way” then supposedly that provides a sufficient answer to any and every problem.

    Decades of work building-out scenarios on how it ‘could have happened’ leading to the tiniest bits of confirmatory evidence create the illusion that we’re ‘getting closer’ to the solution. No, actually we’re not just getting closer, ‘we already have the solution, we’re merely filling in details’.

    Then we read someone like Wagner who gives us hyperastronomical libraries in multidimensional space, simply wiping the slate clean and claiming that there are pre-existing genetic networks that self-organize. So we can forget about Darwin on that point.

    What about the decades of ‘gradualism research’ that supposedly brought us ever-closer to the solution?

    I think that kind of thing exposes the ambiguity and uncertainty that surrounds the topic.

    But I’ll also give Zachriel some praise – he always makes it sound like there’s really nothing to question here at all. The science is settled, apparently. Even when we observe wildly conflicting stories on evolutionary origins (OOL research has an even greater variety of speculative scenarios) these are all presented as if there’s nothing to be skeptical about at all, everything is basically progressing towards firm, materialist conclusions — and the idea that there was some intelligence in the process is shut down completely.

    But the questions are far more open-ended that that. One look at this OP should reveal the challenge. So the attitude that seems as if the origins of even the most bafflingly interactive-complexity that we see are “basically settled” is revealing. It exposes an inconsistency – a defensiveness.

    It would be far more reasonable, and therefore convincing, if there was a real openness to the possibility of intelligent design. When that possibility is shut down or ridiculed, in favor of virtually any other imaginary materialist proposal, it’s easy to see a bias at work.

  508. 508
    Dionisio says:

    #510 Zachriel

    Did you not find the work at Szostak’s lab to be relevant?

    That question was implicitly answered in post #506.
    What they show seems to indicate that it’s mostly ‘work in progress’ with no foreseeable end timing, which confirms that even most eminent scientists can’t explain OOL in a comprehensive and logically coherent way.

    Is that relevant? 🙂

  509. 509
    gpuccio says:

    Silver Asiatic:

    My point is that Zachriel is (IMO!) an intelligent person in a very unhappy situation: he defends a position which he believes in, but which is indefensible. And he does it at his best.

    I appreciate his sincerity and intelligence. But his position is wrong. He has made the wrong choice. That’s all.

  510. 510
    gpuccio says:

    Zachriel:

    “Good, so we agree we have evidence of the broad historical outline.”

    Now, let’s try to understand what we agree upon.

    You say:

    “The basic history was adhesion then differentiation then apoptosis.”

    I certainly agree that those processes are important parts of the development of metazoa. I am not sure of the sequence, or of the historical pattern (I doubt that you are, too). But there is no doubt that an historical pattern exists.

    As you know, I don’t believe that biological design is a supernatural miracle. Not necessarily, at least (I try to have no prejudices). I am sure that design happens in time and space, and has a specific history of development. That is obvious from what we know.

    But it is design all the way. Complex solutions are found, complex programmes are implemented, and nothing of that happens by RV and NS. That is “the key”, as you would say: a stepwise increase in complexity, by stepwise design. With many sudden jumps (OOL, origin of eukaryota, origin of metazoa, Cambrian explosion, and probably many others).

  511. 511
    Silver Asiatic says:

    Thanks, Gpuccio. That’s a very nice way to say it. 🙂

  512. 512
    Zachriel says:

    Box: The starting point is pretty irrelevant in Wagner’s hyperastronomical library in 5,000-dimensional space, since about everything is interconnected – that’s the whole bizarre point.

    It still depends on the particulars of the landscape, though it will be much more connected in higher dimensions than in naïve notions of a two-dimensional landscape.

    Box: What exactly do you think that you and GPuccio agree on?

    The reasonable list of complex processes; adhesion, differentiation, apoptosis; in other words, it was an historical process.

    Dionisio: To me, it’s much more important for science today to dedicate more time and resources to the research of the biological systems and their functioning.

    There’s a huge amount of time and resources dedicated to research of biological systems and their functioning, especially human biology; but sure, more would be nice.

    Dionisio: Unfortunately some delays might have been indirectly caused by misleading presuppositions based on unfounded worldview positions, which kept researchers from being open-minded and thinking out of the box.

    It’s only natural for humans to explore blind alleys—you never know what you’ll find until you look—; but to which “unfounded worldview positions” are you referring?

    Silver Asiatic: brief, reasonable, ambiguous comments pointing out that we don’t know certain things and referencing other works which are equally ambiguous and speculative.

    As scientists don’t claim to have a working theory of abiogenesis, it is reasonable to qualify any such claims.

    Silver Asiatic: When an expert says “it could have happened this way” then supposedly that provides a sufficient answer to any and every problem.

    No. It calls for evidence. So if someone hypothesizes that lipid vacuoles might grow and divide spontaneously, then this is something that can be tested. Similarly, if someone claims that RNA may have the capability of self-replication, then this too might be subject to testing.

    Dionisio: That question was implicitly answered in post #506.

    As there is no complete theory of abiogenesis, there is no “comprehensive, logically coherent, step-by-step explanation”. However, that hardly means that the work at Szostak’s lab is irrelevant.

    gpuccio: But there is no doubt that an historical pattern exists.

    Common ground!

    gpuccio: With many sudden jumps (OOL, origin of eukaryota, origin of metazoa, Cambrian explosion, and probably many others).

    Our knowledge of those processes certainly is more finely gradated than what you suggest. For instance, adhesion exists in single-celled and simple colonial organisms.

  513. 513
    Joe says:

    Zachriel, Queen of the double-talk- mostly meandering nonsense that doesn’t address what is being discussed.

  514. 514
    Dionisio says:

    gpuccio

    Agree, biological design is not supernatural. Many scientists and bioengineering specialists do a lot of biological design these days too.

    Software design is not supernatural either. Engineers and computer scientists design complex machines and software all over the world these days.

    They don’t perform miracles. They just study a lot and work very hard, for many years, using highly sophisticated technology.

    However, I have a few questions:

    What are the main issues of contention here?

    Definition of design? What does it mean as an action? What does it mean as an object or a system?

    Determination of design? How to determine whether something is designed or not?

    Are the above issues interrelated?

    Are they associated with certain concepts we often encounter in discussions here in this site, like irreducible complexity, CSI, dFCSI (or is it dFSCI?), FSCO/I?

    Do all those things have to do with the ‘D’ in ‘ID’?

    Is the ‘I’ in ID a cause of contention?
    Is there a problem with the definition of the term? Or is the application of the term to particular cases?

    Perhaps this post will turn so heavy off topic that may have to move out to another thread?

    Since the neo-Darwinian approach to interpretation, with their formula (RM + NS + HGT + T +…= e) is under so much criticism these days, is Dr. Shapiro’s ‘third way’ approach to interpretation of the observed biological objects the leading option now?

    Could ID be considered the 4th alternative?

    Is it possible that the third way might include ID at some point?

    The main web page of the third way site clearly distinguishes the first and second ways. But they don’t seem to refer explicitly to the ID way. Obviously we would have to ask them why not. Any guess?

    Thank you in advance for any comments on this.

    BTW, my ‘learning phase’ is approaching its end. Soon I may have to move on to work on the next phase of the project I’m involved in. I’ll try to keep an eye on this blog, specially the discussions that attract me most, including your insightful commentaries. But it’s possible that my spare time will be much more limited.

  515. 515
    gpuccio says:

    Dionisio:

    You probably know many of my ideas well, but I will try to briefly sum up some definitions and concepts to answer the questions in your post #521:

    a) Design: any process where a conscious intelligent being purposefully outputs a specific form to a material object from a conscious representation of that form.

    b) We can know that an object is designed in two different ways:

    1) Directly: we have direct observation, or some equivalent evidence, of the process in which the object acquires its form, and therefore we know that a conscious agent outputted intentionally that form into the object. That’s the case with many human artifacts.

    2) By inference. If no direct evidence of the process of origin is available, the best design inference can be made by the observation in the object of the property of CSI or some equivalent concept, which is empirically a very reliable marker of design.

    c) The I and D in ID are in reality connected. Design is by definition “intelligent”, in the sense that the designer must have some cognitive representation to design. And it is also purposeful, because the designer must have a motivation to design. So, IMO, the word “design” would be enough. But I suppose that “intelligent” adds some protection from possible attempts at defining forms of “non designed design”, like it has been done with “non free free will”, and so on. I suppose that “conscious cognitive and purposeful design” would be too long! 🙂

    d) I don’t believe there is any “third way”. Nor that there are really two ways as defined in that thread, because Creationism, IMO, is not really a scientific position (although it is a perfectly acceptable philosophic and religious position).

    As far as I understand, neo darwinism (RV + NS) and ID are the only games in town, for a scientific debate about the origins of biological information. All the rest is bafflegab.

  516. 516
    Dionisio says:

    eccellente!!!

    Mile grazie mio caro Dottore!

  517. 517
    Box says:

    Zachriel,

    Box: What exactly do you think that you and GPuccio agree on?

    Zachriel: The reasonable list of complex processes; adhesion, differentiation, apoptosis; in other words, it was an historical process.

    What was an historical process – and what kind? In a functional computer we can also distinguish between several complex processes. What kind of historical process does that imply?

  518. 518
    Zachriel says:

    Box: What was an historical process

    The origin of the various processes that distinguish metazoans; e.g. adhesion, differentiation, apoptosis; as well as their diversification.

    Box: – and what kind?

    Evolutionary.

  519. 519
    Box says:

    Zachriel,

    Zachriel: evolutionary.

    I thought so. Well, contrary to what you claim in #510, a list of complex processes is no evidence whatsoever for an evolutionary history. Just like a list of complex processes wrt a functional computer is no evidence whatsoever for an evolutionary history. Further I expect that there is no agreement between Gpuccio and you that there is any evidence for an evolutionary history.

  520. 520
    Zachriel says:

    Box: Well, contrary to what you claim in #510, a list of complex processes is no evidence whatsoever for an evolutionary history.

    A list is not evidence. Observations are evidence. See Abedin & King, Diverse evolutionary paths to cell adhesion, Trends in Cellular Biology 2010; or Miller et al., The evolutionary origin of epithelial cell-cell adhesion mechanisms, Current Topics in Membranes 2013.

    Box: Further I expect that there is no agreement between Gpuccio and you that there is any evidence for an evolutionary history.

    gpuccio: there is no doubt that an historical pattern exists.

    While gpuccio didn’t indicate an evolutionary history, he clearly stated that an historical pattern exists. Gpuccio pointed to large gaps. We pointed out that the gaps are not as large as gpuccio suggests.

  521. 521
    gpuccio says:

    Zachriel:

    Just a question. Why “we”? Are you a team? Or is it just plurale maiestatis? 🙂

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