Information Intelligent Design

The highly engineered transition to vertebrates: an example of functional information analysis

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In the recent thread “That’s gotta hurt” Bill Cole states:

I think over the next few years 3 other origins (my note: together with OOL), will start to be recognized as equally hard to explain:

  • The origin of eukaryotic cell: difficult to explain the origin of the spliceosome, the nuclear pore complex and chromosome structure.
  • The origin of multicellular life: difficult to explain the origin of the ability to build complex body plans.
  • The origin of man: difficult to explain the origin of language and complex thought.

That thought is perfectly correct. There are, in natural history, a few fundamental transitions which scream design more that anything else. I want to be clear: I stick to my often expressed opinion that each single new complex protein is enough to infer design. But it is equally true that some crucial points in the devlopment of life on earth certainly stand out as major engineering events. So, let’s sum up a few of them:

  1. OOL
  2. The prokaryote – eukaryote transition (IOWs, eukaryogenesis)
  3. The origin of metazoa (multicellular life)
  4. The diversification of the basic phyla and body planes (IOWs, the Cambrian explosion)

Well, saurian-1358308_1280to those 4 examples, I would like to add the diversification of all major clades and subphyla.

Of course, another fundamental transition is the one to homo sapiens, but I will not deal with it here: I fully agree with Bill Cole that it is an amazing event under all points of view, but it is also true that it presents some very specific problems, which make it a little bit different from all the other transitions we have considered above.

I will state now in advance the point that I am trying to make here: each of the transitions described requires tons and tons of new, original, highly specific functional information. Therefore, each of those transitions commands an extremely strong inference to design. I will deal in particular with the transition to the subphylum of vertebrates, for a series of reasons: being vertebrates, we are naturally specially interested in that transition; there are a lot of fully sequenced genomes and proteomes of vertebrate species ;  and a lot is known about vertebrate biology. IOWs, we have a lot of data that can help us in our reasoning. So, I will  try to fix a few basic points which will be the foundation of our analysis:

  • a) The basic phylum is Chordates, which are characterized by the presence of a notochord. Chordates include three different clades: Craniata, Tunicata, Cephalochordata.
  • b) Vertebrates are a subphylum of the phylum Chordates, and in particular of the clade Craniata. They represent the vast majority of Chordates, with  about 64,000 species described. As the name suggests, they are characterized by the presence of a vertebral column, either cartilaginous or bony, which replaces the notochord.
  • c) The phylum Chordate, like other phyla, can be traced at least to the Cambrian explosion (540 million years ago).
  • d) Chordates which are not vertebrates are quite rare today. They include:
    • 1) Craniata: the only craniates which are not vertebrates are in the class Myxini (hagfish), whose classification however remains somewhat controversial. All other craniates are vertebrates.
    • 2) Tunicata (or urochordata): about 3000 species, the best known and studied is Ciona intestinalis.
    • 3) Cephalochordata: about 30 species of Lancelets.
  • e) The phyla most closely related to Chordates are Hemichordates (like the Acorn worm) and Echinoderms (Starfish, Sea urchins, Sea cucumbers).
  • f) Vertebrates can be divided into the following two groups:
    • 1) Fishes: 3 Classes:
      • 1a) Jawless  (lampreys)
      • 1b)  Cartilaginous (sharks, rays, chimaeras)
      • 1c) Bony fish
    • 2) Tetrapods: all the rest (frogs, snakes, birds, mammals)

For the following analysis, I will consider vertebrates versus everything which preceded them (all metazoa, including “pre-chordates” (Hemichordates and Echinoderms) and “early chordates”  (Tunicata and Cephalochordata). So, everything which is new in vertebrates had to appear in the window between early chordates and the first vertebrates: cartilaginous fish and bony fish (I will not refer to lampreys, because the data are rather scarce). So, let’s try to define the temporal window, for what it is possible:

  • Chordates are already present at the Cambrian explosion, 540 my ago.
  • Jawless fish appeared slightly later (about 530 my ago), but they are mostly extinct.
  • The split of jawless fish into cartilaginous fish and bony fish can be traced about at 450 my ago

Therefore, with all the caution that is required, we can say that the information which can be found in both cartilaginous fish and bony fish, but not in non vertebrates (including early chordates), must have been generated in a window of less that 100 my, say between 540 my ago and 450 my ago. Now, my point is very simple: we can safely state that in that window of less than 100 million years a lot of new complex functional information was generated. Really a lot. To begin our reasoning, we can say that vertebrates are characterized by the remarkable development of two major relational systems:

  1. The adaptive immune system, which appears for the first time exactly in vertebrates.
  2. The nervous system, which is obviously well represented in all metazoa, but certainly reaches new important adaptations in vertebrates.

Muperch-62855_640ch can be said about the adaptive immune system, and that will probably be the object of a future OP. For the moment, however, I will discuss some aspects linked to the development of the nervous system. The only point that is important here is that the nervous system of vertebrates undergoes many important modifications, especially a process of encephalization.  My interest is mainly in the developmental controls that are involved in the realization of the new body plans and structures linked to those processes. Of course, we don’t understand how those regulations are achieved. But today we know much about some molecules, especially regulatory proteins, which have an important role in the embryonal development of the vertebrate nervous system, and in particular in the development and migration of neurons, which is obviously the foundation for the achievement of the final structure and function of the nervous system. So, I will link here a recent paper which deals with some important knowledge about the process of neuron migration. I invite all those interested to read it carefully: Sticky situations: recent advances in control of cell adhesion during neuronal migration by David J. Solecki Here is the abstract:

The migration of neurons along glial fibers from a germinal zone (GZ) to their final laminar positions is essential for morphogenesis of the developing brain, aberrations in this process are linked to profound neurodevelopmental and cognitive disorders. During this critical morphogenic movement, neurons must navigate complex migration paths, propelling their cell bodies through the dense cellular environment of the developing nervous system to their final destinations. It is not understood how neurons can successfully migrate along their glial guides through the myriad processes and cell bodies of neighboring neurons. Although much progress has been made in understanding the substrates (14), guidance mechanisms (57), cytoskeletal elements (810), and post-translational modifications (1113) required for neuronal migration, we have yet to elucidate how neurons regulate their cellular interactions and adhesive specificity to follow the appropriate migratory pathways. Here I will examine recent developments in our understanding of the mechanisms controlling neuronal cell adhesion and how these mechanisms interact with crucial neurodevelopmental events, such as GZ exit, migration pathway selection, multipolar-to-radial transition, and final lamination.

In brief, the author reviews what is known about the process of neuronal cell adhesion and migration. Starting from that paper and some other material, I have chosen a group of six regulatory proteins which seem to have an important role in the above process. They are rather long and complex proteins, particularly good for an information analysis. Here is the list. I give first the name of the protein, and then the length and accession number in Uniprot for the human protein:

  • Astrotactin 1,     1302 AAs,     O14525
  • Astrotactin 2,    1339 AAs,     O75129
  • BRNP1 (BMP/retinoic acid-inducible neural-specific protein 1),     761 AAs,     O60477
  • Cadherin 2 (CADH2),      906 AAs,    P19022
  • Integrin alpha-V,    1048 AAs,      P06756
  • Neural cell adhesion molecule 1 (NCAM1),   858 AAs,  P13591

This is a  very interesting bunch of molecules:

  • Astrotactin 1 and 2 are two partially related perforin-like proteins. ASTN-1 is a membrane protein which is directly responsible for the formation of neuron–glial fibre contacts. ASTN2 is not a neuron-glial adhesion molecule, but it functions in cerebellar granule neuron (CGN)-glial junction formation by forming a complex with ASTN1 to regulate ASTN1 cell surface recruitment. More about these very interesting proteins can be found in the following paper:

Structure of astrotactin-2: a conserved vertebrate-specific and perforin-like membrane protein involved in neuronal development by Tao Ni, Karl Harlos, and Robert Gilbert

  • BRNP1 is another  protein which functions in neural cell migration and guidance
  • Cadherin 2, or N-cadherin, is active in many neuronal funtions and in other tissues, and seems to have a crucial role in glial-guided migration of neurons
  • Integrin alpha-V, or Vitronectin receptor, is one of the 18 alpha subunits of integrins in mammals. Integrins are transmembrane receptors that are the bridges for cell-cell and cell-extracellular matrix (ECM) interactions.
  • NCAM1 is a cell adhesion molecule involved in neuron-neuron adhesion, neurite fasciculation, outgrowth of neurites

Now, why have I chosen these six proteins, and what do they have in common? They have two important things in common:

  • They are all big regulatory proteins, and they are all involved in a similar regulatory network which controls endocytosis, cell adhesion and cell migration in neurons, and therefore is in part responsible for the correct development of the vertebrate nervous system
  • All those six proteins present a very big informarion jump between pre-vertebrate organisms and the first vertebrates

The evolutionary history of those six protein is summarized in the following graph, realized as usual by computing the best homology bit score with the human protein in different groups of organisms.

Neuron_migration

Very briefly, all the six human molecules have low homology with pre-vertebrates, while they already show a very high homology  in cartilaginous fishes. The most striking example is probably Astrotactin 2, which presents the biggest jump from cephalochordata (329 bits) to cartilaginous fishes (1860 bits), for a great total of 1531 bits of jump! The range of individual jumps in the group is 745 – 1531 bits, with a mean jump of 1046 bits per molecule and a total jump of 6275 bits for all six molecules. The jump has always been computed as the difference between the best bit score in cartilaginous fishes and the best bitscore in all pre-vertebrate metazoa. We can also observe that the first three proteins have really low homology with everything up to tunicates, but show a definite increase in Cephalochordata, which precedes the big jump in cartilaginous fishes, while the other three molecules have a rather constant behaviour in all pre-vertebrate metazoa, with a few hundred bits of homology, before “jumping” up in sharks. One could ask: is that a common behaviour of all proteins? The answer is no. Look at the following graph, which shows the same evolutionary history for two other proteins, both of them very big regulatory proteins, both of them implied in the same processes as the previous six.

Neuron_migration2

Here, the behaviour is completely different. While there is a slight increase of homology in time, with a few smaller “jumps”, there is nothing comparable to the thousand bit jumps in the first six molecules. IOWs, these two molecules already show a very high level of homology to the human form in pre-vertebrates, and change only relatively little in vertebrates. We can say, therefore, that most of the functional information in these two proteins was already present before the transition to vertebrates.

So, to sum up:

  • a) The six proteins analyzed here all exhibit a huge informational jump between pre-vertebrates and vertebrates. The total functional informational novelty for just this small group of proteins is more than 6000 bits, with a mean of more than 1000 bits per protein.
  • b) These proteins are probably crucial agents in a much more complex regulation network implied in neuron adhesion, endocytosis, migration, and in the end in the vast developmental process which makes individual neurons migrate to their specific individual locations in the vertebrate body plan.
  • c) The above process is certainly much more complex than the six proteins we have considered, and implies other proteins and obviously many non coding elements. Our six proteins, therefore, can be considered as a tiny sample of the general complexity of the process, and of the informational novelty implied in the process itself.
  • d) Moreover, the process regulating neuron migration is certainly strictly integrated, with so many agents working in a coordinated way. Therefore, there is obviously a strong element of irreducible complexity implied in the whole informational novelty of the vertebrate process, an element that we can only barely envisage, because we still understand too little.
  • e) The neuron regulation process, of course, is only a part of the informational novelty implied in vertebrates, a small sample of a much more complex reality. For example, there is a lot of similar novelty implied in the workings of the immune system, of the cytokine signaling system, and so on.
  • f) The jump described here is really a jump: there is no trace of intermediate forms which can explain that jump in all existing pre-vertebrates. Of course, neo darwinists can always dream of lost intermediates in extinct species. This is a free world.
  • g) Are these 6000+ bits of functional information really functional? Yes, they are. Why? because they have been conserved for more than 400 million years. Remember, the transition we have considered happens between the first chordates and cartilaginous fish, and it can be traced to that range of time. And those 6000+ bits are bits of homology between cartilaginous fish and humans.
  • h) How much is 6000 bits of functional information? It is really a lot! Remember, Dembski’s Universal Probability Bound, taking in consideration the whole reasonable probabilistic resource of our whole universe from the Big Bang to now, is just 500 bits. 6000 bits correspond to a search space of 2^6000, IOWs about 10^2000, a number so big that we cannot even begin to visualize it. It’s good to remind ourselves, from time to time, that we are dealing with exponential values.
  • i) How great is the probability that 6000 bits of functional information can be generated in a window time of less than 100 million years, by some unguided process of RV + NS in six objects connected in an irreducibly complex system, even if RV were really helped by some NS in intermediates of which there is no trace? The answer is simple: practically non existent.
  • j) Therefore, the tiny sample of six proteins that we have considered here, which is only a small part of a much bigger scenario, points with extreme strength to a definite design inference:

The transition to vertebrates was a highly engineered process. The necessary functional information was added by design.

 

297 Replies to “The highly engineered transition to vertebrates: an example of functional information analysis

  1. 1
    News says:

    Anyone who thinks cats are not a product of design should just not be in engineering.

  2. 2
  3. 3
    Dionisio says:

    News: Anyone who thinks cats are not a product of design should just not be in engineering.

    Well, anyone who thinks cats are not a product of design has no idea what the words ‘design’ and ‘engineering’ really mean.

  4. 4
    gpuccio says:

    News:

    Cats are one of the best things in the world! 🙂

  5. 5
    gpuccio says:

    KF:

    Thank you! Your attention is always appreciated. 🙂

  6. 6
    gpuccio says:

    Dionisio:

    Perfectly right!

    OK, in a moment of extreme magnanimity I could probably extend the concept to dogs… 🙂

  7. 7
    Dionisio says:

    KF: Sobering

    Yes, indeed.

  8. 8
    mk says:

    cat is the most sophisticate mouse trap in the world. it can even get down in the stairs. so its an ic system.

    by the way- what if all the dna sequuences was functional? in this case we will conclude that nature was designed or evolved? plus: i think that even in this case the chance that a match part will exist is zero. like to find a match part for my watch that evolved naturally (battery for example).

  9. 9
    gpuccio says:

    mk:

    Thank you for connecting cats to Behe’s tradition.

    DNA sequences are certainly functional with regards to protein coding genes, and probably functional for great part of non coding sequences.

    However, that does not mean that the whole sequence is always functionally specific. We do know that part of coding sequences can change without affecting the function. That is called neutral variation, and happens all the time. We see it happen even in human genes.

    That’s why sequence conservation for very long times in natural history is a certain sign of functional constraint, and therefore of functional specificity. It means that negative selection is preserving a precious specific sequence of AAs.

    Of course, the higher the functional specificity, the more we can be certain that those features were designed, and are not the result of unguided evolution.

    And, of course, IC is an even higher level of structured complexity, pointing to a design origin.

  10. 10
    Dionisio says:

    gpuccio:

    Thank you for writing this new ‘juicy’ OP.

    Regarding the ‘designed cat’ issue, on behalf of my family, I appreciate that you could extend the ‘design’ concept to dogs too. 🙂

    Some of my children have both a cat and a dog living in almost* complete harmony in their home.

    When relatives and friends visit their home, their cat hides away until the guests leave. However, when my wife and I visit their home, their cat doesn’t hide away. Perhaps their cat recognizes some familiar ‘feline’ phonotypical traits in me? 🙂

    When we arrive in their home, their dog welcomes us so effusively that we can’t hug our children right away. It’s like saying ‘first things first’. :):)

    Our other children don’t have any pets in their home. Actually, one of our children is allergic to cats, though the allergy hasn’t been confirmed 100%.

    As far as I know I’m only allergic to some of your interlocutors. 🙂

    When our children were little, we had a very friendly** golden retriever for almost 16 years in our home.
    Until not long ago -as empty nesters- my wife and I had a beautiful orange tabby cat. My wife claimed that’s the nicest being she has ever met. Obviously I was included in that comparison too. 🙂 The death of that beautiful cat was very painful to us, specially to my wife.

    Now let’s try to chew and digest what you wrote here in this new OP.

    BTW, -off topic- did you read the reference to the paper on cybernetic embryo? Apparently they finally realized that the “morphogen gradient” model didn’t answer all the questions in morphogenesis, and actually raised new questions. Hence they came up with this breakthrough “cybernetic embryo” model, which sounds like music to my ears. However, it’s possible that their concept of ‘cybernetic’ has nothing to do with ‘design’. 🙂
    This ‘cybernetic embryo’ model seems just taken out of the oven, hence the concept perhaps hasn’t been ‘tasted’ much yet.

    (*) sometimes their cat and dog have minor ‘arguments’, but never as heated as some debates I’ve seen in this site. 🙂

    (**) much friendlier than some people I know, including myself. 🙂

  11. 11
    gpuccio says:

    Dionisio:

    I have three cats. They are wonderful, but one of them (a female) is probably as aggressive as some interlocutors here (but she is very beautiful!). The other two are very meek.

    I like dogs, but you are right: they are a little bit too “effusive”. 🙂 However, I remain a cat guy!

    Yes, I looked at the “cyberbetic embryo” paper, but I must still read it with more attention. Morphogen gradients are interesting, but I agree that they cannot explain everything. Let’s see…

  12. 12
    Dean_from_Ohio says:

    So there IS something to King of Beasts being a great cat! 🙂

  13. 13
    Dionisio says:

    mk @8

    “what if all the dna sequences were functional?”

    That would be kind of interesting, given the messy lifestyle humans have had through their history (outside Eden), exposing our robust/delicate biological systems to all kinds of bad stuff, some causing deleterious physiological changes but others not so biochemically dangerous.
    The so called ‘neutral variations’ mentioned by gpuccio @9 seem quite logically understandable from a biological perspective. Hence, nonfunctional segments of DNA could be reasonably expected.
    However, determining the functionality of anything may not be as simple as some reductionist folks make it look.
    Have you seen the illustration of functionality using the example of the TV screens on the back of the airplane seats?

  14. 14
    Dionisio says:

    @10 misspelling error correction

    “phonotypical traits” should read “phenotypic traits” instead.

    Sorry for that mistake.

  15. 15
    Dionisio says:

    This OP covers a subject -which gpuccio has discussed before- that is associated with a (overwhelmingly?) large amount of terms. However, as in previous occasions, this article is very well structured, with the information being introduced gradually, hence even biology-illiterate folks like me can read this article without too many difficulties, though I have to search for some terms while reading this. Overall I appreciate this pedagogical approach.

    For example, after reading:

    […] vertebrates are characterized by the remarkable development of two major relational systems:
    1.The adaptive immune system, […]
    2.The nervous system, […]

    I paused to chew and digest what I had read to that point. Then continued.

  16. 16
    Dionisio says:

    Much can be said about the adaptive immune system, and that will probably be the object of a future OP.

    That’s an encouraging statement. Can’t wait to read that future OP (hey, no pressure on the doctor). Specially given that more discoveries have been made since the last OP on that subject appeared in this site. 🙂

  17. 17
    Dionisio says:

    Dean_from_Ohio @12

    So there IS something to King of Beasts being a great cat!

    Wasn’t

    the lion, which is mightiest among beasts
    and does not turn back before any
    [Proverbs 30:30 (ESV)]

    designed too?

    🙂

  18. 18
    bill cole says:

    Hi Gupuccio
    Thank you for the very interesting op. 🙂

    I have studied cadherins in my research but mostly e cadherin. It is indeed one of the key components of intercellular adhesion and when it is under transcribed in the cell mitosis can be initiated which is a cancer trigger. The control mechanism appears to be the active form of vitamin d which is mostly processed through skin exposure to sunlight then an OH is added in the liver then another OH is added in the kidney before it moves inside our cells. This active form is part of the transcription complex of e cadherin, therefore when our cells are low a cancer chain reaction can occur. Everyone needs to make sure they get sun exposure. If not take vitamin d supplements and get your blood levels tested.
    50% of the US population is vitamin d deficient.

  19. 19
    gpuccio says:

    bill cole:

    Thank you for your very interesting contribution. And for inspiring my OP with your statements! 🙂

    Yes, cadherins are a fascinating group of molecules.

    As I have tried to clarify, my list of six proteins is just a sample of an unfathomable abundance of functional complexity, which is there, waiting for us to study and try to understand it.

    ID is a precious paradigm to do that, while neo darwinism, with its pernicious need to underestimate the complexity that it cannot explain (IOWs, practically all the complexity) is a really heavy hindrance to our understanding of the wonderful plans developed in nature, and of the amazing intelligence displayed in them.

  20. 20
    mk says:

    “Have you seen the illustration of functionality using the example of the TV screens on the back of the airplane seats?”

    no. what is about?

    i have a very interesting argument: lets say that someone will need to made a watch by finding parts that evolved in natural process. now: what is his chance to get one part of the watch? and 2? and 10? even if we assume that the chance to find any part is about 50% (lets say a hand)- then the chance for him to find about 50 matching parts for a functional watch made by 50 different parts is about one in 2^50. in similar way we can conclude this for any biological system. the interesting part is that this argument is true even if evolution is possible.

  21. 21
    mk says:

    hi gpuccio. yes, the cat is indeed a behe mouse trap:).by the way- what is your thought about my argument above? its showing that even if evolution is true- its still need a designer.

  22. 22
    gpuccio says:

    mk:

    2^50 is not such a big number, if you have enough probabilistic resources. 50 bits (50 events with one bit of complexity) are not 6000 bits.

    The point is: each complex protein is completely unlikely. Of course, many complex proteins are even more unlikely. So, if each protein has a complexity of 1000 bits, six events have a complexity of 6000 bits, and 50 events will have a complexity of 50000 bits.

    So, the probability of each event is at least as important as the number of events.

    In the end, the important thing is the probability of the whole system.

    Behe’s concept of IC is very important because it shows that each single part cannot be helped by NS if only the whole system is functional. Behe’s argument is about NS, rather than RV.

    The important point is: evolution is not true. Absolutely not true. It cannot generate the single parts, as much as it cannot generate the whole system. It cannot generate Functional Complexity, and it cannot generate Irreducible Complexity. It cannot generate codes (semiotic systems).

    And so on, and so on.

  23. 23
    J-Mac says:

    This is one of the best posts I have ever read on UD…

    I know very, very well that this post, just as many, many other great posts, will have no effect on the people who do not what to understand it or accept the evidence.

  24. 24
    Dionisio says:

    mk @20

    “no. what is about?”

    It was posted @1030 in the thread titled “A third way of evolution?” in the following link:

    http://www.uncommondescent.com.....ent-612770

    But I will repost it here for you:

    Testing for functionality could be misleading in some cases.

    For example, let’s assume we don’t know what the small dark screens attached to back of many airline seats in economy class (mainly long routes) are for.

    Now let’s say we want to thoroughly test their functionality regarding several important criteria:

    1. The airplanes capability to take off and land.
    2. The fuel efficiency of the airplanes.
    3. The maximum number of passengers that can be transported on every flight.
    4. The maximum altitude the airplane can reach.
    5. The maximum speed the airplanes can fly at.
    6. The easiness of boarding and deplaning at the terminals.
    7. The ruggedness and reliability of the cockpit instruments.
    8. The experience of the pilots.
    9. The flight schedules.
    10. The airport fees.

    At the end of the thorough examination -performed redundantly by several teams of experts- we conclude -without any doubt- that the small dark screens attached to the back of the economy seats are definitely non-functional.

    Would such a conclusion be accurate?

  25. 25
    Dionisio says:

    J-Mac @23

    This is one of the best posts I have ever read on UD…

    I know very, very well that this post, just as many, many other great posts, will have no effect on the people who do not want to understand it or accept the evidence.

    Agree. However, many anonymous visitors could read this new OP and follow-up thread to draw their own conclusions.

    I’m still processing the information in the OP. It’s quite technical for me.

    BTW, have you noticed that the “aggressive” interlocutors have not posted any comments yet? 🙂

  26. 26

    A really excellent read GP, thank you and congratulations.

  27. 27
    Mung says:

    Can’t wait to see the Kenneth Miller cat-trap tie clip.

  28. 28
    Mung says:

    gpuccio,

    I think your OP could only be improved if it had a References section at the end.

    I’ve always found the immune system to be fascinating. It doesn’t hurt that the immune system itself is supposed to be an example of evolution in action. Can’t wait to hear more on that.

    Evolution is True.

  29. 29
    Anaxagoras says:

    UNDENIABLE!!!

    The intuition for a designed system is impossible to avoid.

    Scientific homework confirms that a naturalistic unguided explanation lacks any credibility

  30. 30
    gpuccio says:

    J-Mac:

    Thank you! 🙂

  31. 31
    gpuccio says:

    UB:

    Thank you, my friend. 🙂

  32. 32
    gpuccio says:

    Anaxagoras:

    I am happy you liked my homework! It was hard work… 🙂

  33. 33
    gpuccio says:

    Mung:

    “Can’t wait to see the Kenneth Miller cat-trap tie clip.”

    🙂 🙂 🙂

    Mung, you are priceless!

  34. 34
    gilthill says:

    A great post indeed. Many thanks to gp for this gem.
    Also, do you ear the deafening silence of the opposition ?

  35. 35
    gpuccio says:

    gilthill:

    Thank you! 🙂

  36. 36
    gpuccio says:

    Dionisio:

    “BTW, have you noticed that the “aggressive” interlocutors have not posted any comments yet? ”

    gilthill:

    “Also, do you ear the deafening silence of the opposition?”

    True. Maybe it’s only a question of time.

    OK, I will say it: Alicia, I miss you! 🙂

  37. 37
    Dionisio says:

    gpuccio

    One can easily tell that you did a very thorough research for this OP. Thank you.

    As usual, the graphs are very helpful to visualize the information jumps explained in the text.

    Also, you have mastered the art of making such a technical subject as this a little more ‘chewable’ and ‘digestible’ for the biology-illiterate folks like me. That effort is very appreciated.

    BTW, very interesting papers referenced in your OP:

    Sticky situations: recent advances in control of cell adhesion during neuronal migration by David J. Soleck

    Structure of astrotactin-2: a conserved vertebrate-specific and perforin-like membrane protein involved in neuronal development by Tao Ni, Karl Harlos, and Robert Gilbert

    Much food for thoughts in this OP. Still processing it.

  38. 38
    mk says:

    hi gpuccio.

    i actually refer to the chance that any match part will exist and not the chance to find it in the sequence space. its very unique argument that i never found in any id\creation site. i also have a very good analogy for your claim about ic. lets say that we will have a self replicating car with dna. what is the chance that this kind of car will evolve into an airplane?

  39. 39
    mk says:

    hi dionisio. my answer to the question(if i undnerstand it correctly)will be no. because it doesnt have any connection to this screen.

  40. 40
    Dionisio says:

    The 10-point summary at the end of the OP is very helpful.

  41. 41
    Dionisio says:

    mk @40

    Your answer is correct. Thank you.

    Basically none of the 10 tests performed were related to the actual function of the small TV screens.

    In order to find the functional value of those artifacts they could have done other (more sophisticated) tests.
    For example, remove the TV screens from some of the airplanes have various groups of passengers fly the same long route with and without the TV screens. Then ask the passengers to complete a thorough survey about their flights. Perhaps some of the passengers will point to the TV screens as a nice feature for long flights.
    Boring folks like me who read PDF documents stored in tablets instead of watching some videos or playing games might not notice the presence or lack of those TV screens. But passengers like my wife, who watches films during the transoceanic flights, would complain about the lack of those things. 🙂
    Eventually some passengers might decide to book their future trips with other airlines that have TV screens in the economy class seats.
    The economic effect of the decision to remove or not install such TVs could be felt by the mistaken airline at some point.
    Similarly, certain things in biological systems might have functionality that is not easily detectable because it isn’t that obvious or it could be hard to determine, unless more thorough examination is done.

  42. 42
    gpuccio says:

    Dioniso at #41:

    “Similarly, certain things in biological systems might have functionality that is not easily detectable because it isn’t that obvious or it could be hard to determine, unless more thorough examination is done.”

    Exactly!

    That’s why the test of long conservation in natural history is the best test of functionality.

    If variation is not allowed for 400+ million years, you can bet that what you have is functional! 🙂

  43. 43
    gpuccio says:

    mk:

    “what is the chance that this kind of car will evolve into an airplane?”

    Non existent.

    The fact is, new functions do not arise, especially if they are complex, unless someone designs them.

    That’s one of the biggest problems with the concept of NS. NS can only tweak what already exists.

    As a car will not become an airplane, so a snake will not become a bird without some new original complex design.

    Berlinski has pointed exactly to that concept in his famous and priceless video about whale evolution.

  44. 44
    CLAVDIVS says:

    gpuccio

    I suspect ID objectors are not commenting because they are bored. I know I am.

    I acknowledge you’ve invested time and effort into the OP, but it appears to be yet another God-of-the-gaps argument. You are putting the label “design” on gaps in our understanding of nature, but you are not telling us anything about the design process or the designer. This approach does not add anything to our knowledge so far as I can see.

    Around 10 years ago ID was in the media, academic and political spotlight. But not any more. CSI, the explanatory filter, and irreducible complexity are now moribund God-of-the-gaps arguments too, and ID has not come up with anything else new. ID discussions are confined virtually completely to this blog, which has banned most of the interesting opponents and now seems to focus on topics related to Christian apologetics.

    Just telling it how I see it.

    Sincerely
    CLAVDIVS

  45. 45
    gpuccio says:

    CLAVDIVS:

    Thank you for commenting.

    You are definitely the first from the other side who comments about this post, so you deserve special attention. 🙂

    I don’t know if your colleagues are “bored”, as you assume. Certainly, they have been very active in other threads, including some of mine. And they are certainly very active in some threads which, as you say, “focus on topics related to Christian apologetics”, where I rarely take part.

    Human behaviour is really mysterious, after all.

    Of course, I don’t agree with your pessimistic views about ID. I am sure that we will be around for a long, long time (at least until neo-darwinist understand their errors!) 🙂

    I don’t understand your “God of the gaps” reasoning. Excuse me, I have pointed to objective patterns which, IMO, can never be explained by the current theories about evolution. Being an ID proponent, I strongly suggest that a design explanation is warranted.

    You may disagree, but even if you don’t like the design paradigm, having definite objective and scientific patterns which falsify the current explanations that everybody seems to accept should get your attention anyway, even in a blog which focuses on topics related to Christian apologetics, and in which you are however taking part.

    Calling those concepts “God of the gaps arguments” will not solve the problem. I think I can expect something better from an intelligent person as you certainly are, something like: “No, look, your argument is wrong for this and that reason, and those patterns that you show in your post can easily be explained in this or that way”. The “God of the gaps” escape, frankly, is a little disappointing.

    OK, I am just telling it how I see it. We are, perhaps, kindred souls.

  46. 46

    Irreducible complexity is an indisputable fact Claud. Neither you nor anyone else can overcome the physics. Your only option is to ignore the physics and assume your conclusions in its place. And that’s why you do it.

  47. 47
    bill cole says:

    Gpuccio
    I agree with you on the God of the gaps argument. When someone resorts to that tactic I assume victory 🙂

    Scientism assumes a natural scientific explanation sometime in the future i.e. naturalism of the gaps.

    Design is an inference of what we are observing today and our current knowledge, however we know science is always tentative.

  48. 48
    gpuccio says:

    bill:

    “naturalism of the gaps” is a great way to describe what we daily see in our opponents’discourse.

    However, while “God” is a rather precise concept, at least in its general meaning, I would say that “nature” and “naturalism” have no definite meaning at all, as I have argued many times.

  49. 49
    gpuccio says:

    bill (and CLAUDIUS):

    Moreover, to invoke a “god of the gaps” objection when I have never, either directly or indirectly, referred to God in my post (as I never do when I discuss science) is rather surprising.

    Maybe I should focus more on “Christian apologetics”! 🙂

  50. 50

    It is amazing the number of otherwise intelligent people who (over and over and over again) repeat the same fallacy. They certainly would not go out in public and proclaim “I merely assume my conclusions”, yet, that is exactly what they do every time the speak the words “God of the Gaps”. Moreover, they expect everyone else to simply assume they are right as well. Must be nice.

    It’s not so good for the practice of science though. It’s the ultimate science stopper, leaving the institution with no way to correct itself.

  51. 51
    Dionisio says:

    gpuccio @42

    That’s why the test of long conservation in natural history is the best test of functionality.

    If variation is not allowed for 400+ million years, you can bet that what you have is functional!

    Yes, that’s a very good point.
    Now, how did we get that conserved functional stuff in there to begin with?
    That’s probably a challenging issue, isn’t it?
    🙂

    Maybe your interlocutors can help to answer that?
    🙂

  52. 52
    gpuccio says:

    Dionisio:

    Well, just to help our interlocutors to join the discussion, I will try to highlight a few points which can be derived from this post (and from those which have preceded it). They are, IMO, points which deserve discussion, beyond any “God of the gaps” distraction:

    1) Our opponents have often stated, during the last years, that CSI or dFSCI is an abstract and useless concept, that it cannot be measured, that even if measured it has no meaning and practical application

    Well, I have tried to apply a very simple method to measure dFSCI in the existing proteome, and to derive interesting conclusions from those measurements.

    2) The method is simple enough: I use the bit score of homology which can be easily found by comparing proteins in the publicly available BLAST software. That bit score is a good measure of functional information in a molecule, provided that the molecules we are comparing can be traced to some ancient split (in this case, the 400+ million years that divide cartilaginous fish from humans). With such chronological separations, any important homology conserved through time can be explained only as the result of strong negative selection, and therefore strong functional constraints. In many cases, a computation of the ka/ks ration can confirm the degree of functional constraints acting on the molecule.

    3) Applying that method to a specific split, and therefore to a specific time window, and to specific proteins (long regulatory proteins which are implied in important developmental organization) I have found consistent results indicating a very important generation of functional information, in many similar molecules, and with a potential component of high irreducible complexity. IMO, that is a very interesting result.

    4) The same method allows us to distinguish between proteins which undergo some massive growth of functional information, and other proteins, implied in similar networks, which instead simply retain their original information in the same time split. That is again an interesting result, and can be a starting point to try to understand the behaviour of these proteins, given that at present we understand very little of the whole developmental regulation, in this case, of the nervous system.

    OK, my point is simply: right or wrong, these ideas are scientific ideas, and deserve, IMO, to be addressed on a scientific plane, and not only with some philosophical attempt at denial.

  53. 53
    gpuccio says:

    Dionisio and all:

    Ah, I was forgetting an important thing.

    The method I have applied, even if simpler and a little different, owes everything to the concepts developed by Durston et al. in this fundamental paper of 2007:

    Measuring the functional sequence complexity of proteins

    https://tbiomed.biomedcentral.com/articles/10.1186/1742-4682-4-47

    I could not be more grateful to him and to all those who, like him, are trying to develop some scientific perspective based on the ID paradigm, against untold difficulties.

  54. 54
    Dionisio says:

    This excellent OP clearly points to the undeniable fact that substantial amounts of complex specified information appear to be added to the referred proteins within a relatively short biological time interval.

    Some interlocutors may express their dissatisfaction with the logical conclusions derived from this OP. That’s fine. They have the right to believe whatever they want. But people’s beliefs don’t change the evidences that point to reality.

    Note that even figuring out how the complex specified information got added to those proteins won’t take us far from the starting point on the way to fully understand the whole enchilada of the development process of biological systems.

    For example, this was posted @1026 in the thread under this link:
    http://www.uncommondescent.com.....ent-612183

    Given any case of known evolutionary divergence, it could be described as:

    Dev(d1) = Dev(ca) + Delta(d1)
    Dev(d2) = Dev(ca) + Delta(d2)

    Where

    Dev(x) is the developmental process of any given biological system x

    Delta(x) is the whole set of spatiotemporal procedural differences required to produce Dev(x).

    d1 and d2 are two descendants of their common ancestor (ca).

    Assuming the Dev(x) are well known, what hypothetical Delta(d1) and Delta(d2) could be suggested for the following cases?

    Case 1: d1 = placental mammals; d2 = marsupials;
    Case 2: d1 = placental; d2 = monotreme;

    Just point to the literature that explains this in details.
    The explanation must be comprehensive, logically coherent and it must hold water under any kind of thorough examination.

  55. 55
    Dionisio says:

    gpuccio @52-53

    Ok, now it seems like you have turned up the thermostat in this discussion thread. 🙂
    Thank you!

  56. 56
    bill cole says:

    Gpuccio

    Moreover, to invoke a “god of the gaps” objection when I have never, either directly or indirectly, referred to God in my post (as I never do when I discuss science) is rather surprising.

    Exactly, your opponent invoked a strawman argument.

  57. 57
    Dionisio says:

    gpuccio @52

    Well, I have tried to apply a very simple method to measure dFSCI in the existing proteome, and to derive interesting conclusions from those measurements.

    As far as I can tell, the method you have applied seems so clear that even I have started to understand it. Hence, other biology-illiterate folks like me should have no problem understanding your point.

    However, here’s an important caveat: one must be willing to understand it. Otherwise, it won’t matter how simple the method you apply is or how well you try to explain it, or how much effort you put into writing the OP, with the best known pedagogical approach, even using the ‘state of the art’ latest and greatest techniques for science education as described in the papers available from Springer today (see News post on this).

    Any person participating in this discussion but unwilling to at least understand your message -though not necessarily agreeing with it- should go back to their natural habitat in the beautiful Norwegian fjords! 🙂

    One humble way to understand anything is asking questions to learn.

    One way to discern the real motives of any participant in a discussion is asking them simple questions and watching how they react.

    Regarding the outdated (worn out) ‘gods of the gaps’ argument, I prefer the title “God of the entire show” coined by professor John Lennox.

    No one hiding behind such a vacuous ‘gods of the gaps’ concept would post over 2,500 references to most recent biology research papers within the last couple of years in just two threads in this site (“Mystery at the heart of life” and “Third way of evolution?”). Interesting if there’s another similar blog, on the opposite side of the ongoing argument, that has posted at least that many paper references within that time period lately.

    The opposite worldview is the one hiding behind outdated neo-Darwinian pseudoscience that leads nowhere. They better wake up and join us in this cheerful celebration of every new discovery before their ship sinks completely.

    We ain’t seen nothing yet. The best is still ahead.

    We should look forward, with increasing anticipation, to reading future research papers shedding more light on the elaborate molecular and cellular choreographies orchestrated within the biological systems.

    Every new discovery unveils parts of the biological systems that can only be explained through design principles.

  58. 58
    ellazimm says:

    gpuccio

    Excuse me, I have pointed to objective patterns which, IMO, can never be explained by the current theories about evolution

    When you say ‘can never be explained’ then polite dissenters probably don’t see the point of discussion. It does sound like you’ve made up your mind.

    You may disagree, but even if you don’t like the design paradigm, having definite objective and scientific patterns which falsify the current explanations that everybody seems to accept should get your attention anyway,

    Again, what is the point of raising objections when you are already convinced that you have falsified current explanations?

    Calling those concepts “God of the gaps arguments” will not solve the problem. I think I can expect something better from an intelligent person as you certainly are, something like: “No, look, your argument is wrong for this and that reason, and those patterns that you show in your post can easily be explained in this or that way”. The “God of the gaps” escape, frankly, is a little disappointing.

    It is also disappointing for someone to continually assume that some effect is impossible based on their interpretations of current theory.

    Your knowledge or lack of knowledge nor my knowledge or lack of knowledge is not the point. The point is: what is the most parsimonious explanation, the one that matches most of the data AND requires the least amount of special pleading.

    Intelligent design frequently ignores much data and research AND posits an undefined, undetected, uncommunicative and unknowable designer. That’s why it’s NOT the best explanation.

    However, while “God” is a rather precise concept, at least in its general meaning, I would say that “nature” and “naturalism” have no definite meaning at all, as I have argued many times.

    I’d love to hear your rather precise concept of ‘God’. And then I’d like to compare it to all the other concepts of ‘God’ that have existed throughout the ages.

    OK, my point is simply: right or wrong, these ideas are scientific ideas, and deserve, IMO, to be addressed on a scientific plane, and not only with some philosophical attempt at denial.

    Fine. Discuss them with biologists. Submit them to a journal. Discuss them at a seminar. Have an argument at a conference. It’s not hard to get your academic ideas addressed. You just have to be brave enough to take the reactions.

  59. 59
    CLAVDIVS says:

    gpuccio

    By ‘God-of-the-gaps’ I am referring to the form of the argument:
    * There is a gap in our understanding of the natural world
    * Therefore, the cause is supernatural

    You have not specifically referred to God or supernatural causes in your argument, but neither have you ruled them out … because you have not told us anything whatsoever about the design process or the designer. This is the pattern of most ID arguments, and it is indeed God-of-the-gaps reasoning.

    Accordingly, even if your argument is accepted as correct, it does not reveal to us anything we did not already know. If you disagree, can you tell me what new things we learn by accepting your argument?

    Regards
    CLAVDIVS

  60. 60
    gpuccio says:

    ellazimm:

    Well, second comment from the other side, and still strange “arguments”.

    Let’s see.

    “When you say ‘can never be explained’ then polite dissenters probably don’t see the point of discussion. It does sound like you’ve made up your mind.”

    This is really bizarre. So, you and other “polite dissenters” don’t feel any need to express your views, or explain the reasons of your dissent, simply because I have “made up my mind”?

    Is that your idea of communication, in science or anywhere else? You never debate with those who have some different idea, and are convinced of what they think? You only discuss with people who are unsure, or confounded?

    You know, I can have made up my mind, as I am sure you have too, and still we can reasonably and constructively confront our ideas. It happens. Sometimes.

    “Again, what is the point of raising objections when you are already convinced that you have falsified current explanations?”

    Maybe showing where I am wrong?

    You know, I think we come her, you and me and the others, not so much to convince our interlocutor, but rather to express our ideas by means of an intellectual confrontation with some valid interlocutor, so that other onlookers may “make up their mind”. Are you really so discouraged only because you don’t really hope to convince this foolish and obstinate guy?

    “It is also disappointing for someone to continually assume that some effect is impossible based on their interpretations of current theory.”

    Should I make my assumptions based on your intepretation of current theory? Just to know.

    “Your knowledge or lack of knowledge nor my knowledge or lack of knowledge is not the point. The point is: what is the most parsimonious explanation, the one that matches most of the data AND requires the least amount of special pleading.”

    I have a very definite idea of what the answer is. I also believe that you have “made up your mind” already.

    “Intelligent design frequently ignores much data and research…”

    What data and research?

    “..AND posits an undefined, undetected, uncommunicative and unknowable designer.”

    ID posits that all complex functional information comes from some conscious intelligent agent. Defined or not. Detected or not. Communicative or not. Knowable or not. ID infers the intervention of a conscious designer, if you really want to use the correct verb. In ID theory, the designer is inferable.

    “That’s why it’s NOT the best explanation.”

    Why am I not surprised of your conclusion? Ah, yes… You had probably made up you mind.

    “I’d love to hear your rather precise concept of ‘God’. And then I’d like to compare it to all the other concepts of ‘God’ that have existed throughout the ages.”

    Well, we were referring to the “God of the gaps” idea. I suppose that, in that context, God is just some being that we can refer to to fill the gaps. That’s a rather precise concept, for me. I did not mean that all the aspects of the idea of God are precise, or shared by all religious people. I can certainly agree with you that there are all sorts of different and often contrasting interpretations of the idea of God. But again, I was referring to “God of the gaps” versus “Nature of the gaps”. You see, I am convinced that “nature” is really an ambiguous concept. You give me your definition, and we can discuss. If you have not already made up your mind, of course. 🙂

    “Fine. Discuss them with biologists. Submit them to a journal. Discuss them at a seminar. Have an argument at a conference. It’s not hard to get your academic ideas addressed. You just have to be brave enough to take the reactions.”

    Why do all you guys want to tell me what I should do? I do what I like to do. I like to write on this blog. I try to do that at my best. I like to answer the comments of my interlocutors, especially those from the other side.

    When there are comments…

    Now, just answer a very simple question: what pertinent comment have you made about my OP in your post #58?

  61. 61
    Dionisio says:

    Discuss them with biologists. Submit them to a journal. Discuss them at a seminar. Have an argument at a conference. It’s not hard to get your academic ideas addressed. You just have to be brave enough to take the reactions.

    Who is this telling gpuccio what to do?

    I know gpuccio has coauthored medical papers in the official Journal of the American Academy of Pediatrics and perhaps other journals too.

    I have never published any paper, and most probably never will, except a few handwritten notes stuck to the refrigerator door as a reminder for grocery shopping. 🙂
    Hence, I’m not qualified to tell gpuccio what he should do with his time and knowledge.

    But I’m very glad gpuccio decided to write this OP and I look forward to reading his future OPs too. I’m sure other folks in this blog think similarly about this.

    Any person participating in this discussion but unwilling to at least understand gpuccio’s clear message -though not necessarily agreeing with it- should consider going back to their natural habitat in the beautiful Norwegian fjords!

  62. 62
    gpuccio says:

    CLAVDIVS:

    “By ‘God-of-the-gaps’ I am referring to the form of the argument:
    * There is a gap in our understanding of the natural world
    * Therefore, the cause is supernatural”

    OK. My objections:

    1) ID theory is not about a gap in our understanding. ID theory is about the observable origin of all complex functional information from conscious processes.

    IOWs, we are not saying: OK, there is this thing which is dFSCI, and we have no idea of how it comes into existence, so let’s attribute it to God, or to some other supernatural cause!”.

    No. Not at all.

    What we are saying is: OK, there is this thing which is dFSCI, and we can observe that it comes always from conscious processes.

    Can you see the difference? There is no gap here. Then an inference by analogy follows. But gaps have nothing to do with the reasoning, least of all gods and supernatural beings.

    ID is empirical. It is not a philosophy. It is science.

    2) The “supernatural” aspect. You may know how hostile I am to the words “nature”, “natural” and “supernatural”. What are they supposed to mean?

    I can observe that Hamlet came from the conscious representations of Shakespeare. I see that this post comes from my conscious representations. Is Shakespeare supernatural? Am I supernatural?

    Let’s say that, for some miracle, you (even if you have already made up your mins, see precious two posts 🙂 ) accept for a moment that vertebrates were designed at some definite time of natural history. Does that make the event supernatural?

    You will say: but we know no “natural” designer who could have done that.

    OK, let’s get rid of the “bad word”. What remains is: but we know no designer who could have done that.

    And I say: OK, the designer must exist, because I infer him from the design. But you are right, we don’t know him (or them).

    Where is the scandal? Do you really believe that we know all that exists? I don’t.

    We don’t know what dark energy is, and yet it is at the center of all scientific discussions. Just to give an example.

    Luckily, our knowledge is not a necessary condition for something to be real, otherwise the universe would have collapsed a lot of time ago.

    “Accordingly, even if your argument is accepted as correct, it does not reveal to us anything we did not already know. If you disagree, can you tell me what new things we learn by accepting your argument?”

    Yes, I disagree. As I have tried to point out in my post #52, my humble and simple reasonings offer some interesting proposals. I have tried to identify definite places and times where a lot of functional information appears rather suddenly. I have described different behaviours of similar proteins with regard to their informational content. Just forget for a moment the problem of the designer. Just accept for a moment that what we can see in natural history is a series of rather sudden generation of complex functional information, and that the current theory of RV + NS can in no way explain those facts, indeed can only sidetrack our reasonings.

    Now, who is the designer is not the only interesting question. There are many other important questions, if you start reasoning in terms of intentional design and functional information. For example, what is the purpose of the new information. What is the general plan, or plans, that we can observe. That can really help to see and understand things, while the sterile attempt to explain them by a theory which cannot explain them can only, in the end, be a source of ignorance and error.

  63. 63
    Dionisio says:

    gpuccio @53

    The method I have applied, even if simpler and a little different, owes everything to the concepts developed by Durston et al. in this fundamental paper of 2007:

    Measuring the functional sequence complexity of proteins

    https://tbiomed.biomedcentral.com/articles/10.1186/1742-4682-4-47

    Thank you for referring to that paper.

  64. 64
    Dionisio says:

    gpuccio @62

    We don’t know what dark energy is, and yet it is at the center of all scientific discussions. Just to give an example.

    We’ve used the empirical effects of gravity and electromagnetism very productively for many years, but do we really understand exactly what gravity and electromagnetism are and their origin?

    🙂

  65. 65
    Dionisio says:

    gpuccio

    After reading your posts @52-53 I warned @55:

    it seems like you have turned up the thermostat in this discussion thread

    Well, now we know that it did work! 🙂

    The ‘polite dissenters’ have jumped into the ‘arena’!

    Apparently you’ve removed the ‘boring’ aspects of this discussion?

    🙂

  66. 66
    Dionisio says:

    @54 let’s restate this once more:

    This excellent OP clearly points to the undeniable fact that substantial amounts of complex specified information appear to be added to the referred proteins within a relatively short biological time interval.

    Some interlocutors may express their dissatisfaction with the logical conclusions derived from this OP. That’s fine. They have the right to believe whatever they want. But people’s beliefs don’t change the evidences that point to reality.

    Note that even figuring out how the complex specified information got added to those proteins won’t take us far from the starting point on the way to fully understand the whole enchilada of the development process of biological systems.

    See the serious “evo-devo” issue presented @54
    As gpuccio and other ID proponents have stated, conscious design appears to be the only known source (so far) of functional specified complex information.

    But they politely ask: if anyone is aware of another source, what is it?

    Now, let’s make this clear:

    It’s obvious to any seriously thinking person reading this blog, that ID proponents stop short of trying to identify the conscious designer. They try hard to keep their biology-related discussions within the strict domain of biology. Nothing less. Nothing more.
    Our beloved Italian doctor gpuccio is an excellent example of this. His highly insightful and always welcome OPs and follow-up comments don’t leave any doubts about him being a strong ID proponent.

    Why do I refer to the ID-proponents as “they”/”them” instead of “we”/”us”?
    Well, simply because I’m not an ID proponent.
    Why?
    Because I’m always willing to publicly admit that the ultimate reality is summarized in the first few verses of the 4th book in the Christian Bible New Testament. Hence, I believe that I know the identity of the Designer, because I believe He has revealed Himself in both:
    1. the whole Creation (His General Revelation) which we observe in awe and study meticulously and
    2. the Holy Scriptures (His Special Revelation to His chosen people).
    That’s all. That simple. As y’all can see, I’m disqualified to be counted among the ID proponents.
    However, I like and enjoy reading some of the ID propositions, which I see very serious and definitely scientific.

    Theologically speaking gpuccio and I might be on different pages. I really don’t know. But I enjoy reading what he writes here and look forward to reading his future OPs and comments.

    Perhaps that’s why this blog literally seems like a very colorful philosophical/theological ‘eintopf’!

    After all, science can be done by people with different worldviews. Different Nobel Prizes in sciences have been given to atheists, agnostics, Jews, Christians, etc.

    Now, all that said, let’s get back to the discussion topic initiated by gpuccio’s excellent OP.

    Thank you.

  67. 67
    CLAVDIVS says:

    gpuccio

    1) ID theory is not about a gap in our understanding. ID theory is about the observable origin of all complex functional information from conscious processes. … What we are saying is: OK, there is this thing which is dFSCI, and we can observe that it comes always from conscious processes.

    2 points.

    First:

    The observable origin of all complex functional information is from the conscious processes of humans (and some other animals) who are vertebrates.

    You cannot therefore argue, by analogy as you say, that the complex functional information in vertebrates comes from the conscious processes of vertebrates – because this is absurd.

    Your argument must be that the complex functional information in vertebrates comes from non-vertebrate consciousness.

    But non-vertebrate consciousness has never been observed to produce complex functional information.

    Your argument from analogy thus undermines itself and fails.

    Second:

    I asked “… even if your argument is accepted as correct, it does not reveal to us anything we did not already know. If you disagree, can you tell me what new things we learn by accepting your argument?”

    Your response makes my point: you still have not told us any new things we learn from accepting your argument. You said:

    Yes, I disagree. As I have tried to point out in my post #52, my humble and simple reasonings offer some interesting proposals. I have tried to identify definite places and times where a lot of functional information appears rather suddenly. I have described different behaviours of similar proteins with regard to their informational content. Just forget for a moment the problem of the designer. Just accept for a moment that what we can see in natural history is a series of rather sudden generation of complex functional information, and that the current theory of RV + NS can in no way explain those facts, indeed can only sidetrack our reasonings.

    Now, who is the designer is not the only interesting question. There are many other important questions, if you start reasoning in terms of intentional design and functional information. For example, what is the purpose of the new information. What is the general plan, or plans, that we can observe. That can really help to see and understand things, while the sterile attempt to explain them by a theory which cannot explain them can only, in the end, be a source of ignorance and error.

    You’re just pointing to gaps in our knowledge, which we already know about, and asking more questions.

    I want you to tell me something new, that we didn’t know before, that results from your argument.

    Otherwise, what’s the point?

  68. 68
    gpuccio says:

    CLAVDIVS:

    I appreciate your good will in the discussion, but I have to dissent:

    “The observable origin of all complex functional information is from the conscious processes of humans (and some other animals) who are vertebrates.”

    OK.

    “You cannot therefore argue, by analogy as you say, that the complex functional information in vertebrates comes from the conscious processes of vertebrates – because this is absurd.”

    Of course.

    “Your argument must be that the complex functional information in vertebrates comes from non-vertebrate consciousness.”

    My argument is that complex functional information, either in vertebrates or anywhere else, comes only from conscious representation. While that is an empirical observation which has no exceptions (no systems exists which can generate dFSCI without any conscious intervention), it has also an obvious explanation: only the conscious experiences f understanding and purpose can overcome the probabilistic barriers intrinsic in dFSCI.

    So, my argument, which is ID argument, is simple, strong, rational and beautiful.

    “But non-vertebrate consciousness has never been observed to produce complex functional information.”

    This is a very wrong way to put it. Let’s say that we have experience of consciousness in living physical beings, and of conscious intelligent consciousness which can easily generate dFSCI only in humans. Therefore, our inferences about consciousness come obviously from our observations of consciousness in humans. That’s very reasonable: we get information from what we know.

    The point is: you believe that only physical beings can be conscious, and I don’t have that prejudice. That comes obviously from different world views. I am OK with that, but again the point is:

    1) There is a strong and obvious inference by analogy which is commanded by observed facts and good reason: the design inference for biological information.

    2) You refute it only in name of your personal world view.

    3) I accept it, not because it is compatible with my personal world view (it is), but rather because it is a strong and obvious inference by analogy which is commanded by observed facts and good reason, and of course I have no prejudice in my world view which prevents me from accepting what is obvious and rational.

    So, who is biased here?

    You say:

    “You’re just pointing to gaps in our knowledge, which we already know about, and asking more questions.”

    No, I am pointing to facts: those six molecules, and not others, present a sudden and important generation of specific dFSCI. This is not a gap. As far as I know, it is not even something we “already knew about”: can you please point to some paper which had already said that?

    And of course I am asking more questions: that’s the beauty of science. The more we know, the more new questions we can ask. That’s how our knowledge grows.

    Only error and bias are science stoppers, and kill the true questions instead of revealing them.

  69. 69
    gpuccio says:

    CLAVDIVS:

    Ah, and even of your contribution to the discussion is reasonable and constructive, still you must admit that you have not yet said anything about the arguments presented in the OP.

    Do you agree with what I say, even if not with the final design inference? Do you accept that the facts presented there defy any explanation by the currently accepted theory?

  70. 70

    2 points

    Your first point appears to be nothing more than another useless attempt to control what can be considered evidence. These little chestnuts of materialist’ defense have gone on for so long we may legitimately ask the question – will materialist ever be able to defend their creation myth with actual science and reasoning?

    There is a single observable quality on record that is capable of producing the effects in question. That quality is intelligence. It’s a real thing. What in the world makes you think you can remove it from science just because humans have it? And let us not forget, science keeps a little caveat on the side for intelligence whenever it wants to evoke it for its own projects. If we receive a narrow-band radio signal from across the cosmos, these little attempts to dismiss intelligent action as a legitimate observable will suddenly disappear. And if we find semantic content encoded in that signal there won’t be a doubt in anyone’s mind. Encoded semantic content just doesn’t occur without intelligent action.

    If you need to demand that any intelligence that originated the encoded information in the cell must have been a vertebrate – then knock yourself out. It would be a refreshing change from the materialist’ hackneyed bromides about dismissing intelligence from science. The inconsistencies would at least be less embarrassing.

    As for your second point, it accomplishes as little as your first. I don’t know if you’ve noticed, but the materialist ideology hasn’t produced one iota of observation that supports a non-intelligent origin of encoded semantic content – the d in GP’s dFSCI. On the contrary, the d in dFSCI can be exclusively identified by its physical organization, yet with the exception of a few non-conformists (mostly in Europe), the remainder of biology doesn’t even give it a thought. It’s a hoot! The very center of the problem – which absolutely must be resolved — is virtually ignored, while the public is fed the possibility of life on some distant planet because a particular chemical substance might be found there.

    Instead of simultaneously asking for something new while you cleverly overlook what is already known, perhaps you might rethink your position. Will you be calling for an end to the war on the legitimate design inference in biology (based on universal evidence) or will you support the continued avoidance of that evidence because – if we take your objection at face value — you cannot conceive of an intelligent vertebrate forming anywhere else but on Earth?

  71. 71
    ellazimm says:

    gpuccio,

    Of course I don’t only discuss things with people who haven’t made up their mind. But my experience on this forum is that ID supporters are generally firmly entrenched and will not acknowledge even a small problem with their views. In that light I am less and less interested in pursuing discourse in this venue.

    I suppose that, in that context, God is just some being that we can refer to to fill the gaps. That’s a rather precise concept, for me. I did not mean that all the aspects of the idea of God are precise, or shared by all religious people.

    I don’t think ‘some being’ that can fill the gaps is precise.

    Now, just answer a very simple question: what pertinent comment have you made about my OP in your post #58?

    Since I consider your entire argument, including your original post, a god-of-the-gaps argument and I’m quite sure after years of reading your posts and comments that you won’t change your mind then I consider my comments at least peripherally pertinent.

    you believe that only physical beings can be conscious, and I don’t have that prejudice.

    Why is that a prejudice? What evidence do you have for your view?

    And, as has been pointed out, you have no experience of intelligent agents other than those who have existed on this planet. But you allow a powerful one in through the back door when you look at a gap in current scientific knowledge. You can’t logic up God.

  72. 72
    ellazimm says:

    UP

    That quality is intelligence. It’s a real thing. What in the world makes you think you can remove it from science just because humans have it? And let us not forget, science keeps a little caveat on the side for intelligence whenever it wants to evoke it for its own projects. If we receive a narrow-band radio signal from across the cosmos, these little attempts to dismiss intelligent action as a legitimate observable will suddenly disappear. And if we find semantic content encoded in that signal there won’t be a doubt in anyone’s mind. Encoded semantic content just doesn’t occur without intelligent action.

    It has already happened that a signal has been received that, at first, was considered to come from an intelligent source. And it was examined and scrutinised and analysed. And a non-intelligent source was discovered. Something as important as non-terrestial intelligence will be heavily examined before acceptance. When science examines the claims of ID proponents that a non-human intelligence has been ‘detected’ then those claims are not upheld. Your case has not yet been proven. You need to do more work.

    Will you be calling for an end to the war on the legitimate design inference in biology (based on universal evidence) or will you support the continued avoidance of that evidence because – if we take your objection at face value — you cannot conceive of an intelligent vertebrate forming anywhere else but on Earth?

    We can conceive of it. (And he didn’t say it had to be a vertebrate, read his comment again.) We just have no evidence it has happened.

  73. 73

    When science examines the claims of ID proponents that a non-human intelligence has been ‘detected’ then those claims are not upheld.

    Yes they have. Both IC and dFSCI (and all of their children) have been upheld, without exception.

    We just have no evidence it has happened.

    Except for all the observations you cannot explain without intelligent action. Has this not occurred to you?

  74. 74
    Origenes says:

    CLAVDIVS, gpuccio.

    CLAVDIVS: The observable origin of all complex functional information is from the conscious processes of humans (and some other animals) who are vertebrates. You cannot therefore argue, by analogy as you say, that the complex functional information in vertebrates comes from the conscious processes of vertebrates – because this is absurd.

    gpuccio: Of course.

    Why can’t it be the case that conscious alien vertebrates designed life on earth — ‘Venters’ from space? One may object that this hypothesis doesn’t offer an ultimate explanation for life in the cosmos, but science doesn’t concern itself with ultimate explanations.

    CLAVDIVS: Your argument must be that the complex functional information in vertebrates comes from non-vertebrate consciousness.

    Not so. The design inference works, even under the restrictive view that intelligence can only spring from vertebrate consciousness. IOWs CLAVDIVS does not present a valid counter-argument.

  75. 75
    gpuccio says:

    Origenes:

    “I don’t agree. Why can’t it be the case that conscious alien vertebrates designed life on earth — ‘Venters’ from space?”

    You are correct, in principle. But I have never been a great fan of the alien hypothesis, although it is a perfectly correct scientific hypothesis and ID hypothesis. As I assumed that CLAUDIUS too was not sponsoring that kind of solution, I just agreed with him on something about which we had a similar view.

    But your observation is epistemologically impeccable, thank you for making it.

  76. 76
    gpuccio says:

    ellazimm at #71:

    Well, another post and still no comments about any of the specific arguments in the OP. That’s really good! 🙂

    But…

    We learnt that “of course” you “don’t only discuss things with people who haven’t made up their mind.”

    That’s real progress.

    And:

    you “consider your entire argument, including your original post, a god-of-the-gaps argument”. OK, that’s a really amazing point, never heard of it before. 🙂

    And:

    you “consider my comments at least peripherally pertinent”.

    OK, my sincere compliments here. “Peripherally pertinent” is brilliant. I am serious here!

    Now, a more interesting point:

    Me (to CLAUDIUS): “you believe that only physical beings can be conscious, and I don’t have that prejudice.”

    You: “Why is that a prejudice? What evidence do you have for your view?”

    OK, shall I state the obvious? The nature of consciousness is one of the biggest cognitive problems in the history of human thought.

    The idea that consciousness arises from the physical body is only one of the many theories about the nature of consciousness. Although many devotees of scientism accept it as a dogma today, there are a lot of reason to refute that position. And we have discussed those reasons many times here.

    Whatever you can believe, you should agree that there is at present no final truth about that important point, and you should acknowledge that many thinkers, religious or not, do believe that consciousness is an independent principle that cannot be explained in terms of physical configurations.

    That’s why I say, with good reason, that believing that “only physical beings can be conscious” is a prejudice in a scientific discussion. If you prefer, we can say that is is a specific world view, certainly not shared by all, probably not shared by most.

    So, my point is that we have to remain flexible about the nature of consciousness and of possible conscious agents. If you look at a scientific problem like the nature of dFSCI and of its expression in biological beings with the caveat that only explanations compatible with your personal world view about consciousness can be accepted, that’s a prejudice.

  77. 77
    gpuccio says:

    ellazimm at #72:

    “It has already happened that a signal has been received that, at first, was considered to come from an intelligent source. And it was examined and scrutinised and analysed. And a non-intelligent source was discovered. Something as important as non-terrestial intelligence will be heavily examined before acceptance. When science examines the claims of ID proponents that a non-human intelligence has been ‘detected’ then those claims are not upheld. Your case has not yet been proven. You need to do more work.”

    I really think that you should make up your mind! 🙂

    It’s one of the two.

    Either:

    1) Your argument is that no amount of evidence for design in biological beings will ever do, because we know of no possible designers who are not physical beings on our planet.

    Or:

    2) Your argument is that we have not presented enough evidence that “non-human intelligence has been ‘detected’”, and we need to do more work.

    But how can you say that, if you have said absolutely nothing about the evidence presented, for example in this OP?

    If your position is the second one, please take your responsibilities, do your homework, and make some specific comment or criticism about the evidence presented.

  78. 78
    Origenes says:

    GPuccio @75,

    I’m no fan of the the alien hypothesis either. However, post #74 is about protecting the design inference from the tiresome objection that intelligence can only be human.
    We’ve been told again and again by atheists how irrational it is to hold that we are alone in the universe. They conveniently forget about that when they argue against ID.

    Neil deGrasse Tyson:
    Ordinarily, there is no riskier step that a scientist (or anyone) can take than to make sweeping generalizations from just one example. At the moment, life on Earth is the only known life in the universe, but there are compelling arguments to suggest we are not alone. Indeed, most astrophysicists accept a high probability of there being life elsewhere in the universe, if not on other planets or on moons within our own solar system. The numbers are, well, astronomical: If the count of planets in our solar system is not unusual, then there are more planets in the universe than the sum of all sounds and words ever uttered by every human who has ever lived. To declare that Earth must be the only planet in the cosmos with life would be inexcusably egocentric of us.

  79. 79
    gpuccio says:

    Origenes:

    OK, I perfectly agree. Thank you again. 🙂

  80. 80
    EugeneS says:

    Actually, dismissing intelligence from science as genuine causation is absurd because science itself is an intelligent enterprise. Intelligence is written all over it.

    This is why we see drastic departure from reason in the recent attempts to reconcile materialism with contemporary science. This departure comes in different forms: the multiverse, denial of fine tuning and of the objectivity of design detection.

  81. 81
    gpuccio says:

    EugeneS:

    Well said! 🙂

  82. 82
    J-Mac says:

    What gaps are you talking about here when referring to the “God of the gaps”?

    Are you talking about minuscule, insignificant gaps of knowledge that Darwinians that are about to be resolved? No way. You are talking about a chasm (s) of plausibility that Darwinists have not been able to bridge. Being positive about it or critical of those who point them out doesn’t change a thing.

    The good thing is that ordinary public is well informed and pretty educated now and they are not going to be bullied into believing that if something is “called science” it is actually science.

  83. 83
    J-Mac says:

    I remember one very, very wise man once told me:

    “If you were the designer of a masterpiece and someone else was taking credit for it, how long would you wait to expose it if you had the power to do it even though you had an eternity to wait?”

    150 years might seem like a long time from human prospective that is limited by time. Is it a lot for Someone who is not restricted by time?

  84. 84
    Dionisio says:

    J-Mac @82-83

    You’ve asked a valid question.

    gpuccio, UB, and other nice folks here evidently dislike any knowledge gaps. One can tell by their interest in learning and sharing what they’ve learned.

    The ‘gods of the gaps’ is a figment in some people’s minds.

    The real God is the God of he entire show, as professor John Lennox have said.

  85. 85
    Origenes says:

    J-Mac: What gaps are you talking about here when referring to the “God of the gaps”?
    Are you talking about minuscule, insignificant gaps of knowledge that Darwinians that are about to be resolved? No way. You are talking about a chasm (s) of plausibility that Darwinists have not been able to bridge.

    Indeed. And it is not the case that theses gaps are embedded in coherent materialistic explanations for other aspects of the organism. The “gaps” which are pointed out here are the ones that can be backed up by calculations. It is, in fact, the case that materialism cannot accommodate life at all. We are not talking about gaps in understanding; we are talking about a theory that is utterly incompatible with life.

    According to any materialistic explanation of life, there are only particles which create the illusion of one thing — the organism. However, in reality, instead of an organism, there is nothing over and beyond blind particles bumping into each other. IOWs there is, in fact, not one thing. Given materialism, there is nothing that wants to live, struggles to survive and/or organizes its parts.

    Yet the unfounded, incompatible idea that organisms want to live — struggle to survive — has great force in the materialistic Darwinian narrative. Darwinism assumes, without any basis, that an organism is compatible with materialism and uses it at a starting point of a “materialistic” explanation.

    Materialism holds that only fermions and bosons exist, organisms are and do things that don’t fit that picture. Given fermions and bosons why would there be organisms? Essentially, materialism needs to explain how intricate flexible coherence — the viability of an organism — can exist at levels above and beyond fermions and bosons. Producing such a materialistic explanation, bottom-up from the level of fermions and bosons, is a daunting task indeed. But, to be clear, organisms can never be a starting point of any materialistic explanation. One cannot assume what needs to be explained.

    How can living systems be so robust (dynamically stable), when they consist of thousands of chemical interactions that must all be coordinated precisely in time and space? From the point of view of physics, cells (not to speak of more complex organisms) should not exist, and yet they do. How is that possible?
    http://jamesabarham.com/my-blo.....t-darwin-i

  86. 86
    gpuccio says:

    J-Mac, Dionisio:

    Thank you for contributing to criticism of the “God of the gaps” argument.

    A few more thoughts on the issue.

    A gap of knowledge is always the origin of scientific understanding. Science arises because our consciousness is intuitively motivated to understand the things that it does not understand. Hence science, and indeed all cognition, arise.

    So, there is nothing wrong in gaps of knowledge. Any argument against gaps is indeed an argument against science itself.

    So, I suppose that, as we could expect, the problem lies in the “God” part. We can have gaps, we can have theories to try to explain them. The important thing is to keep “God” out of that, because then it’s no more science.

    OK, I am fine with that. But I would call that “methodological avoidance of the concept of God”, rather than “methodological naturalism”. At least, that would be a more meaningful name.

    But my problem is: when have I used the name, or concept, of God in mt reasoning? Maybe it’s my old age, but I don’t remember doing that!

    I have inferred the existence of a designer of biological information, not a transcendent creator of everything.

    So, we have a “designer of the gaps” argument. Well, is that a problem?

    Let’s see. We already agree that there is no problem in using a gap of knowledge to build an explanatory theory. All science does exactly that.

    Is the problem in the concept of a conscious designer? I can’t see why. Conscious designers exists, ans we know that conscious designers design objects which exhibit great quantities of dFSCI. Great quantities of dFSCI are exactly what is observed in my OP. So, it seems rather “natural” to use the concept of a conscious designer to explain what is observed.

    So, where is the problem? It’s simple. Our friends cannot accept the hypothesis that in reality there may be conscious agents who could design biological objects.

    OK, but why?

    They say: we have never observed that kind of conscious agents. Let’s concede that (I am not sure it is exactly true, but that’s another story). But I ask: are you really sure that we have observed all that exists in reality?

    Few people would really answer yes to that question even among the most convinced devotees of scientism.

    But we can observe the results which point to a conscious designer: dFSCI in biological objects. That’s what the OP is about.

    So, if we can reasonably infer the existence of dark energy from its effects, even if we have no idea of what it is, why can’t we reasonably infer the existence of a biological designer, even if we don’t know who he is (or they are)?

    The answer is simple, and disappointing: because the idea of a biological designer is too similar to the idea of a God.

    With dark energy, we are still more safe (at least for the moment). After all, there is energy in the name, and energy is somewhat reassuring. Even the “dark” is not bad: it sounds more like Star Wars than religion.

    So, I have a proposal: why can’t we call ID the inference to a “Conscious dark energy designer of biological information”?

    Maybe we could find a way to a truce with our interlocutors, after all! 🙂

  87. 87
    gpuccio says:

    To all:

    Just a simple ackowledgement.

    After a couple of days, there is still no pertinent comment from the other side about the content of the OP.

    I am obviously grateful to CLAUDIUS and ellazimm for constructively joining the discussion, but I think that they would be the first to admit that their arguments, valid or not that they are, have nothing to do with the specifics of the OP. We could well say that they are not even “peripherally pertinent”, in that regard.

    So, I will try again to emphasize what, in my OP, could perhaps deserve some discussion, kindly or not, aggressive or not, constructive or not.

    My title is:

    “The highly engineered transition to vertebrates: an example of functional information analysis”.

    OK, I think there are two different things at issue here.

    “The highly engineered transition to vertebrates” refers to a specific design inference, based on the data proposed in the OP.

    Here, the arguments presented by CLAUDIUS and ellazimm are maybe pertinent, but really peripherally. Indeed, they have kindly offered basic objections to any design inference for biology, and not to my specific inference. The arguments they used (God of the gaps, and similar) would refute any such inference, whatever the motivations of the inference itself.

    OK, let’s go to the second part of the title, which IMO is probably the most relevant:

    “an example of functional information analysis”

    Now, this is potentially more interesting. Functional information analysis? An example? Am I kidding? Have I succeeded, or am I completely out of my mind?

    In either case, some discussion could help.

    After all, we have been hearing for years, from the other side, that CSI and dFSCI are frauds, false concepts, logical fallacies, circular reasonings, you say it.

    Now, this foolish IDist (or IDiot, as you prefer) posts an “example” of “functional information” analysis!!!

    And nobody says a word (from the other side, I mean).

    And I think: how many times have we been requested to show how the concept of CSI, or dFSCI, could be applied to a real context? Well, right or wrong, this is a real context. Is it wrong? OK, I am here to listen: this is wrong because…

    I apologize for these (maybe too personal) considerations, but I thought that some of these things had to be said.

  88. 88
    gpuccio says:

    Origenes:

    I agree with you that life is more than blind matter. I also believe that life is more than just information in matter. In that sense, the concept of life is elusive even to ID, because ID deals only with the informational aspect.

    I would say that the nature of life is still elusive.

  89. 89
    Dionisio says:

    gpuccio @86

    why can’t we call ID the inference to a “Conscious dark energy designer of biological information”?

    Well, I guess that the ‘itchy’ terms ‘conscious’ and ‘designer’ are unacceptable in the given biological context.

    Perhaps if you call ID the inference to the “natural dark energy design of biological information” it would be more acceptable?

    You may keep trying to accommodate your OPs to the ‘taste’ of your interlocutors or just ignore all the whining and complaining coming from your ‘polite dissenters’ and call things by their names.

    In Spanish we say ‘al pan pan y al vino vino’.

    There’s a phrase -perhaps incorrectly associated with Cervantes’ Don Quixote- that says that when you advance some dogs bark. 🙂

    Ignore the barking and keep writing your insightful OPs and posting your follow-up comments.
    Many folks will appreciate it.

  90. 90
    Dionisio says:

    gpuccio @86

    A gap of knowledge is always the origin of scientific understanding. Science arises because our consciousness is intuitively motivated to understand the things that it does not understand. Hence science, and indeed all cognition, arise.

    So, there is nothing wrong in gaps of knowledge. Any argument against gaps is indeed an argument against science itself.

    Exactly.

    I believe Kopernik did not get inspired to write his breakthrough astronomic conclusions while looking at the birds during a pleasant walk in Frombork.
    He was motivated by difficult unanswered questions.
    His thorough research led him to discoveries that helped him to answer the outstanding questions, but raised new ones.

    We see the same in biology all the time.

    For example, here you posted this excellent OP pointing to the fact that 6 proteins show a relatively huge jump in functional complex information within a relatively short biological time interval. That intriguing observation raises interesting questions, which motivate you to search for logically coherent answers.

    How could we get that information added to the given proteins?

    One way could be to make it happen through a guided process under laboratory conditions. How would you do it?

    Is there another way?

    On the other hand, could it be that some questions raised by the published research papers are related to the established approach of doing bottom-up research of top-down design?

  91. 91

    After a couple of days, there is still no pertinent comment from the other side about the content of the OP. I am obviously grateful to CLAUDIUS and ellazimm for constructively joining the discussion…

    GP, I applaud your attempts to keep the conversation on course, and I apologize if my response to the ”God of Gaps, irreducible complexity, and dFSCI” comments did not help your cause, or gave your interlocutors a reason to not return.

  92. 92
    gpuccio says:

    UB:

    I have really appreciated your comments on those points. I think we are in such harmony of thoughts that what you write could well have been written by me! 🙂

    If my interlocutors find reasons not to return, the reason should probably be searched in the substance of the debate.

    In a sense, I could easily interpret their silence as a confirmation that what we write and say is not easily denied, but if I must be sincere I miss the confrontation. 🙂

  93. 93
    Dionisio says:

    gpuccio @92

    In a sense, I could easily interpret their silence as a confirmation that what we write and say is not easily denied,…

    Your interpretation seems very logically accurate.
    Keep posting your OPs.
    Many of us here like to read them.
    And perhaps many onlookers/lurkers/anonymous visitors enjoy reading your explanations too.

  94. 94
    Dionisio says:

    Since this OP might become part of a permanent reference publication, it’s worth correcting “fat finger” errors:

    In brief, the author reviews what is known about the process of neuronal cell adhesion and migration. Starting from that paper and some other material, I have chosen a group of six regulatory proteins which seem to have an inportant role in the above process. They are rather long and complex proteins, particularly good for an information analysis. Here is the list.

    Didn’t notice the misspelled word the first time I read this. The mind makes the correction automatically.

    Now I’m trying to answer these questions:
    How are these proteins produced?
    i.e. what genes get expressed and how?
    what GRN get activated? What signaling pathways?

    Then we could try to see what genetic/epigenetic changes needed to occur in order to get the enhanced version of the proteins.

    Does this make sense?

  95. 95
    Dionisio says:

    They all seem to be produced from straightforward gene expression, no pleiotropic cases, no splicing, PTM, etc. Did I get this right?

    If that’s the case, then the expressed genes in the ancestor and descendant should display differences that correspond to the differences observed in the actual proteins.

    Is this correct?

    ?Astrotactin 1, http://www.ncbi.nlm.nih.gov/gtr/genes/460/
    http://www.ncbi.nlm.nih.gov/gene/460
    http://www.uniprot.org/uniprot/Q61137

    ?Astrotactin 2,
    http://www.uniprot.org/uniprot/O75129

    ?BRNP1
    http://www.uniprot.org/uniprot/O60477

    ?Cadherin 2
    http://www.uniprot.org/uniprot/P15116

    ?Integrin alpha-V,
    http://www.uniprot.org/uniprot/P06756

    ?NCAM1
    http://www.ncbi.nlm.nih.gov/gene/4684

    Basically, in addition to comparing the actual proteins, also compare the processes to make them.

    Is this the correct path to get the information I’m looking for?

  96. 96
    Dionisio says:

    gpuccio

    RE: @95

    Am I barking up the wrong tree?

    🙂

  97. 97
    Dionisio says:

    gpuccio

    In this paper you referenced in your OP:

    Structure of astrotactin-2: a conserved vertebrate-specific and perforin-like membrane protein involved in neuronal development
    Tao Ni, Karl Harlos, Robert Gilbert
    DOI: 10.1098/rsob.160053
    Open Biology
    The Royal Society Publishing

    I read this:

    Our structure reveals how different functions, such as membrane binding via an annexin-like domain, have been co-opted to enable the functioning of a modified MACPF/CDC domain in a novel context […]

    What does “have been co-opted” mean in the given context?
    How does that work in this case?

  98. 98
    gpuccio says:

    Dionisio:

    No, all that you say makes sense, and of course it deverves attention.

    I will try to deepen some of these topics.

    As I have said many times, I am not sure that our understanding of the regulatory networks is enough to clarify many of the aspects you point to.

    I believe that the identification of specific and highly conserved sequences in such a group of related proteins should help to ask new questions. If those sequences arise in vertebrates, they must be related to specific properties of the vertebrate body plan and functions, like neuron organization and so on.

    One of the most intriguing possibilities is to try to match the information about sequence conservation (functional information) and biochemical structure and activity. The problem is that we understand enough about specific domains and structures with known biochemical functions (for example, DNA binding domains in transcription factors), but much less is understood about sequences which are conserved but have no obvious domain structure and probably regulatory functions. Starting from conservation, correctly interpreted as functional information, to get to the regulatory functions would be a fascinating way to understand new levels of organization.

    Another stimulating topic could be to enquire about the coordinated engineering and function of those proteins, IOWs the irreducible complexity aspect: how much are these sequences which arise in the same time window and subphylum related one to the other? How do they contribute to body plan, development and organization?

    My simple point is: reasoning in terms of design, intention and plans is a true science promoter which can help give new perspective to our approach to biology. Questions simply change. The question is no more:

    how did this sequence evolve by some non existent neo darwinian mechanism giving reproductive advantage?

    but rather:

    why was this functional information introduced at this stage? what is the plan? what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?

    By the way, I am going to correct the mispelled word. 🙂

  99. 99
    gpuccio says:

    Dionisio:

    I suppose that, in this particular case, they mean “co-option” in the sense of joining many different domains with different functions to get a new original result.

    However, we must consider that the domains are redefined, acquire new sequence features, and that the general result is much more than the original functions of the individual domains.

    These are very complex proteins, and only part of their structure-function relationship is understood. Here, individual bits of information can make a real difference, and there are a lot of them to be considered. Even the known domains are identified by some definite homology, but are very different from one protein to another one.

    The truth is: these are very complex realities, and we cannot simplify them, we have to understand them for what they are.

  100. 100
    Dionisio says:

    gpuccio @98

    […] the identification of specific and highly conserved sequences in such a group of related proteins should help to ask new questions.

    Excellent point!

    If those sequences arise in vertebrates, they must be related to specific properties of the vertebrate body plan and functions, like neuron organization and so on.

    Excellent point!

    One of the most intriguing possibilities is to try to match the information about sequence conservation (functional information) and biochemical structure and activity.

    Excellent point!

    Starting from conservation, correctly interpreted as functional information, to get to the regulatory functions would be a fascinating way to understand new levels of organization.

    Excellent point!

    Another stimulating topic could be to enquire about the coordinated engineering and function of those proteins, IOWs the irreducible complexity aspect: how much are these sequences which arise in the same time window and subphylum related one to the other? How do they contribute to body plan, development and organization?

    Excellent point!

    […] reasoning in terms of design, intention and plans is a true science promoter which can help give new perspective to our approach to biology.
    why was this functional information introduced at this stage? what is the plan? what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?

    Excellent point!

  101. 101
    Mung says:

    gpuccio: …but if I must be sincere I miss the confrontation.

    gpuccio is a nutjob and anyone who believes that anything he writes is true needs to have their head examined.

    Is that better?

    😀

  102. 102
    gpuccio says:

    Mung:

    Ah, Mung! What could I do without you? 🙂

  103. 103
    Dionisio says:

    gpuccio @99

    Thank you for the clear explanation.

  104. 104
    Origenes says:

    gpuccio: Just a simple ackowledgement.

    After a couple of days, there is still no pertinent comment from the other side about the content of the OP.

    A similar complaint has been expressed by Douglas Axe:

    … we’ve nailed this thing, there is nothing more that we need to do. We’ve made these arguments and nobody has responded to these arguments, at least not in the technical literature as a lot of people do. I mean, on their blogs, they say that we are full of … whatever. No one has done the kind of work that we’ve done, with the care that we’ve done it, to show that our results are wrong. ….
    On the other hand it is not by any means acknowledged by the academic scientists, not by any means acknowledged in the universities and the textbooks that our point is correct. So, we are largely ignored by the academic establishment. And, as I was scratching my head with the opportunity to write a book, I was wondering: what do you do in a situation when you have done all the work and it turned out beautifully clear — in my mind it shows very clearly that design is the correct way to explain life; not the Darwinian explanations — but it is not changing anything.

    [Douglas Axe, youtube 14 min 20 sec]

  105. 105
    gpuccio says:

    Dionisio:

    A few more thoughts about the idea of co-option in astroctin, and in general of re-use of existing domains.

    The main recognizable domain in astrotactins is the MACPF domain (membrane attack complex-perforin) which in astrotactin 2, for example, is located at the 852-1035 interval, and which strongly characterizes astrotactins as perforin related proteins.

    So, form the quoted paper about astrotactins:

    The N-terminus of the endodomain structure is formed by the canonical MACPF domain consisting of a central, broken, antiparallel four-stranded ?-sheet that possesses a distinctive central approximately 90° bend. Figure 2 shows a structure-based phylogenetic comparison of the ASTN-2 MACPF domain and other known equivalent structures from the MACPF/CDC superfamily.

    Now, a first important point is that the similarity of the MACPF domain in astrotactins with the same domain in other perforin related proteins, although undeniable, is more a general structure similarity than a sequence similarity, more than enough to classify those domains in the same protein family, but certainly not to believe that they are really the same thing.

    For example, is we blast human astrotactin 2 (the MACPF domain part only) against human perforin 1, the sequence similarity is really low:

    8 identities
    16 positives just 21.9 bits of homology
    an expect of 0.015, barely statistically significant.

    Consider, for comparison, that blasting the same domain sequence of human astrotactin 2 with lepisosteus oculatus, a bony fish, we get:

    158 identities (86%)
    171 positives (92%)
    333 bits of homology
    expect 2e-106

    A remarkable difference indeed!

    What does that mean?

    It means that the MACPF sequence that we find in astrotactin 2, both in humans and in fish and in all vertebrates, is certainly a sequence which can be traced to the MACPF protein family, but it is extremely different in sequence from the other MACPF domains found in other perforin like proteins, even in humans, while it is extremely similar in sequence to all astrotactin 2 proteins, even between distant species like human and fish.

    IOWs, the MACPF domain that we observe in astrotactins is highly specific for astrotactins, and highly conserved at sequence level in astrotactins, and in astrotactins only.

    The paper about astrotactins confirms this conclusion. Please, read carefully the part:

    2.2. MACPF and EGF-like domain structures

    I quote a relevant paragraph:

    All MACPF/CDC proteins that form pores have to date been shown to do so using a ?-stranded barrel in which each subunit contributes two ?-strand hairpins to generate a structure similar to a bacterial outer membrane porin, but formed by multiple subunits rather than a single polypeptide chain [3,61]. This requires the two ?-hairpins to be not significantly different in length to each other and that they are long enough to span a bilayer membrane. Two factors suggest that ASTN-2 loops 1 and 2 may not function in pore formation or that, if they do, the mechanism of pore formation by ASTN-2 differs significantly from that of the pore-forming members of the MACPF/CDC superfamily

    Emphasis mine.

    The same paper suggest a similar conclusion for the annexin like domain in astrotactin 2, as you can read in the part:

    2.6. The annexin-like domain

    The relevant passage:

    Thus, despite no sequence homology ASTN-2 and human annexin have very similar structures; their charge distributions, however, are very different (electronic supplementary material, figure S9b). For example, with the annexin V domains and the ASTN-2 annexin-like domain all oriented equivalently, the most-similar annexin V domain 3 presents a highly positively charged face whereas ASTN-2 presents a mixed face with regions of positive and negative charge.

    Again, emphasis mine.

    Co-option?

    In my world, this is heavy and brilliant engineering!

    So, we must be very careful. The biological literature correctly recognizes domains using both structural similarities and even weak sequence similarities. That’s perfectly fine.

    But that does not mean that those domains are the same thing in different proteins. They can be very different, and have very different functions.

    IOWs, what usually is labeled as co-option, or simply as re-use of the same domain, is really a process characterized in many cases by a whole re-formulation of the information in that sequence and structure.

    A design process, under all points of view.

  106. 106
    Dionisio says:

    gpuccio @99

    […] in this particular case, they mean “co-option” in the sense of joining many different domains with different functions to get a new original result.

    This concise statement should help to understand some important concepts you have referred to in this discussion thread.

    However, since this OP and your follow-up comments tend to be very technical –as it’s the case of your very insightful explanation @105, which I’m in the process of chewing and digesting before commenting on it later– understanding some basic concepts like “protein domains” is required.

    For example, are these good basic references?

    http://www.ebi.ac.uk/training/.....in-domains

    https://en.wikipedia.org/wiki/Protein_domain

    Here’s an interesting paper on the subject of protein domains:

    […] the way domains are defined needs to shift, if the concept of the domain is to maintain coherence when applied to conditionally disordered proteins.
    […]
    For a long time domain definition has ignored the linkage between structure and the physiochemical environment, because many proteins fold into a singular and structurally specific state at regular temperature and pressure, and in the absence of other molecules.

    The discovery of increasing numbers of proteins that do not behave in this fashion requires a changed emphasis in heuristic definitions of the protein domain.

    Protein domain definition should allow for conditional disorder
    Kavestri Yegambaram, Esther MM Bulloch, and Richard L Kingston
    Protein Sci. 22(11): 1502–1518.
    doi: 10.1002/pro.2336

    BTW, perhaps the technical level of your explanations is one of the reasons the “polite dissenters” from the opposite side of the debate seem mostly absent from this highly interesting discussion. However, the topic of the OP is technical, hence there’s no way around. Now, isn’t ironic that some of your opponents complain quite often that your ‘intelligent design’ proposition is not scientific? Can a discussion get more scientific than this?

    I’m processing the rest of your explanations @99 & @105 which provide much foods for thoughts. 🙂

    One issue I’m trying to understand has to do with the relation between the central dogma of biology (or its updated versions) and the co-option. IOW, the whole enchilada: DNA protein-coding exon sequences, transcription, promoters, operons, transduction signaling pathways, TFs, splicing, translation, PTMs, etc.

    Are the domain reshaping, their swapping, their co-options or multi-domain fusions, etc. sometimes associated with DNA changes, other times with epigenetic mechanisms, other with other post-transcriptional and/or post-translational events, others with combinations of the above?

    Disclaimer: as usual, my biology-illiterate condition may explain the noticeable dumbness of some of my questions. One of the advantages of this discussion is the forgiving attitude of the moderator. 🙂

  107. 107
    gpuccio says:

    Dionisio:

    Well, there is no doubt that all the factors that you mention can contribute to the final form and function of a protein. However, the basic discussions about protein domains and their functions, and their classification into superfamilies, families, and so on, derive essentially from a limited source of knowledge:

    a) The sequence: domains are usually recognized by sequence homology. For example, when we blast a protein at the NCBI site, the software recognizes the presence of possible domains in the sequence we are blasting because of its homology with the reference sequence for that domain. However, even low homologies are enough to identify a domain. That’s why the software states, in its output: “Putative conserved domains have been detected”.

    b) The structure: this is the main level at which a domain is defined. Domains have some known folding and tertiary structure. Here, again, the structure can be more or less similar.

    c) The function: in general, some similarity of function is expected from domains in a same family. However, as we have seen, it is perfectly possible for domains with similar structure to have different functions, and it is perfectly possible that similar functions are implemented by different domains.

    The classification of protein domains in superfamilies, like for example in the SCOP database, is largely based on the concept of finding groups of protein domains which share no similarity, either in sequence or in structure or in function, and for which, therefore, no derivation can be objectively hypothesized from one to any other.

    As Wikipedia puts it:

    Protein superfamilies represent the current limits of our ability to identify common ancestry. They are the largest evolutionary grouping based on direct evidence that is currently possible.

    SCOP 1.75 lists 2020 individual superfamilies.

  108. 108
    Dionisio says:

    gpuccio @107

    Interesting points. Thank you.

    BTW,

    SCOP 1.75 lists 2020 individual superfamilies

    I kind of like that number 2020! 🙂

    Isn’t it also used for referring to good vision?

    [Emphasis mine]

  109. 109
    gpuccio says:

    Dionisio:

    Yes, it’s amazing, isn’t it?

    2020 groups of basic protein information which are, admittedly, beyond the “current limits of our ability to identify common ancestry”.

    IOWs, they are completely separated islands of function.

    And the example of the MACPF domain in astrotactin 2, that we discussed above, shows clearly that there may be huge differences in sequence and function even between domains classified in the same family (not even superfamily), in different proteins!

    Consider this: blasting the sequence of the MACPF domain in human astrotactin 2 versus the whole human proteome, we get only 43 hits. About half of them, ranging from 186 to 374 bits, are with various isoforms of astrotactin 2. The rest, ranging from 139 to 141 bits, are with various isoforms of astrotactin 1.

    So, this particular implementation of the MACPF domain seems really quite specific to astrotactins, and nothing else.

    So, it is in itself an isolated island of function! 🙂

  110. 110
    Dionisio says:

    Mung @101

    gpuccio: …but if I must be sincere I miss the confrontation.

    gpuccio is a nutjob and anyone who believes that anything he writes is true needs to have their head examined.

    Is that better?

    Not bad. Really.

    That was a very creative idea to please gpuccio by ‘faking’ a confrontational comment. Definitely the comment was funny, it made me laugh, but perhaps it would be better to have a real serious discussion, not pretended confrontational ‘acting’? 🙂

    Since this discussion has turned so technical (above the pay grade of low-IQ biology-illiterate folks like me), maybe we all could learn more by inviting to this ‘arena’ real accredited biology scientists like Professor Larry Moran and/or Professor S. Joshua Swamidass. Regarding the latter, perhaps Dr. V J Torley can give a hand with this using his connection? 🙂

    As all can see, gpuccio has raised very interesting questions about profound issues in biology.

    Where are those professors when we need them more? 🙂

    We have seen them actively involved in previous occasions in this site. Their involvement should be highly appreciated again.

  111. 111
    Dionisio says:

    gpuccio:

    Perhaps I’ve said this funny anecdote here before, but I’ll say it again:

    A few years ago, when I was exploring the idea to switch career, I met a couple of biology professors at a university in Poland. While we were at lunch in a local restaurant, one of the scientists briefly told me about his research on protein folding. That was the first time I had heard about such a thing. At some point he suddenly stopped his talk and asked me if I didn’t like the food, because he noticed I wasn’t eating more. That unexpected question kind of woke me up from a strange hypnotism. Then I told him that I was so fascinated by what he was saying about protein folding issues that I literally had forgotten I was in a restaurant. My mind had been just blown away by his overwhelmingly fantastic description of that stuff I had never heard about until then. He just laughed out loud.

    Well, I think that conversation was one of the tipping points in my decision to change career.
    Since then the fascination has only increased and eventually became an irresistible obsession.

    Here we are now.

    Life goes on…

    🙂

  112. 112
    bill cole says:

    Dionisio

    But that does not mean that those domains are the same thing in different proteins. They can be very different, and have very different functions.

    IOWs, what usually is labeled as co-option, or simply as re-use of the same domain, is really a process characterized in many cases by a whole re-formulation of the information in that sequence and structure.

    A design process, under all points of view.

    I completely agree with Gpuccio here. If you see a claim of co option there is never a detailed discussion of how the reorganization of the genome could have facilitated that co option. The claim that co option is the answer to evolution forming the bacterial flagellium has never been validated in any detail of how the genome reorganized.

  113. 113
    gpuccio says:

    Dionisio:

    Yes, these small protein objects made of even smaller aminoacids are really fascinating! Hypnotic, I would say.

    So, let’s enjoy our common passion in this quiet solitude… 🙂

  114. 114
    gpuccio says:

    bill:

    IMO, co-option is a very lame concept used by neo darwinists as an extreme weapon of defense. In particular, it had its moment of pseudo-glory when neo darwinists had to desperately find some counter-argument to Behe’s brilliant introduction of the idea of irreducible complexity, which has since been a real pillar of ID theory.

    Co-option, like convergent evolution, is just a poor tool of bad magics, to convince your audience that you can explain what cannot be explained.

  115. 115
    bill cole says:

    gpuccio Dionisio

    Remember Ken Millers attempt to show a Darwinian account of the bacterial flagellum.:-)
    https://youtu.be/K_HVrjKcvrU

  116. 116
    gpuccio says:

    bill:

    Pitiful!

  117. 117
    bill cole says:

    here is Behe’s response.
    https://youtu.be/vEGjMgPOGeM

  118. 118
    gpuccio says:

    bill:

    Thank you for the very interesting links.

  119. 119
    gpuccio says:

    Dionisio:

    Thank you for linking, in your ever zealous search for new and interesting material, the following paper:

    “Cellullar insights into cerebral cortical development: focusing on the locomotion mode of neuronal migration”

    Takeshi Kawauchi1

    http://www.ncbi.nlm.nih.gov/pm.....-00394.pdf

    which adds a lot of details to this extremely fascinating topic.

    It is particularly obvious, reading the paper, that the six proteins I have considered are just a tiny sample of an interacting regulation network that includes a lot of other “agents”, all strictly integrated to allow and tightly control one of the most important functions for the ordered development of nervous system.

    Thank you again.

  120. 120
    Origenes says:

    Gpuccio: The most striking example is probably Astrotactin 2, which presents the biggest jump from cephalochordata (329 bits) to cartilaginous fishes (1860 bits), for a great total of 1531 bits of jump!

    1531 bits in just one protein … and we know that Astrotactin 2 is just one of the many influencers of the development of the nervous system.

    In the light of these huge numbers what to think of the “340” number, recently used by Swamidass and Torley wrt ape human transition:

    VJTorley:

    You [Eric Anderson] ask: “Do you seriously think 340 beneficial mutations in DNA could turn an ape-like creature into a human, and 3000 beneficial mutations in DNA could turn a land animal into a whale?”
    I have to say (reluctantly) that I haven’t seen any rigorous quantitative argument yet as to why this could not be the case.
    … For human evolution, I’m guessing that 30 to 50 separate organs (or systems) underwent transformation, and that there were 10 mutations per organ, with these mutations occurring more or less in sync (due to intelligent guidance), making 300 to 500 mutations.

    ~ source ~

  121. 121
    gpuccio says:

    Origenes:

    I agree with you: I definitely disagree with VJ on that point.

    Tons of evidence demonstrate that huge numbers of new functional information are needed for the transition from one species to another one, and much more when sudden jumps. like the emergence of a new clade or subphylum, like vertebrates, are implied.

    Just think how different are the genomes of C. elegans and C. briggsae, two small nematodes which appear almost identical phenotypically, and are separated by “only” 80 – 120 million years.

    From the “wormbook” site:

    One way C. briggsae and C. elegans orthologs were identified was by searching for C. briggsae/C. elegans pairs that were each other’s best BLASTP (Altschul et al., 1997) match in the opposite species. Synteny was subsequently used as a criterion to search for more orthologous pairs. These combined approaches produced altogether 12,155 ortholog pairs, or 62% of the C. briggsae gene set or 65% of the C. elegans gene set (Stein et al., 2003). After the publication of the initial C. briggsae genome analysis paper, a recently developed program InParanoid (O’Brien et al., 2005) was applied to identify orthologs between C. briggsae and C. elegans. The InParanoid database (April 2005 release), using a recent C. elegans gene set, lists 12,858 C. briggsae and C. elegans ortholog pairs. Therefore the numbers of orthologs obtained by these two different approaches agree well with each other. However, the number of identified orthologs will change over time as the genome assembly and gene annotation, especially for C. briggsae, improve.

    So, only 62-65% of ortholog genes in two almost identical organisms!

    Of course, the emergence of vertebrates required probably an unimaginable quantity of original functional information, if we consider that my 6000+ well defined bits come from a really tiny sample of specific proteins.

    So, what’s the problem with the transition to humans?

    In my OP, I have said:

    Of course, another fundamental transition is the one to homo sapiens, but I will not deal with it here: I fully agree with Bill Cole that it is an amazing event under all points of view, but it is also true that it presents some very specific problems, which make it a little bit different from all the other transitions we have considered above.

    There are reason for that statement.

    The problem is that the transition form primates to humans, a very recent one, shows the apparent paradix of a huge phenotypic and functional difference with, apparently, a rather small genomic difference.

    Now, there could be various explanations for that. The one preferred by neo-darwinists is that even a small difference can be enough to explain the different results in humans. I absolutely refute that explanation, which has the only purpose to “salvage” the foolish theory of neo-darwinism. It is refuted also by the whole corpus of information in the existing proteomes and genome, where huge differences in functional information are required to achieve new complex phenotypic functions, as showed by this OP and by the following discussion.

    Moreover, neo-darwinists also state that those small difference between, say, human and chimp, are exactly what is expected by the neutral theory.

    So, if you sum the two statements, you have the amazing paradox that the huge phenotypic and functional differences between chimp and humans are due essentially to a bunch of neutral variations!

    OK, let’s leave that kind of belief to our kind neo darwinist friends: after all, they are well accustomed to believe in myths! 🙂

    What other explanations are possible?

    First of all, we have to consider that, the more we go upward in the evolution/design process, the more functional differences are mainly achieved by changes in regulation networks, rather than in brute effectors.

    Regulation networks are much more elusive that gross biochemical functions, and we certainly understand much less about them. Moreover, a great part of those regulation networks is probably implemented at the level of non coding DNA, and we understand even less of that.

    There is also the epigenetic level that we have to consider: epigenetic differences can certainly have a great role. Although many, especially in the neo darwinist field, tend to believe that all epigenetic information derives essentially from the genome, that is in no way an established fact. I have proposed in another thread to consider the genectic-epigenetic system as a whole, where information is continually exchanged dynamically between the two parts of the system.

    Finally, there is another consideration, which IMO is very important: even with all that we know of genetic and epigenetic organization, the fact remains that the true procedures which govern the whole process of cell differentiation remain elusive.

    Now, neo darwinists tend to suggest that the information for those governing procedures simply does not exist, and that everything happens because a great number of lucky independent cascades of complex events just happen, and nothing really controls them. OK, let’s leave that belief to them (see above).

    Others, like me (and certainly my friend Dionisio) firmly believe that there must be a lot of specific and complex information there, in some form, in some place, which governs those complex development of different complex procedures which generate so many different cell types and body forms and functions.

    Why do we believe that? Because that’s the way, the only way, that complex information systems work.

    But there is no doubt that the information about those governing procedures remains really elusive.

    What is the most reasonable conclusion? I will state it, and then let my darwinist friends free to consider it a “God of the gaps” argument! 🙂

    There is still “a lot” that we don’t understand and cannot even vaguely figure out, in how cell development works.

    The differences that make humans human will probably be found in that “a lot”.

  122. 122
    Dionisio says:

    gpuccio @119

    […] the six proteins I have considered are just a tiny sample of an interacting regulation network that includes a lot of other “agents”, all strictly integrated to allow and tightly control one of the most important functions for the ordered development of nervous system.

    You’ve said it all. Additional comments are not required.

    Would anyone out there dare to argue against that statement within the context @119?

    Where are the professors when we need them?

    🙂

  123. 123
    Dionisio says:

    gpuccio @109

    […] it is in itself an isolated island of function!

    Would anyone out there dare to argue against that statement within the context @109?

    Where are the professors when we need them?

    🙂

  124. 124
    Dionisio says:

    gpuccio @105

    Co-option?

    In my world, this is heavy and brilliant engineering!

    […] what usually is labeled as co-option, or simply as re-use of the same domain, is really a process characterized in many cases by a whole re-formulation of the information in that sequence and structure.

    A design process, under all points of view.

    Would anyone dare to argue against that statement within the context @105?

    Where are the professors when we need them?

    🙂

  125. 125
    Mung says:

    As usual gpuccio ignores all the missing intermediates. An astounding display of a lack of imagination.

    The reason we haven’t heard from Alicia is because she is off compiling that list of missing intermediates that we have no evidence for, and it’s a very long list, and Alicia’s imagination has limits too.

    It’s just not as limited as gpuccio’s.

  126. 126
    Dionisio says:

    gpuccio @121

    Tons of evidence demonstrate that huge numbers of new functional information are needed for the transition from one species to another one, and much more when sudden jumps. like the emergence of a new clade or subphylum, like vertebrates, are implied.

    Just think how different are the genomes of C. elegans and C. briggsae, two small nematodes which appear almost identical phenotypically, and are separated by “only” 80 – 120 million years.

    From the “wormbook” site:

    One way C. briggsae and C. elegans orthologs were identified was by searching for C. briggsae/C. elegans pairs that were each other’s best BLASTP (Altschul et al., 1997) match in the opposite species. Synteny was subsequently used as a criterion to search for more orthologous pairs. These combined approaches produced altogether 12,155 ortholog pairs, or 62% of the C. briggsae gene set or 65% of the C. elegans gene set (Stein et al., 2003). After the publication of the initial C. briggsae genome analysis paper, a recently developed program InParanoid (O’Brien et al., 2005) was applied to identify orthologs between C. briggsae and C. elegans. The InParanoid database (April 2005 release), using a recent C. elegans gene set, lists 12,858 C. briggsae and C. elegans ortholog pairs. Therefore the numbers of orthologs obtained by these two different approaches agree well with each other. However, the number of identified orthologs will change over time as the genome assembly and gene annotation, especially for C. briggsae, improve.

    So, only 62-65% of ortholog genes in two almost identical organisms!

    Of course, the emergence of vertebrates required probably an unimaginable quantity of original functional information, if we consider that my 6000+ well defined bits come from a really tiny sample of specific proteins.

    So, what’s the problem with the transition to humans?

    In my OP, I have said:

    Of course, another fundamental transition is the one to homo sapiens, but I will not deal with it here: I fully agree with Bill Cole that it is an amazing event under all points of view, but it is also true that it presents some very specific problems, which make it a little bit different from all the other transitions we have considered above.

    There are reason for that statement.

    The problem is that the transition from primates to humans, a very recent one, shows the apparent paradox of a huge phenotypic and functional difference with, apparently, a rather small genomic difference.

    Now, there could be various explanations for that. The one preferred by Neo-Darwinists is that even a small difference can be enough to explain the different results in humans. I absolutely refute that explanation, which has the only purpose to “salvage” the foolish theory of Neo-Darwinism. It is refuted also by the whole corpus of information in the existing proteomes and genome, where huge differences in functional information are required to achieve new complex phenotypic functions, as showed by this OP and by the following discussion.

    Moreover, Neo-Darwinists also state that those small difference between, say, human and chimp, are exactly what is expected by the neutral theory.

    So, if you sum the two statements, you have the amazing paradox that the huge phenotypic and functional differences between chimp and humans are due essentially to a bunch of neutral variations!

    OK, let’s leave that kind of belief to our kind neo darwinist friends: after all, they are well accustomed to believe in myths! 🙂

    What other explanations are possible?

    First of all, we have to consider that, the more we go upward in the evolution/design process, the more functional differences are mainly achieved by changes in regulation networks, rather than in brute effectors.

    Regulation networks are much more elusive that gross biochemical functions, and we certainly understand much less about them. Moreover, a great part of those regulation networks is probably implemented at the level of non coding DNA, and we understand even less of that.

    There is also the epigenetic level that we have to consider: epigenetic differences can certainly have a great role. Although many, especially in the neo darwinist field, tend to believe that all epigenetic information derives essentially from the genome, that is in no way an established fact. I have proposed in another thread to consider the genetic-epigenetic system as a whole, where information is continually exchanged dynamically between the two parts of the system.

    Finally, there is another consideration, which IMO is very important: even with all that we know of genetic and epigenetic organization, the fact remains that the true procedures which govern the whole process of cell differentiation remain elusive.

    Now, neo darwinists tend to suggest that the information for those governing procedures simply does not exist, and that everything happens because a great number of lucky independent cascades of complex events just happen, and nothing really controls them. OK, let’s leave that belief to them (see above).

    Others, like me (and certainly my friend Dionisio) firmly believe that there must be a lot of specific and complex information there, in some form, in some place, which governs those complex development of different complex procedures which generate so many different cell types and body forms and functions.

    Why do we believe that? Because that’s the way, the only way, that complex information systems work.

    But there is no doubt that the information about those governing procedures remains really elusive.

    What is the most reasonable conclusion? I will state it, and then let my darwinist friends free to consider it a “God of the gaps” argument! 🙂

    There is still “a lot” that we don’t understand and cannot even vaguely figure out, in how cell development works.

    The differences that make humans human will probably be found in that “a lot”.

    I assumed the “wormbook” quote ends right before this statement:

    So, only 62-65% of ortholog genes in two almost identical organisms!

    Here’s a request:
    In the following statement, can you provide the link to the referred thread? Thank you.

    I have proposed in another thread to consider the genetic-epigenetic system as a whole, where information is continually exchanged dynamically between the two parts of the system.

    Would anyone dare to argue against the comments posted @121?

    Where are the professors when we need them most? 🙂

    Hello! Anybody out there? 🙂

  127. 127
    Dionisio says:

    Mung @125

    As usual gpuccio ignores all the missing intermediates. An astounding display of a lack of imagination.

    Yes, he seems to have serious intellectual problems accepting what is so obvious to everyone and their cousins out there: that the neo-Darwinian theory (+extensions) can answer all his questions and many more, including why aunt Matilda baked that yummy cake for her nephew Johnny and not for me. 🙂

  128. 128
    Dionisio says:

    Mung @125

    The reason we haven’t heard from Alicia is because she is off compiling that list of missing intermediates that we have no evidence for, and it’s a very long list, and Alicia’s imagination has limits too.

    Ok, that explains one missing ‘polite dissenter’ but what about the professors?

    🙂

  129. 129
    Dionisio says:

    Ok, enough joking here, let’s get serious now.

    I appreciate Mung’s very creative (and funny) comments to make gpuccio happy by providing some missing confrontation. But, besides the one Mung mentioned, why don’t we see the other ‘polite dissenters’ here? Where did they go? Have they been banned from this site? Do they need a GPS to find this thread? 🙂

    Would anyone dare to argue against gpuccio’s OP and follow-up comments in this thread?

    Where are professors M, S, etc. when we need them most? 🙂

    Hello! Anybody out there? 🙂

  130. 130
    gpuccio says:

    Dionisio:

    I fixed the blockquote error. Thank you.

    You are right, the silence of the other side is specially evident in this thread. And yet, we have tried to touch many topics, apparently interesting and intriguing.

    I wonder, as you do, what’s happened. I hope they are well, anyway. 🙂

    Regarding my statement about the genetic – epigenetic system, I think it was a comment, recent but not too recent, and I really don’t know how to retrieve it.

    A stupid question: is there a way to see a list of all my comments (not just the posts) in my author’s page? That would help.

  131. 131
    gpuccio says:

    Mung:

    Ah, yes, my personal fight with the missing intermediates has been around for a very long time. It has even been debated in great detail in enemy field (at Mark Frank’s blog, and probably also at TSZ). So, it’s an old story (but always stimulating).

    I don’t know if Alicia is busy elsewhere, or what else. I really miss the old good interlocutors: Mark Frank, Zachriel, and many others.

    Intellectual confrontation is a value in itself: the merit ( if there is any! 🙂 ) for my personal ideas about ID can be given, for the best part, to my interlocutors.

  132. 132
    Dionisio says:

    gpuccio

    Check this out:

    Note you posted several comments in that same thread.

    http://www.uncommondescent.com.....ent-603834

  133. 133
    gpuccio says:

    Dionisio:

    Yes, that’s it!

    How did you do it?

    I copy it here, in case someone is interested (ah, ah!):

    “Indiana Effigy:

    It’s not that simple.

    Epigenetics is a constant interaction between a static form of information (the nucleotide sequence stored in DNA, both protein coding and non coding) and its dynamic expression as transcriptomes and proteomes in each different cell state.

    In that sense, there is no condition in the cell life which is not at the same time genetic and epigenetic.

    For example, the zygote which originates multicellular beings hai its own distinctive epigenetic state: the DNA is expressed in the zygote in different ways than it will be expressed in different states of the embryo, or in different specific tissue cells, both stem cells and differentiated cells.

    The epigenetic state of the zygote, in turn, is derived mainly from the cytoplasm of the oocyte, but also from epigenetic messages in the sperm cell.

    So, at each moment of the life of a cell, or even more of a multicellular being, the total information which is being expressed is a sum of genetic and epigenetic information.

    And, whatever you may think, any theory about the origin of biological information must explain how the total information content which is expressed during the life span of some biological being came into existence.”

    And:

    “Indiana Effigy:

    “But if I am reading you correctly, the actual “information” still relies on the DNA.”

    Not all of it, certainly. The cytoplasm, as I said, bears information too. And so does the state in which DNA is when it is transmitted in cell division.

    There is never a moment where DNA is in some “absolute” state. It is always in some epigenetic state.

    And the cytoplasm, or the nucleus itself as a whole, have specific information content at each state. The sum total of proteins and RNAs expressed, for example.

    As “life always comes from life”, life is always a continuous dynamic expression of genetic and epigenetic information.

    When Venter builds his “artificial” genomes, copying and modifying natural genomes, he has to put them into a living cell. IOWs, he is introducing a modified genetic component into a specific existing epigenetic condition.

    Remember, life is a dynamic, far from equilibrium condition, not a static storage of information.”

  134. 134
    Dionisio says:

    gpuccio:

    I simply Binged*:
    gpuccio epigenetic
    and Bingo!
    BTW, the resulting list included other blogs where they quoted or referred to you. I can tell you’re popular among the polite dissenters out there. Apparently they like your comments as much as we do here. 🙂

    Here I quoted your comments, but apparently forgot to provide a link to the source:

    http://www.uncommondescent.com.....ent-528378

    I use Bing in my Surface tablet. It’s the default search engine and it works for me, as you can see. 🙂

    The interactive animation software development project I’ve worked on is mostly based on MSFT / Xamarin platforms, hence I’m sold to them. 🙂

    BTW, Xamarin main conference is titled ‘Evolve’ which confirms that highly controversial term is context-dependent. In their case it refers to intelligent guided evolution. 🙂

  135. 135
    Dionisio says:

    gpuccio:

    in the first lecture of the 2014 Systems Biology course by professor Uri Alon, around time mark 34:50 Dr. Alon talked about the remarkable genetic machinery and asked how it came to be? Please note this isn’t a transcript, but just an approximate interpretation of what I heard in the video.
    Anyone interested in hearing exactly what the professor said may want to watch the video.
    Apparently he said that supposedly it was not an engineer who designed it so beautifully like this. Then adding another sense of wonder, he said that this machinery is almost universal. For example genes in E-coli bacteria and human beings look very similar, same genetic code. Take a gene that encodes for a protein that turns jellyfish green (green fluorescent protein) and using molecular biology tools add that piece of DNA code from the jellyfish to the E-coli DNA promoter activated by the TF associated with sugar level and the bacteria will turn green depending on the concentration level of sugar.
    @35:50 Amazing modularity!
    That’s a big experimental tool used to study the dynamics of gene regulatory circuits playing with this modularity.
    @36:30 BTW, it doesn’t work the other way, i.e. take the corresponding promoter from the jellyfish DNA to the E-coli and it won’t work inside the E-coli because E-coli doesn’t make the transcription factor that activates the promoter copied from the jellyfish. That’s an interesting asymmetry of the modularity.
    The way this came about… this thing… the process we think, believe it or not, is by [through?] a framework they call natural selection: every time DNA replicates there’s a probability to make a one-letter error called [random?] “mutation”. Due to these mutations in the genes the proteins could malfunction, i.e. the bacteria will have less than a fighting chance vs. other bacteria that could affect the bacteria reproduction hence the mutation will vanish, but sometimes that mutation may turn into an advantage for reproduction and then that mutated DNA is passed along through the bacteria population.
    So that’s the process they believe -believe it or not- brought about all this kind of machinery.
    That’s a big challenge right now in biology.
    Understand this possibility of the story of natural selection in details to make this modularity for example. A major difference between species is in the regulatory networks.

    Repeating the phrase ‘believe it or not’ in a serious course like this gives a bad impression because it seems kind of wobbling, doesn’t it?
    It almost seemed like it was a required thing he must say or else… well, you know…
    The lecture quality would have improved had the professor completely avoided all that digressing talk about origin and focused on the stuff that is known with certainty, which is related only to how it works and what it does.

    PS. I definitely recommend taking this course if you’re interested in the subject. The lectures are very well structured and the video format makes it easier to understand because the autodidact student can repeat any parts, pause to search for terms, etch, which couldn’t be done sitting in the classroom in real time (in vivo). Professor Uri Alon’s book on systems biology is the main textbook suggested for the 2014 course on systems biology by professor Jeff Gore at MIT.

  136. 136
    bill cole says:

    Hi Gpuccio

    There is a new article at TSZ that uses your article as a basis to discuss ID. From the TMZ article:
    You stated biology was going to move from.

    how did this sequence evolve by some non existent neo darwinian mechanism giving reproductive advantage?

    but rather:

    why was this functional information introduced at this stage? what is the plan? what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?

    The author goes on to claim what you are trying to establish:

    Gpuccio references actual biology in his writings and is one of the few at UD that do, and as such I’m prepared to take him at his word that the ID project is now ready to move from simply determining design to answering the questions he posed:

    why was this functional information introduced at this stage?
    what is the plan?
    what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?
    If any ID supporter would like to provide a specific example with answers for those 3 points for discussion that would be perfect.

    Gpuccio’s OP concludes:

    The transition to vertebrates was a highly engineered process. The necessary functional information was added by design.

    In response I simply repeat back the question what is the plan?

    It appears that the author does not understand your original statement and thus is creating a straw-man argument.

    You and I have had enough discussions that I think I understand what you meant by your original statement but I would be interested to how you would respond to the TSZ comment.

  137. 137
    gpuccio says:

    bill:

    Thank you for referencing that.

    I have gone and given a look to the post and to some of the comments. I must confess that I had not been at TSZ for a while.

    The author of the OP goes under the ID of OMagain. I don’t know him, at least not with this name.

    However, I find his post balanced and interesting.

    He asks, more or less, if:

    the ID project is now ready to move from simply determining design to answering the questions he posed:

    Well, I do hope it is. Indeed, I am not really aware of an “ID project”. For me, ID is a scientific paradigm, open to all, a way of interpreting biological reality according to reasonable inferences. I am not sure that there is an “ID project”, probably not even an “ID movement”, or party, or team.

    There are certainly people, of different kinds and with different approaches, who accept ID as a basic paradigm for biology. That’s what I would simply call “the ID field”.

    And there are (very few) people who work in the biological field trying to apply the ID paradigm, like Durston, Axe, Gauger, and others. To them I am very greatful. They are doing a great job, but obviously their resources are very limited.

    As for me, I am certainly available to discuss, at the level which I can afford, in this blof the questions I have made. But I would like to remind OMagain, and others at TSZ, that ID is not at all accepted by the biological academy as something which should be at least considered, and therefore the work to make others aware that “simply determining design” is possible and must be considered is still a great work that remains to be done.

    That said, I am ready to comment briefly on OMagain questions, and on some of the other comments in that thread. But I will do it in the next posts, as soon as I have a moment.

    Of course, if any of the TSZ commenters who seem to have read my OP and be interested enough to comment on it at TSZ are available to comment here (and if they have not been banned! 🙂 I would really welcome them.

  138. 138
    gpuccio says:

    bill (and OMagain at TSZ):

    OK, OMagain essentially asks: what is the plan?

    That comes from my statement:

    “why was this functional information introduced at this stage? what is the plan? what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?”

    So, in a sense, a partial answer is already in my statement.

    The point is, here I am not speaking of a very general plan, like: why were living beings designed at all. It should be clear that I am speaking very empirically.

    My point is: by a functional information analysis. we can recognize the new functional information added at definite times and in definite places. For example, my brief ans very simple analysis shows that lot of functional information has been added in those six proteins involved in neuronal migration.

    Now the ID point of view is: functional information is added to express new functions.

    This is a very important point where ID is different from neo darwinism. I have highlighted that many times.

    For neo darwinism, the only “purpose” in biological beings (if a purpose can be described at all) is reproductive fitness. That’s the only function that has a role in their theory. That’s also the main difference between NS and design, or even between NS and intelligent selection, as I have discussed some time ago here:

    http://www.uncommondescent.com.....selection/

    So, neo darwinism can only reason in terms of chance and/or reproductive advantage.

    That is a very serious limitation.

    The point of view of ID is completely different. In ID, the center of all is function: any function. A designer can implement any function, not just reproductive fitness.

    So, when we recognize an input of functional information, like for example in the proteins of my OP, the natural questino is: why?

    IOWs, what is the function that requires this sudden increase of functional information?

    Neo darwinism can only answer: there must be some way that those new sequences gave a reproductive advantage. Unfortunately, that answer is usually wrong, and therefore remains only wishful thinking. Those “reproductive advantages”, which should evoke NS, remain in the realm of myth, just like the famous intermediates which have all gone extinct.

    But ID does not suffer from that kind of error. ID can recognize functions for what they are.

    So, we know that six proteins implied in neuronal migration in vertebrates exhibit a definite, huge jump in functional information.

    Now, we know two things: those 6000+ bits of functional information must be functional (we infer that from their high conservation for more than 400 million years).

    At the same time, we don’t know what they do. We can reasonably infer that they confer specificity to neuronal migration in vertebrates, but that is almost all we can say at present.

    Of course, I am not saying that I can answer those questions. I am saying that they are very good questions, and that ID is the correct paradigm to make those questions, and that biological research should look for answers starting from an ID approach.

    It’s always much easier to find the right answers, when you have the right questions.

    So, the answer could be: what is so special in the process of neuronal migration in vertebrates? What is the role of those new specific sequences in so many important proteins? How do they work? Do they implement new cell interactions? Do they have any relationship with the vertebrate body plan? With brain development?

    And so on.

    So, OMagain, as you can see, I am absolutely ready to discuss my point of view in as much detail as it is possible. You are cordially invited to join us here, if you can.

  139. 139
    gpuccio says:

    dazz (at TSZ):

    “I really, really want to know what the mechanism is that this unknown designer used to “introduce functional information”

    I want to know that too!

    The hypothesis that I have proposed many times is that, whatever the mechanism may be, it must be similar to the mechanism used by our human consciousness to interact with our brain.

    IOWs, a consciousness – matter interface.

    OMagain proposes “quantum handwaving”. I have suggested many times that a quantum interface is the most likely solution. Eccles and others have proposed a similar solution for the consciousness – brain interface.

    More “downstream”, possible models for the implementation of functional information are:

    – guided variation
    – intelligent selection of random variation

    Moreover, I have proposed many time an important role for transposons. Many empirical data suggest that. So, I am a great fan of transposons as “tools of design”.

  140. 140
    gpuccio says:

    CharlieM (at TSZ):

    I am prepared to give the question, “what is the plan?” a go.

    Thank you! I already like you. 🙂

    It is my belief that the plan comes from a formative “subtle body” which is beyond our physical perception.

    OK, I am looking for adepts for a new “neo-vitalist” project. Are you on? 🙂

    However, I must always remind everybody that ID deals with information in physical objects. But the concept that there may be things in reality which are not yet understood by our present world view (call it physicalism, materialism, or just naturalism, methodological or else) is important: science is a search for what is real, not for what satisfies our present convictions.

  141. 141
    gpuccio says:

    dazz:

    I’ve been reading Gpuccios article and he seems to compute “functional information” in terms of bit-score BLAST comparisons with human proteins: the higher the match to the human protein, the higher “functional information” is. Clearly he’s assuming the plan has been fulfilled and it’s us

    No. You have understood the methodology, but not the reason for it.

    My fault, certainly. I have used this methodology in previous posts, so I have gone into details here.

    The idea is: I use the human form of the proteins because what I am looking for is conservation form the early vertebrates (especially cartilaginous fish) and humans. That gives ne a good foundation to consider the bitscore as a measure of functional information, because, as I have said many times, 400+ million years of conservation of a complex sequence is guarantee of high functional restraint.

    If you look at my previous posts, especially this one:

    http://www.uncommondescent.com.....ted-genes/

    you will see that I have used exactly the same methodology to identify functional information in Hymenoptera.

    So, as you can see, I am in no way partial to a plan aimed at humans.

    I hope that clarifies the point.

  142. 142
    gpuccio says:

    dazz (at TSZ)

    Thank you for going into some biological detail at your post #35 (at TSZ).

    Yes, the 334 bits of homology between the huma protein and the one in lancelets is highly significant. An expect of 2e-81 is of course very significant: the two proteins are certainly homologues.

    But, as you can see, the identities are only 27%. That’s because 27% of identities in a very long protein are a lot of identical AAs.

    That’s why in my analysis I am looking for information jumps in proteins which already have some homologues in pre-vertebrates. If there were no homology, we would have a de novo gene. But I have been describing jumps.

    I hope that is clear.

  143. 143
    gpuccio says:

    Tom English (at TSZ):

    Respond to gpuccio as though he’s actually trying to do science, rather than to create the appearance in a propaganda outlet that “intelligent design” activists do a different kind of science, and you aid and abet the crypto-creationists.

    Than you! I had never been called a “crypto-creationist” before (not that I know, however). I am rather proud.

    And I just needed some propaganda outlet, after those almost reasonable posts from the other side.

  144. 144
    gpuccio says:

    petrushka (at TSZ):

    Greetings. Just happy to see you are still there. 🙂

    I miss you.

  145. 145
    gpuccio says:

    dazz:

    What a fucking waste of time Gpuccio’s article is. The same old retarded tornado-in-a-junkyard crap, spiced with some bogus self-centric “information” theory

    See post #143!

  146. 146
    gpuccio says:

    dazz:

    Are an OP and 47 comments at TSZ about my “article” also a “fucking waste of time”?

    Or are they fulfilling some privileged mission?

  147. 147
    Dionisio says:

    Wow! In the 1970s a Swedish song started with the question “can you hear the drums, Fernando?”

    But now, I would rather ask “can you hear the commotion gpuccio’s OP has caused?

    Now we know why the polite dissenters were absent here. They were busy somewhere else!

    BTW, it’s kind of funny to see this inter-blogging debate.

    Mung can take a break now.
    🙂

  148. 148
    gpuccio says:

    Dionisio:

    Ah! Some fun at last. 🙂

    In the past I had an interesting inter-blogging debate with TSZ which lasted for some time. In the end, it is rather tiresome, but once in while it can be fun.

    But I would advice our friends at TSZ to be cautious. Maybe Tom English has it right, after all: never respond to a crypto-creationist! 🙂

  149. 149
    gpuccio says:

    Acartia (at TSZ):

    “If Gpuccio is not willing to comment here, maybe he would be willing to ask Barry to grant another amnesty”

    I would like very much to have many of you here. However, Barry is obviously free to decide for himself.

    But are you really all banned? Just to know…

    However, if you want, we can go on with the inter-blogging debate, at least for some while. As I have said, I have already done it in the past.

  150. 150
    Dionisio says:

    gpuccio

    Ok, so what’s their ‘bottom line’ answer?

    How did the functionality could get added to the proteins discussed in your OP?

    BTW, how many biology papers have they referenced in their blog the last couple of years?

  151. 151
    gpuccio says:

    Acartia (at TSZ):

    “But I do do commend your attempt and your civil approach to the issue.”

    Thank you! I commend you for your commending. Indeed, it does not happen often. 🙂

    I think that we could all benefit from keeping the discussion on a scientific plane. I like intellectual confrontation, and I also like it to be strong, even aggressive if necessary, but there is no reason not to have respect for one another.

    I agree that discussing “across two threads” can be tiresome. However, if you have any specific question or comment about my position, you are welcome to express it.

  152. 152
    gpuccio says:

    Alan Fox (at TSZ):

    Greetings to you!

    “the hardest nut to crack regarding life on earth is its origin”

    OK, I agree on that. Apart from the impressive impossibilities of getting from an inanimate system to any living system, apart from the problems of metabolism, genetic code, far from equilibrium systems, what came first, and so on, my simple point is that the information jump from any inanimate system to LUCA is beyond any imagination, if it is true that almost half of known protein superfamilies were already present in LUCA, as far as we may infer.

    You may know that I consider protein superfamilies as super-isolated islands of function, beyond any attempt of explanation by the neo darwinian mechanism. Almost 1000 of them appearing in, at most, a few hundred million years is the biggest information jump we can imagine.

    “Then the biochemical evolution of prokaryotes that continued for two billion years prior to the emergence of anything more complex* can only be considered with circumstantial evidence.”

    OK. that’s probably the least problematic aspect, at present. So, let’s avoid it for the moment.

    “Though that the biochemistry is common across all Earth life is the killer argument for me that we all share a common ancestor.”

    I agree. You may know that I believe that we (probably) share a common ancestor, and I have also defended that point of view many times here.

    “Once you have eukaryotes, for which there is a very satisfying explanation in symbiogenesis, it gets much easier. ”

    I have to disagree:

    1) Symbiogenesis has almost certainly a part in eukaryogenesis, but it certainly does not explain it. I think there is a lot of evidence that eukaryogenesis requires an information jump almost as big as OOL.

    2) Even after eukaryotes, nothing is easy. The transition to metazoa is another huge jump: a lot of complex proteins and regulatory systems practically appear, or are drastically remodeled in multicellular organisms.

    And the emergence of the phyla is not “easy” at all, as you probably could acknowledge if you stop a moment to think of it.

    And my OP here was exactly about that: even the emergence of a subphylum, like vertebrates, implies tons of new complex information which is beyond any capabilities of the current neo darwinian theory.

    Of course you will disagree, but I wanted to make clear my position.

    “Evolve sex, multicellularity, cell specialisation… you’re home free.”

    Free??? The nervous system, all epigenetic mechanisms, the whole transcription factors network, hundreds of different cell types, the immune system, and so on, and so on…

    Free??? If that is your idea of free… 🙂

  153. 153
    gpuccio says:

    Zachriel (at TSZ):

    Hi! Glad to see you again.

    Well, “handwaving” is how OMagain sees it. But I have never denied that I believe in a quantum interface between consciousness and matter. That’s my strong view, and I absolutely stick to it.

    And I am not alone. Eccles. Beck. Penrose (in a different way). And others.

    Is that just handwaving?

    Is it so difficult to accept that others may have different views from yours, in highly controversial topics like the nature of consciousness, without feeling obliged to deride them?

  154. 154
    CharlieM says:

    Hi gpuccio @140

    I’m very short of time at the moment and I wouldn’t describe myself as an adept. But I would be interested in your project. I’ll be posting further when I get more time.

    regards
    Charlie

  155. 155
    gpuccio says:

    CharlieM:

    You are welcome. I will wait for you.

  156. 156
    gpuccio says:

    dazz (at TSZ):

    “I wonder if he also accepts that mutations happen, and that mutations alter the DNA sequence and in turn, protein sequence too. Because comparing protein sequences and rejecting the roll of mutation seems self-refuting. Maybe his “quantum interface” is responsible for those mutations instead of being truly random?”

    dazz, of course I accept that mutations happen. And that they alter the DNA sequence and protein sequence. Do you think I am a fool?

    Moreover, I am convinced that many mutations are completely random. I also believe that those random mutations are most times neutral or quasi neutral, and that they are subject to random drift, so that they can be fixed.

    I don’t believe that random beneficial mutations have any important role in the generation of complex functional information. I think that their role is strictly limited to small “microevolutonary” events.

    I think that the variation which generates complex functional information is guided, and not random. And it acts through guided common descent.

    I hope this clarifies some of my views.

  157. 157
    gpuccio says:

    I am busy now, I will go on answering what should be answered in TSZ’s comments in a while.

  158. 158
    gpuccio says:

    dazz (at TSZ):

    “Can someone please ask gpuccio if he can share the FASTA files he used?”

    Here are the accession numbers (from UNIPROT) of the 6 human proteins I blasted:

    Astrotactin 1 O14525
    Astrotactin 2 O75129
    BRNP1 O60477
    CADH2 P19022
    Integrin alpha-V P06756
    NCAM1 P13591

    If you look at them on uniprot, you can easily download the sequence as a FASTA file.

    You can blast each of those proteins in BLAST, just using the accession number. To get the best non vertebrate homology, I blasted vs Metazoa, excluding Vertebrates.

    Do you need other details?

  159. 159
    gpuccio says:

    Joe Felsenstein (at TSZ):

    “Surely someone needs to mention that LUCA is the oldest species that had two or more living descendant species. It is not the organism at the origin of life, which could be much earlier”

    GlenDavidson (at TSZ):

    “LUCA, not FUCA.”

    Well, LUCA is the oldest species for which we can reasonably infer anything. For what we know, it could have been the first living thing on earth. IOWs, as far as we know from observed facts, LUCA could well be FUCA.

    As far as we don’t find any new facts, I start reasoning with LUCA. Anything else is not supported by facts. I am well available to discuss any FUCA which existed before LUCA, provided that someone shows me some evidence that such an organism ever existed, and that we have objective data which show what it was.

  160. 160
    gpuccio says:

    Alan Fox (at TSZ):

    You raise many different arguments, many of which I have already discussed many times, even with you, I think.

    I cannot restate everything here in brief, of course.

    For the moment, this will suffice:

    Well, all that goes out of the window, if you consider RNA world a plausible precursor to DNA and proteins. I used to be skeptical of RNA world, mainly due to the influence of the late Professor Robert Shapiro but I’ve come around due to persuasive arguments by fellow members here (notably Allan Miller) and also as it answers Upright Bipeds “semiotic” argument, RNA being able to double up on both information storage and catalytic function.

    Well, I had not your fortune, and I am still extremely skeptical of RNA world. Will you accept me at TSZ? 🙂

    Moreover, I don’t agree that “it answers Upright Bipeds “semiotic” argument”. Not at all. Luckily, I have discussed this point recently on another thread, so I will just paste here a few reflections.

    This is the thread:

    http://www.uncommondescent.com...../#comments

    Post #3:

    Me to Matspirit:

    And, always just to know, how would a “direct copy organism”, whatever it may be, “evolve” a whole representation and translation system, with highly symbolic connections between nucleotides and aminoacids, implemented by some 20 highly complex proteins plus some “small” machinery like the ribosome and a lot of other assets?

    IOWs, I suppose that the “direct copy” system was copying RNA to RNA (am I correct, or you mean something else?). So, in the mythical RNA world, the sequence of nucleotides was important for the information about the final RNA effectors (rybozimes, and so on). IOWs, the information was about RNA as a biological effector, and had nothing to do with proteins, aminoacids, and so on.

    So, what happens? One day the DCO (direct copy organism) decides that it is rather old fashioned to store information for the reason it is used (RNA structures which have something to do), and it would be exciting to store completely new symbolic information for some unclear future purpose, having to do with some new molecules (proteins)?

    And what about proteins? Were they present in the DCO? Did they copy themselves? How? Or did they appear suddenly?

    It is fascinating how people who seem otherwise normally intelligent can accept this kind of conjectures as though they were reasonable scientific theories. Maybe my imagination has severe limitations…”

    Post #16:

    Me to MatSpirit:

    Thank you for trying. No name calling, obviously, but I really want to comment on what you say.

    “I was referring to a ten molecule polymer I mentioned in message 128”

    OK, but a ten molecule polymer is not an organism.

    So, my point remains: Direct copy organisms? Examples, please?

    “This would be direct reproduction where the molecule copies itself directly without any DNA or other representations, signs or symbols.”

    I have no problems with simple molecules directly copying themselves in the right context (usually designed ad hoc). That still has nothing to do with living organisms.

    “You can see where this idea upsets the semiotics people, but it seems to be what most of the OOL researchers seem to think happened. It goes under names like “RNA world” or “chemical evolution”.”

    I am certainly part of the semiotic people, but strangely I don’t feel upset at all. And I am well aware that “most of the OOL researchers” believe that kind of things. Look, there is just one argument that you should not use with me: the argument of conformistic thought. I always say that I am a minority guy. I am proud of that. You see, I don’t care how many authoritative people believe one thing: for me, the only importnat thing is if I can be convinced that it is true.

    I am very firmly convinced that a very strong cognitive bias is operating in biological ideology. I understand its origins, which are maybe partly justified (the need to free science from old dogmatisms mainly connected to religion). I can understand that, but the only result of dogmatic anti-dogmatism is a new form of dogmatism. So, I beg your pardon, but the simple fact that many believe something is not, for me, a reason to believe. I like to choose the things I believe in.

    That said, let’s go to the other points.

    “I don’t think the original DCO was “about” anything. It didn’t make proteins or anything else, just copies of itself. I think it was probably a polymer because just about everything alive today is made from them and because the polymer structure is perfect for evolution.”

    Again, a replicating molecule, even if it were really spontaneously possible, is not an organism: life is made first of all of metabolism, separation of environments, far from equilibrium states, and many other things.

    However, let’s say that your “organism” is an RNA organisms. So, we are entering the myth of RNA world. OK, let’s go on.

    “As for how such Direct Copy Organism (thanks for that name, I’ll keep using it)”

    No problem, I like it too!

    “would evolve the complex system we see today, I would guess that DNA backup for fragile RNA came first.”

    I have no problems with that. RNA and DNA are similar molecules, and complementary ones. OK, the scenario has many difficulties, but I don’t want to emphasize them here. Let’s go on.

    “Three of the four codon in DNA are identical to the ones in RNA and the fourth is a close chemical cousin. The backbones of both molecules are also chemical cousins.”

    OK. The origin of nucleotides is not exactly a solved problem, but let’s go on, again.

    “As far as proteins go, amino acids form spontaneously, botherwise on eart and in space. (Miller-Urey found five of them in their famous experiment. Modern researchers have examined vials saved from their experiment with modern instruments and brought the total up to 21.) Proteinoids (short proteins of up to 5 amino acids) form spontaneously. So I would guess that proteins of some kind were present.”

    OK. Having a few aminoacids and maybe some proteinoid is not really the problem.

    Now, let’s understand where the real, big problem is:

    1) Proteins do not copy themselves directly. They can only be reproduced by the information in DNA genes, which uses the symbolic translation system. OK with that?

    2) So, even if we have a proteinoid, and even if it does something useful (very doubtful, but OK, this is the game), my simple question is: how is the information for that simple proteinoid conserved and passed from DCO to DCO? Or are new instances of the same proteinoid created each time by sheer luck? Excuse me, but I don’t understand. And how can the information in the original proteinoid “evolve”, if the information is not copied and translated from some physical storage system?

    3) And the most important point: how is it that some sequence of nucleotides at some point starts representing a sequence of aminoacids, according to some symbolic code? Remember, the sequence of nucleotides in our RNA DCO has only one function: to preserve and pass on the information for RNA enzymes.

    Now, the biochemical rules which govern RNA molecules are completely different from the biochemical rules which govern proteins. And, above all, there is no spontaneous symbolic connection between the two sets of rules.

    So, please, answer this very important point: why should a functional sequence which has a very definite function according to some set of rules, and is conserved and propagated exactly for that reason, become a sequence which has no more relationships with its initial function, but strangely starts to represent another completely different set of rules, according to a purely symbolic code, which can only work if a complex translation apparatus, including 20 aaRNA synthases, the ribosome, and many other components, is already working? This is really beyond my frail imagination.

    “Look at it this way. Life as we see it today, in all its towering complexity, is so well understood that it has become intellectually irresponsible to deny that that it’s material. There is no elan vital. That idea is dead.”

    To say that life is so well understood is really the statement of the millennium! Are you really convinced of what you are saying? I am afraid that there is no hope.

    However, while I would be happy to defend a little the “elan vital” here, I will simply emphasize that nothing in ID theory is denying that the biological information necessary for life is material, or at least implemented in material forms: our only point is that it is designed. A watch, a computer, are material objects, but the information which makes them what they are is designed. So, this is a false argument. We will discuss “elan vital” another time, for the moment let’s just discuss the origin of biological information, as we have always done.

    “So if the extravagantly complex life we see today is material and is known to have come from material causes (other life), why not believe those material causes extend all the way back until life was so simple that non living material causes could produce it?”

    Because it is simply wrong: complex functional information, even if materially implemented, has its origin in conscious intelligent representations. Always. That’s exactly the point of ID theory. Non conscious systems simply cannot generate that kind of physical organization, never have, never will.

    “It is a fact that a lot of very intelligent people who are also very well educated and who have studied the OOL field for decades DO think that conjectures like these are reasonable.”

    The conformistic thought argument again? They may think whatever they like. I don’t.

    “I think that if you understood the field better, you might think they were reasonable too.”

    Here I strongly disagree with you. I think that I understand the field well enough to have very strong and motivated convictions. Maybe I understand it better than you do, but just for fairness, let’s say that we understand the field equally well, and still we have opposite ideas. There is nothing strange in that. It’s called freedom of scientifc thought, and IMO it is the main cognitive manifestation of free will. But that’s another story.

    “I am confident that when you do disagree you will give cogent reason for your disagreement, as above, and not childish name calling and I thank you for it.”

    I have tried to satisfy your expectations. 🙂

    Now, this other point. You say:

    But this argument is only convincing if functional proteins are rare in sequence space. Evolutionary search only needs to stumble on a solution, not the solution. There is plenty of new research since Keefe and Szostak showed ATP binding is common in a random sequence library.

    I would say that Keefe and Szostak was a very bad starting point. I have criticized that paper, and the conclusions which are usually derived from it, many times. can do it again any time you like.

    However, you refer to “plenty of new research”. References, please, so that we can discuss.

    I am absolutely convinced that functional proteins are rare in sequence space. But there are many ways to define functional proteins.

    I must remind you that, in the context of your theory (neo darwinism) only one definition counts: proteins which can confer a reproductive advantage, and therefore can be visible to NS.

    You say: “Evolutionary search only needs to stumble on a solution, not the solution.” OK. but the solution must be a naturally selectable solution. No other function counts.

    I am not aware of any naturally selectable result in Keefe and Szostak’s paper, for example, in spite of all the Intelligent Selection they performed.

    You could be interested, perhaps, in this OP of mine about the differences between NS and artificial selection, a topic which is usually strangely ignored by neo darwinists:

    http://www.uncommondescent.com.....selection/

  161. 161
    gpuccio says:

    dazz:

    “I’m missing:

    Non chordate metazoa
    Echinoderms
    Tunicates
    Cartilaginous fish

    The ASTN1 ones would do”

    Here they are(the accessions are from NCBI, because I derive them from the blast results):

    Best nonchordate (non echinoderm): Lingula anatina XP_002123195 58.9 bits

    Echinoderms: Strongylocentrus purpuratus XP_790940.3 36.6 bits

    Tunicates: Ciona intestinalis XP_002123195 43.5 bits

    Cartilaginous fish: Callorhincus milii XP_007893873.1 1328 bits

  162. 162
    gpuccio says:

    John Harshman:

    And that big jump he makes a big deal out of is just the big slice of time separating the human-shark common ancestor from the human-cephalochordate common ancestor.

    What do you mean? Have you read my OP?

    I quote from it:

    For the following analysis, I will consider vertebrates versus everything which preceded them (all metazoa, including “pre-chordates” (Hemichordates and Echinoderms) and “early chordates” (Tunicata and Cephalochordata). So, everything which is new in vertebrates had to appear in the window between early chordates and the first vertebrates: cartilaginous fish and bony fish (I will not refer to lampreys, because the data are rather scarce). So, let’s try to define the temporal window, for what it is possible:

    Chordates are already present at the Cambrian explosion, 540 my ago.
    Jawless fish appeared slightly later (about 530 my ago), but they are mostly extinct.
    The split of jawless fish into cartilaginous fish and bony fish can be traced about at 450 my ago
    Therefore, with all the caution that is required, we can say that the information which can be found in both cartilaginous fish and bony fish, but not in non vertebrates (including early chordates), must have been generated in a window of less that 100 my, say between 540 my ago and 450 my ago. Now, my point is very simple: we can safely state that in that window of less than 100 million years a lot of new complex functional information was generated. Really a lot.

    So, again, what do you mean? I have explicitly stated in my OP what you say in your comment. What is the problem with you?

  163. 163
    gpuccio says:

    dazz:

    This doesn’t make any sense to me because the match for ASTN2 for example, between humans and sharks is 73%. That doesn’t look so conserved to me. It’s also hard to reconcile the idea that a single fold can diverge more than 25% and still perform the same basic function if “islands of function” was true. And that’s just one pair comparison

    You must be kidding. Or, simply, you are not familiar with protein homologies.

    Believe me, 73% conservation between shark and human is an extremely high conservation. It’s almost 900 identical aminoacids, a bitscore near to 2000 bits, and an expect of 0.0!

    You seem to forget the role of neutral variation. In 400 million years, neutral variation will practically erase any homology in any non functional sequence or position in a sequence. You can see that clearly when you evaluate the Ks values, the rate of mutation for synonimous sites, which are a good measure of neutral variation. At that chronological distance, Ks values tend to reach saturation, that is the point where you cannot any more detect any homology.

    So, this is an extreme conservation, and an extreme functional restraint. If you don’t understand well these issues, just document yourself.

    You also add:

    “In fact, even if it was an entirely different function in my book that would also falsify the “islands of function” hypothesis”

    This is nonsense. Again, you don’t know what you are saying. “more than 25%” is the minimum variation you can expect in 400 million years because of neutral variation, if the function remains exactly the same. That’s why I call them “islands of function”, and not “points of function”.

    We have debated these issues in great detail here. The same does not seem to be true of TSZ.

    Look, myoglobin, which is a much shorter molecule (154 AAs) whose function is well known and rather stable, presents only 62 identities (42%, for a total of 123 bits and an expect of 9e-37) in the comparison between shark and humans.

    Some proteins are more flexible to neutral variation, others much less. That’s exactly what functional information measures: the degree of functional restraint.

    AST2 shows a very high degree of functional restraint in a very long protein: that’s why its functional information is so high.

  164. 164
    Origenes says:

    GPuccio, thank you for your comments on TSZ. It must be a vexing task to make any sense of the meaningless drivel espoused by OMagain and her/his companions. I could not have done it.

  165. 165
    gpuccio says:

    John Harshman:

    It doesn’t make sense to me for quite different reasons. I would consider 73% after 300 million years to be quite conserved.

    Good. At least you seem to understand that basic fact.

    But why should “conservation” refer to matching humans? Why not sharks? Why not fruit flies?

    Have you read my post #141 here, in response to dazz?

    If not, I paste it here for your convenience:

    dazz:

    “I’ve been reading Gpuccios article and he seems to compute “functional information” in terms of bit-score BLAST comparisons with human proteins: the higher the match to the human protein, the higher “functional information” is. Clearly he’s assuming the plan has been fulfilled and it’s us”

    No. You have understood the methodology, but not the reason for it.

    My fault, certainly. I have used this methodology in previous posts, so I have gone into details here.

    The idea is: I use the human form of the proteins because what I am looking for is conservation form the early vertebrates (especially cartilaginous fish) and humans. That gives ne a good foundation to consider the bitscore as a measure of functional information, because, as I have said many times, 400+ million years of conservation of a complex sequence is guarantee of high functional restraint.

    If you look at my previous posts, especially this one:

    http://www.uncommondescent.com…..ted-genes/

    you will see that I have used exactly the same methodology to identify functional information in Hymenoptera.

    So, as you can see, I am in no way partial to a plan aimed at humans.

    I hope that clarifies the point.

    My point was to look at jumps in vertebrates vs non vertebrates. So I use the shark human comparison because, as you certainly understand, that allows me to define a rather precise window pre (something less than 100 million years) and post (400+million years). That’s clearly said in the OP, and further clarified in the comments in the thread.

    You add:

    And what does that have to do with information?

    It has all to do with information. You guys seem really to be unfamiliar with ID.

    The functional information is the information linked to the specific defined function. It is computed as the ratio between the target space (the number of sequences that exhibit the function) and the search space (the total number of possible sequences). So, the target space is the “island” of function, however big it is.

    Measuring the target space directly is very difficult for proteins (and, in general, with complex objects, including language). So. we must proceed with indirect approximations.

    The best way available, as far as I can say, is to measure the conservation across a long period of evolutionary time.

    So, that’s, in a nutshell, what conservation has to do with information.

  166. 166
    gpuccio says:

    Origenes:

    Yes, it’s a little exacting. However, I am grateful to them because they give me a chance to clarify better my points.

    I try to choose those comments which are good for that purpose, and to ignore the rest. 🙂

  167. 167
    gpuccio says:

    Adapa:

    “ID offers no mechanisms, no timeline, not the slightest bit of detail on anything” (emphasis mine)

    I think that we have been debating exactly timelines here. In a thread at UD about an OP at UD based completely on ID theory.

    What’s the problem with you?

  168. 168
    gpuccio says:

    John Harshman:

    “And why is similarity to humans an index of increased information content?”

    No. Its’s not that similarity to humans is an index of increased information content. You are definitely misunderstanding my reasoning.

    There is nothing special in humans.

    Here I have considered sequences which, for a great part, appear in cartilaginous fish and bony fish (so, before the split), and are conserved up to humans. IOWs, sequences which are specific to vertebrates and conserved in the whole subphylum.

    That’s the only role of human proteins in my reasoning.

    As the human line is derived from bony fish, I have used cartilaginous fish for the evaluation of the “jump”, because that guarantees 400+ million years of conservation, which is exactly what I need to infer high functional restraint.

    If you look at my thread about Hymenoptera, you will see that I have inferred functional conservation for the specific sequence of protein Prickle 1 in Hymenoptera comparing wasps, bees and ants, without making any use of human proteins in the reasoning.

    Here is the thread:

    http://www.uncommondescent.com.....ted-genes/

  169. 169
    gpuccio says:

    Dionisio:

    Thank you for linking those papers about the RNA world,a point that has been raised in this discussion.

    I think that this question from one of the papers:

    “5) How can the way information is stored and metabolic complexity coevolve to pave to road leading out of the RNA world to the present protein-DNA world?”

    well expresses the main point I have made here.

    IOWs, let’s assume for a moment that an RNA world existed (I don’t believe it at all, and it remains pure conjecture). The big, big problem is: why should a system based on RNA, and not proteins, and on direct copying of an information which is about RNA enzymes, evolve at all to a system based on symbolic information for protein sequences?

  170. 170
    Dionisio says:

    gpuccio:

    You ask:

    […]
    why should a system based on RNA, and not proteins, and on direct copying of an information which is about RNA enzymes, evolve at all to a system based on symbolic information for protein sequences?

    Your politely-dissenting interlocutors at the opposite blog may know the answer to that important question.
    However, maybe they don’t want to share that information with you? 🙂
    What your interlocutors have written so far seems to lack substance. It definitely reminds me of Mina’s song “parole, parole, parole”. 🙂

  171. 171
    bill cole says:

    Gpuccio

    IOWs, let’s assume for a moment that an RNA world existed (I don’t believe it at all, and it remains pure conjecture). The big, big problem is: why should a system based on RNA, and not proteins, and on direct copying of an information which is about RNA enzymes, evolve at all to a system based on symbolic information for protein sequences?

    Exacto

  172. 172
    Dionisio says:

    gpuccio @162

    So, again, what do you mean? I have explicitly stated in my OP what you say in your comment. What is the problem with you?

    Maybe they simply don’t want to understand your explanations?
    Maybe some people think that understanding someone else’s point of view is the same as agreeing with it?
    Or maybe they think they’ve understood your point, but really they haven’t?

  173. 173
    Dionisio says:

    gpuccio @163

    You must be kidding. Or, simply, you are not familiar with protein homologies.

    What is it that makes me think that in this case it’s the latter?

    🙂

  174. 174
    Dionisio says:

    gpuccio @163

    We have debated these issues in great detail here. The same does not seem to be true of TSZ.

    Have your ‘politely-dissenting’ interlocutors ever seriously discussed any important biology-related issue in great detail in their blog?

    At UD there are over 2,500 biology-related research papers referenced in the last couple of years. How many have they referenced at TSZ?

  175. 175
    Dionisio says:

    Origenes @164

    It must be a vexing task to make any sense of the meaningless drivel espoused by OMagain and her/his companions. I could not have done it.

    I would not have even tried.

    🙂

  176. 176
    Dionisio says:

    gpuccio

    FYI – here’s an invitation to a known scientist to comment on your OP and follow-up thread:

    http://www.uncommondescent.com.....ent-613945

  177. 177
    gpuccio says:

    Alan Miller (at TSZ):

    “Because there are mechanisms by which novel genes can arise, or appear to arise, and there are reasons why homology can be difficult to detect.”

    I respectfully disagree with this point. I don’t think we have a clue how novel genes arrive.

    I obviously agree with you, and I commend you for your intellectual honesty. 🙂

  178. 178
    gpuccio says:

    John Harshman (at TSZ):

    dazz: “Seems to me that in order to provide some meaningful metric of conservation in vertebrates that might help measure functional constrain in vertebrates for those proteins, one would need to align the proteins for ALL current vertebrates and determine what’s conserved across the board. Does that make any sense?”

    I think that at the very least you would have to ignore pseudogenes. I presume the question would be how much a protein could vary and still retain the same function. Proteins that have lost all function (really, genes that don’t produce proteins any more) should not count, nor should proteins that have significantly altered function. And now you have to ask what “significantly” means. Even proteins like cytochrome c, which does the same thing in all eukaryotes, must adapt to their cellular environments: operating temperatures, pH, changes in associated proteins, etc. It’s not a simple question.

    I absolutely agree with you!

    My reasoning in the OP makes the following very reasonable assumptions:

    1) If we find 1000+ bits of homology between shark and humans, we can really infer that that sequence was more or less present in a common ancestor. I think you understand why better than others. 1000+ bits of homology have practically zero probability of being a random observation. There is no way to explain them other than by conservation through evolutionary history. Alicia Cartelli, in the past, tried “convergent evolution”, but after my rather fierce answer she seems to have renounced to that theory. I think you can understand that if we start explaining homologies in proteins by convergent evolution when it is convenient, the whole castle of evolutionary theory becomes senseless.

    2) What can we say of other species in the same class of organisms that have lower homologies?

    For example, blasting ASTN2 vs bony fish, we get a wide range of hits, ranging from 1215 to 2009 (and there can be certainly other minor hits which are not shown in the main blast results).

    Now, as you say, it’s not a simple question. As you say, pseudogenes should not be considered, and the lowest hits, if present, are probably trivial.

    Other hits are with ASTN1. The hits with molecules labeled as ASTN1 show a rather consistent range, 1215 – 1271. Which is consistent with the partial homology between the two molecules in all species.

    However, even hits with ASTN2 molecules vary, from 1294 to 2009. That could be explained as some loss of information in some species, which is possible, or simply as special adaptations. As you say, “Even proteins like cytochrome c, which does the same thing in all eukaryotes, must adapt to their cellular environments”.

    Whatever the cause, it has no relevance for the basic fact that the sequence with maximum homology in sharks must have been passed from the precursor of cartilaginous and bony fish to humans. And of course, as there is no reason to think that it was not subject to neutral variation in those 400+ million years, it was certainly conserved by negative selection.

    3) What can we say of the variation which occurs after? Of course, there are further increases in the homology to humans in snakes, birds, and mammals. I have not interpreted them in my OP because, as you say, it’s not a simple problem. I think that much of those further increases is functional, and is due to new, or simply different, functional requirements in the new classes of organisms. I have just given the values in mouse, and in humans to give the bitscore of identity, as general information.

    But all my reasoning is about the information jump between pre-vertebrates and the first vertebrates.

  179. 179
    gpuccio says:

    dazz (at TSZ):

    “Question for the experts. Is there any know case in which a relatively or even highly conserved protein(s) at some point in some lineage have undergone a faster evolution? IOW, some protein has stopped being subject to significant selective pressure?”

    Your question is not very clear: are you interested to “faster evolution” in the sense of faster degradation (loss of homology because of neutral varition), or rather in the sense of faster change because of beneficial mutations and positive selection?

    Rumraket seems to interpret your question in the first sense, while Dave Carlson answers the second meaning.

    Both their answers are perfectly good. Not so your considerations.

    To Rumraket, you comment:

    Thanks, makes complete sense.

    Seems to me that in order to provide some meaningful metric of conservation in vertebrates that might help measure functional constrain in vertebrates for those proteins, one would need to align the proteins for ALL current vertebrates and determine what’s conserved across the board. Does that make any sense?

    I still wouldn’t call that a measure of “functional information”

    Wrong. See my answer to John Harshman at #178. And I wonser if you have really understood Rumraket’s point. I paste it here for you convenience:

    “Not that I’m an expert, but off the top of my head, genes involved in eye development in blind cave fish.

    Another thing could be genes involved in tooth formation in toothless birds.

    In general, most pseudogenes would more or less qualify. ”

    Just to make it more clear, he is giving examples of genes which are rapidly degraded because there is no more any need for their function in that species, or simply because they are no more functional at all (pseudogenes).

    That is simply a confirmation of how powerful random variation is when there are no functional constraints, and absolutely supports my point that conservation through long periods of time is a very good measure of functional information.

    Is it clear?

    Now, as soon as I find time, I will comments Dave Carlson’s very interesting post about positive selection, which opens new important questions, and then I will go back to your comments about that.

  180. 180
    PeterJ says:

    Fox News has has an article which supposedly reveals what scientists have discovered regarding the origin of life.

    Perhaps it has already been viewed here, but if not, it’s worth looking at.

    http://www.foxnews.com/science.....began.html

  181. 181
    Dionisio says:

    PeterJ @180

    Thank you for indirectly, through a pop-sci article, referring to this paper:

    Weiss, M. C., F. L. Sousa, N. Mrnjavac, S. Neukirchen, M. Roettger, S. Nelson-Sathi and W. F. Martin, 2016, The physiology and habitat of the last universal common ancestor. Nature Microbiology. vol. 1, Article number: 16116 (2016) doi:10.1038/nmicrobiol.2016.116
    http://www.nature.com/articles/nmicrobiol2016116

    Did you read this paper completely?
    Did you understand it?

  182. 182
    Dionisio says:

    PeterJ @180

    Here’s a link to an ePDF copy of the paper you referenced:

    http://www.nature.com/articles.....oxnews.com

  183. 183
    Dionisio says:

    PeterJ @180

    [follow-up to comments @181-182]

    Here’s a summary of the paper contents:

    Page 1:
    – Tracing proteins to LUCA by removing transdomain LGTs.
    – LUCA’s microbial ecology reconstructed from genomes.

    Page 2:
    – Figure 1: Phylogeny for LUCA’s genes
    – LUCA’s genes point to acetogenic and methanogenic roots
    – Hydrothermal vents, methyl groups, and nucleoside modifications

    Page 3:

    and so on…

    Can you open it?

  184. 184
    Dionisio says:

    PeterJ @180

    [follow-up to comments @181-183]

    Here’s a summary of the paper contents:

    Page 1:
    – Tracing proteins to LUCA by removing transdomain LGTs.
    – LUCA’s microbial ecology reconstructed from genomes.

    Page 2:
    – Figure 1: Phylogeny for LUCA’s genes
    – LUCA’s genes point to acetogenic and methanogenic roots
    – Hydrothermal vents, methyl groups, and nucleoside modifications

    Page 3:
    – Figure 2: Taxonomic distribution of LUCA’s genes grouped by functional categories

    Page 4:
    – Figure 3: LUCA reconstructed from genome data
    – Spelling out caveats and allowing for some LGT

    Page 5:
    – Figure 4: Methyl groups in conserved modified nucleosides and in anaerobic autotroph metabolism

    Page 6:
    – Discussion
    – Methods

    Page 7:
    – References

    Page 8:
    – References (continuation from page 7)

  185. 185
    gpuccio says:

    Dionisio and others:

    I have no time now, but I have just noticed this new thread:

    http://www.uncommondescent.com.....rinciples/

    and the very interesting paper linked.

    Just two brief comments:

    1) Please, look at Figure 1 in the paper, and just tell if that reminds you of anything (isolated islands of function?) 🙂

    2) Beautiful quote from Einstein in the paper: “One can best feel in dealing with living things how primitive physics still is.” And a question: is invoking “new laws of physics, hitherto unknown . . . ” (Schroedinger) still “methodological naturalism? Materialism? Physicalism? Or what else?

    Well, I would say: it really depends on what those “new laws” look like! 🙂

    And if the “hard problem of life” were strictly connected to the “hard problem of consciousness”?

    And if the “new laws of physics” were strictly connected to consciousness and design?

  186. 186
    kairosfocus says:

    GP, IIRC, I got that from you first. KF

  187. 187
    Dionisio says:

    gpuccio @185

    1) Please, look at Figure 1 in the paper, and just tell if that reminds you of anything (isolated islands of function?) 🙂

    Esattamente! They just call them ‘disconnected regions’ but your term ‘IIOF’ seems more accurate.

    [Top of Page 5]

    Figure1:
    Reversible causal graphs demonstrate that ‘you can’t always get there from here’ as the state space is composed of many disconnected regions

  188. 188
    gpuccio says:

    dazz (at TSZ):

    I understand that conservation strongly suggests negative selective pressure and therefore, functional constraint. I also understand that neutral evolution is an indication of lack of function. What I don’t think is meaningful is your metric for “functional information”:

    Is seems odd to me to quantify “functional information” by comparing proteins that retain the same function. For all I know most of the “information” that makes a shark different to a bony fish, or a mouse, is in gene regulation anyway.

    Again, you seem not to understand. In my OP I am comparing proteins in shark (and bony fish) to all pre-vertebrates. That’s where the jump takes place.

    IOWs, those 6000+ bits of information which appear in sharks are nowhere to be seen before.

    So, the reasoning has two steps:

    1) There is a sudden jump in the first vertebrates

    2) Those 6000+ bits are conserved up to humans

    The two thin gs together make my argument. My argument is about information which appears rather suddenly and which must be functional because, after it appears, it is conserved.

    Is that so difficult to understand?

    Of course those six proteins in vertebrates must have some function different from the function of their weak homologues in pre-vertebrates. And that function must be specific for vertebrates, all vertebrates.

    A reasonable hypothesis is that neuronal migration in vertebrates is regulated differently in vertebrates, and that the new functional information in those six proteins, which are implied in neuronal migration, is related to the vertebrate body plan.

    So, why do you speak of “proteins that retain the same function”? My point is that the jump is due to a different function, and that the conservation after the jump is due to the maintenance of the new function.

    Is it clear?

  189. 189
    gpuccio says:

    Alicia Cartelli (at TSZ):

    “Hi Pucci! I’ve missed you as well!
    Unfortunately I can’t comment on your post because (I’m assuming) you had me blocked. I assume this because you were the only person I was really talking to last time I was at UD. I even tried to make a new account while you were gone for a bit, but it appears you guys know my IP.”

    Alicia, glad to find you in your usual form!

    You can believe me or not, but I never “had you” (or anyone else) “blocked.

    Alan Fox:

    “I suspect Barry Arrington keeps a tight hold on the reins of power. It is simple to block IPs from the admin dashboard. I doubt gpuccio had a hand in it.”

    Well, it seems that Alan Fox believes me. 🙂

    Alicia Cartelli:

    “I guess, but my silent ban coinciding with gpucci’s immediate absence after talking to him for a while was a bit too much of a coincidence for me.
    Oh well.”

    And you apparently don’t. Not too much, at least. OK, I can live with that, I suppose.

    However, as a convinced neo darwinist, you should have more faith in coincidences. 🙂

  190. 190
    Dionisio says:

    PeterJ @180

    [follow-up to comments @181-184]

    Page 6.

    Discussion
    [second paragraph]

    Although the paucity in LUCA of genes for aminoacid and nucleoside biosynthesis could, in principle, be attributable to post-LUCA LGT, we note that there is no viable alternative to the view that LUCA, regardless of how envisaged, ultimately arose from components that were synthesized abiotically via spontaneous, exergonic syntheses somewhere during the history of early Earth.

    [beginning of right column]

    Prior to the origin of genes, proteins and the code, LUCA’s origin was hence dependent on spontaneous organic syntheses, which are thermodynamically favourable under the high H2 activities of submarine hydrothermal vents, and which still occur today in some geochemical environments.

    Where’s the beef?

    Can they reproduce all that in a lab?

    Where is the detailed description of the spatiotemporal mechanisms that produce all that?

  191. 191
    Dionisio says:

    gpuccio @188

    Hard to tell why that “politely dissenting” interlocutor does not seem to understand your clear explanations.

    Could it be that their motives are…? Oh, no, let’s not talk about that now. 🙂

  192. 192
    Dionisio says:

    gpuccio @189

    However, as a convinced neo darwinist, you should have more faith in coincidences. 🙂

    Yes, good point. How else can they support all the nonsense they write?
    🙂

  193. 193
    gpuccio says:

    Now, let’s go to serious things.

    Dave Carlson, at TSZ, gives this very interesting answer to dazz:

    dazz:
    Question for the experts. Is there any know case in which a relatively or even highly conserved protein(s) at some point in some lineage have undergone a faster evolution? IOW, some protein has stopped being subject to significant selective pressure?

    Yes, there are many such examples. In fact, one popular method for identifying sequences under positive selection is to look for lineages in a phylogeny that have undergone relatively rapid amino acid substitution in comparison with lineages in which the sequence is more highly conserved is (more specifically, looking for elevated rates of non-synonymous substitutions compared to synonymous substitutions).

    Here is an example of such a case from my own research (as yet unpublished, though I’m working on it!). This is small snippet of an alignment of tropomyosin sequences found in six spider species from 3 genera (two species per genera). There are very few amino acid substitutions in any of the species over most of the length of the sequence, but here toward the middle there is a relatively high concentration of non-synonymous substitutions in two of the species from the same genera. This is a pretty strong signal of positive selection acting in the ancestor of these two species.

    There many more published examples of this kind of analysis.

    He also gives the alignment.

    Of course, dazz is ready to equivocate:

    “So in this case, a loss of conservation led to speciation, or played a roll in it. I guess that would imply a loss of functional restraint and therefore, a loss of information according to gpuccio?”

    It’s strange how some self-proclaimed darwinists understand so little of their own theory.

    So, let’s discuss a little this misunderstood point: positive selection.

    Now, positive selection is a strange paradox: it should be the strong mechanism in all neo darwinian explanation, the core of the theory. It is, indeed, the basic foundation of the neo darwinian theory; that RV which generates a reproductive advantage is positively selected, expanded and fixed.

    But the paradox is that positive selection is really, really rare.

    Let’s understand better. There is a kind of positive selection that we can observe directly. It is well documented, and is found in those well known cases of “microevolution”; simple antibiotic resistance, S hemoglobin in malaria zones, the rugged landscape experiment with phages, and so on.

    Well, they are not so many, after all. But they exist, they are well documented, and they are well understood.

    What do they have in common? They are all about small transition, a few bits, one, two aminoacids, maybe sometimes three or four.

    In no case those transitions, while giving some reproductive advantage in the appropriate environment, are steps to some more complex transition. They remain, absolutely, micro-transitions.

    But there is also an indirect way to “detect” positive selection. The idea is, is some sequences change more that they should by neutral variation, or if some sequences are conserved for long times, and suddenly they change a lot, then we can infer positive selection: those changes are positively retained because they give some advantage.

    The simplest way is to compare non synonymous mutation rate with synonymous mutation rate ( which is a measure of neutral variation): the Ka-Ks ratio.

    If the ratio is much lower than 1, then the sequence is conserved, and is subject to negative selection. That’s the case with almost all proteins genes, with different degrees of low Ka-Ks ratio.

    On the other hand, if the ratio is higher than 1, positive selection is assumed.

    That’s exactly the case with Dave Carlson’s example.

    He does not give us an explicit Ka-Ks analysis, but he observes “elevated rates of non-synonymous substitutions compared to synonymous substitutions”, which is the same idea.

    Now, the point is: these cases exist, but they are definitely rare. An important example, which applies a similar concept. is the detection of HARs in humans: segments of the human genome that are conserved throughout vertebrate evolution but are strikingly different in humans.

    So, what does the example presented by Dave Carlson mean? Is it an example of possible design inference?

    Well, it’s not so simple.

    First of all, we have to try to infer if the changes documented here (in spiders) can be reasonably considered functional. There are many ways to do that. One would be, as I have done for my proteins, to check if the changed sequences have been conserved for a long enough time. Another way (more difficult) would be to understand the function of those changed sequences. IOWs, we should try to exclude the possibility that the changes are simply random neutral variation (maybe the result of some random insertion).

    If we can reasonably argue that the changes are functional (and I am absolutely open to that interpretation) the question remains: should they, in the light of ID theory, be considered as some random variation subject to positive selection, or can we infer a design intervention?

    According to ID theory, the answer is simple: we have to measure the functional complexity of the transition. Only a very high level of functional transition allows a design inference.

    How high? Well, 500 bits is Dembski’s UPB. That is a safe threshold, and it corresponds to about 115 necessary AAs. I have suggested a more realistic threshold of 150 bits for the biological world (about 35 necessary AAs). Empirical data (Behe, Axe) suggest that the real threshold could be more near to 5 – 10 necessary AAs (22 – 43 bits).

    I will stick here to my 150 bits as a safe threshold.

    So, what can we say of Dave Carlson’t example? If we have no data about conservation, or about function, we can only compute the total potential information content of the transition: 20^n. That is the search space, not the functional information. However, the functional information in a sequence can never be higher than the search space, so the search space is an upper limit for it.

    Now, I don’t know how many AAs are implied in the positive selection. If I look at his image, I would say only a few, maybe more than 10, but not much more. But his image could be only part of the whole process.

    However, under at least 35 AAs implied in the transition, I would not consider a design inference. That’s not to say that the transition was not designed (as our enemies often argue, correctly, it is impossible to exclude design), but certainly there is no real reason to invoke design for such a simple transition, which could still be explained, with some concessions, by non design mechanisms.

    Moreover, in the absence of functional data, we can only say that the search space is an upper limit for functional information, but the true value could be much lower. One more reason not to try any design inference here.

    I hope that is clear. This is an important point which is often misunderstood (not only by dazz).

  194. 194
    Dionisio says:

    @189

    gpuccio quoted one of his politely-dissenting tsz interlocutors saying:

    I assume this because you were the only person I was really talking to last time I was at UD.

    Well, wrong assumption (again). They make wrong assumptions too often. 🙂

    Even in the cases where gpuccio has been the explicitly addressed person, in public discussion threads other persons may read those comments too and could tip the administrators of the blog, or even request the banning.

    gpuccio is well known in UD for his patient and polite treatment of his dissenting interlocutors. He even publicly misses debating with those interlocutors, probably because they make him write more to the benefit of the anonymous visitors (a.k.a. onlookers or lurkers) who may draw their own conclusions based on what they read here.

    I lack that kind of patience, hence I consider some interlocutors unnecessary distractions and welcome their absence. Good riddance. 🙂

    Biology-related discussions demand serious concentration.

    Participants should be willing to understand all presented positions well. Otherwise should go back to their natural habitat in the beautiful Norwegian fjords. 🙂

  195. 195
    Dionisio says:

    gpuccio @193

    Glad you’ve explained the concept of “positive selection”, which I had not understood before. Maybe I’ve got it now? 🙂
    Thank you.

  196. 196
    Dionisio says:

    @193
    “Now, the point is: these cases exit, but they are definitely rare.”

    “If we can reasonably argue that he changes are functional […]”

    “So, what can we say of Dave Carlson’t example? If we have no data bout conservation, […]”

  197. 197
    gpuccio says:

    Dionisio:

    Corrected! 🙂

  198. 198
    Dionisio says:

    gpuccio @193

    One more reason not to try any design inference here.

    Here you’ve demonstrated honesty by observing the established rules.

  199. 199
    Dionisio says:

    gpuccio @197

    Anyway, the indicated ‘mutations’ did not affect the functional information in the associated statements. 🙂

    But definitely they were not designed. 🙂

  200. 200
    Dionisio says:

    Positive selection:

    PPO ¦ PP
    POP ¦ P P
    PPO ¦ PP
    POO ¦ P
    POO ¦ P

    Negative selection:

    NOOON ¦ OOO
    NNOON ¦ OO
    NONON ¦ O O
    NOONN ¦ OO
    NOOON ¦ OOO

    🙂

  201. 201
    bill cole says:

    Gpuccio
    Here is a question to me regarding you from Alan Fox at TSZ. I wanted your thoughts before I responded.

    @ colewd. This is the crux of arguments over functionality. Gpuccio talks about superfamilies of related functional proteins as if the distribution of functional proteins varies between proteins that are known and putative proteins that have not been already exploited by some organism. Why should the density vary across sequence space? Why should not the occurrence of functional proteins turn out to be near constant across the whole space of all possible protein sequences?

  202. 202
    gpuccio says:

    bill:

    I am not sure that I understand well colewd’s point, and now I have not the time to look at all his posts at TSZ (which seem to be many!).

    I talk about superfamilies of related functional proteins because that’s what we observe. It’s not me that classify proteins in superfamilies. It’s SCOP and other important databases.

    What I don’t understand is what he means by “putative proteins that have not been already exploited by some organism”. For example, we have ATP synthase, and the alpha and beta chains, as I have debated many times, are very specific and extremely conserved, from prokaryotes to humans. So, it is perfectly reasonable to consider those two sequences as islands of function.

    Maybe colewd thinks that there are a lot of completely different sequences, with a near constant distribution across sequence space (whatever that means), which could easily work in ATP synthase in the place of the alpha and beta chain. But why should that be true? Has he any reason to believe such a weird thing, beyond simple imagination?

    The movements in sequence space are realized, as should be obvious, at sequence level. If two sequences have no detectable homology, what is the probability of getting from one to the other by simple random variation? Practically non existent.

    So, the only sequence space where you could find another beta chain which works, and is not related to our well known beta chain, is a sequence space which is practically filled by different sequences which would all works as beta chains of ATP synthase. Such a space exists, I am afraid, only in the fervid imagination of those who cannot admit the simple truth taught by observed facts: protein superfamilies are isolated islands of function in the sequence space, and there are 2000+ of them in the known proteome.

    If I am misunderstanding colewd’s point, I am ready to listen to his clarifications. Just let me know.

  203. 203
    bill cole says:

    Gpuccio
    The question came from Alan Fox to Colewd. Since it referenced you I thought I would bring it to you since I am colewd 🙂 I will edit colewd and put Alan in and respond.

    Thanks

  204. 204
    gpuccio says:

    bill:

    Thank you for clarifying. I apologize for misunderstanding the roles. Indeed, I had suspected that colewd could be you, but frankly I had not the time to follow well the whole discussion there.

    I suppose that my points at @202 remain valid as an answer to Alan Fox. 🙂

  205. 205
    gpuccio says:

    bill:

    I just saw that at TSZ:

    From Rumracket:

    “The first number is 1 in every 10^11 randomly generated protein sequences 80 amino acids in length, will have [The Function In Question]. It’s based on this paper: Functional proteins from a random-sequence library by Keefe & Szostak.”

    So, I see they are still using that paper for their propaganda. They are shameless!

    “The second number is a creationist number, IIRC spuriously calculated by Douglas Axe back in some work he did in 2004.”

    So, the completely biased paper by Keefe & Szostak, which shamelessly uses intelligent selection to get some folding about a completely non selectable function, is great, while Axe’s work is “spurious”.

    Why don’t we add the 10^70 starting sequences computed to be necessary to get the wildtype sequence in the rugged landscape paper?

    The way neo darwinists try to convince us that their fantasies about a function filled protein space have any objective support range from pitiful to dishonest.

    By the way, have you noticed that the total functional information content of the beta chain of ATP synthase as conserved from E. coli to humans (about 6oo bits), while huge and amazing, is still much lower than the mean functional information jump of the six proteins in my OP?

    Ah, but certainly neo darwinists do not want to deal with those numbers! Coming from a crypto-creationist, they must certainly be “spurious”, at best! 🙂

    So, let them stick to their lies about Keefe & Szostak’s paper.

  206. 206
    gpuccio says:

    Patrick at TSZ goes on inviting me to comment at their blog, instead of continuing with the interblog issue.

    While I thank him for the kind interest, I must remind him that I post here, because here is my place, here are the people who care about ID, which the theory I love, and so here I must express my ideas.

    Just answering some of the comments from TSZ is big work for me, and as you can see from my little misunderstanding with bill cole at #202, it is really done in a rush most of the time. But, at least, the discussion happens here, where those who come at UD can see it, if they like.

    Posting at TSZ, which I have done in the past, would take too much of my time and subtract it to my activity here.

    So, Patrick, just accept my choice. After all, you are not obliged to be interested in my thoughts, or if you are, you can always read them here (I suppose you are not banned from reading) and answer at TSZ, and if what you say is interesting, and if I have the time, I will answer here. It’s cumbersome, but it’s he best I can do.

  207. 207
    gpuccio says:

    bill:

    I just found this statement you made at TSZ:

    The papers that I have read give two proposals on de novo genes. 1. Gene duplication 2. NC RNA. In one paper there is a vague proposal on once a gene is duplicated and finds new function, how it then gets transcribed. The real challenge is finding new function through almost infinite mathematical space. First a mechanism of change needs to be identified. Then a mathematical model that can repeatably get you from functional space A to functional space B which is the new gene as a result of gene duplication. The additional challenge here is natural selection does not help until function is found and successfully transcribed.

    While Lenski’s experiment showed through gene duplication and transcription of a duplicated gene how a new feature could evolve (the ability to consume citrate in an aerobic condition) how did the original 480AA enzyme sequence that breaks down the citrate molecule evolve?

    You said it perfectly! I wholly agree with you. 🙂

    I must say that the way our interlocutors arrogantly exhibit their few examples of microevolution, involving one or two simple events (including Lenski’s), as though they were splendid answers to the information problem frankly nears intellectual dishonesty.

    And about Lenski and the meaning of the Cit+ phenotype, it can be useful to read again this simple summary from Wikipedia:

    Other researchers, have experimented on evolving aerobic citrate-utilizing E. coli. Dustin Van Hofwegen et al., working in the lab of Scott Minnich, were able to isolate 46 independent citrate-utilizing mutants of E. coli in just 12 to 100 generations using highly prolonged selection under starvation, during which the bacteria would sample more mutations more rapidly.[43] In their research, the genomic DNA sequencing revealed an amplification of the citT and dctA loci and rearrangement of DNA were are the same class of mutations identified in the experiment by Richard Lenski and his team. They concluded that the rarity of the citrate-utilizing mutant in Lenski’s research was likely a result of the selective experimental conditions used by his team rather than being a unique evolutionary speciation event.[43]

    John Roth and Sophie Maisnier-Patin reviewed the approaches in both the Lenski team’s delayed mutations and the Van Hofweges team’s rapid mutations on E. coli. They argue that both teams experienced the same sequence of potentiation, actualization, and refinement leading up to similar Cit+ variants.[44] According to them, the period of less than a day during which citrate usage would be under selection, followed by 100-fold dilution, and a period of growth on glucose that would not select for citrate use, ultimately lowered the probability of E. coli being able accumulate early adaptive mutations from one period of selection to the next.[44] On the other hand, Van Hofwegen’s team allowed for a continuous selection period of 7 days, which yielded a more rapid development of citrate-using E. coli. Roth and Maisnier-Patin suggest that the serial dilution of E. coli and short period of selection for citrate-use under the conditions of the LTEE perpetually impeded each generation of E. coli from reaching the next stages of aerobic citrate utilization.[44]

    In response, Blount and Lenski acknowledge that the problem is not with the experiments or the data, but with the interpretations made by Van Hofwegen et al. and Maisnier-Patin and Roth.[45] Lenski notes that the rapid evolution of Cit+ was not necessarily unexpected since his team was also able to produce multiple Cit+ mutants in a few weeks during the replay experiments they reported in the 2008 paper in which his team first described the evolution of aerobic citrate use in the LTEE.[46] Furthermore, Lenski criticizes Van Hofwegen et al.’s description of the initial evolution of Cit+ as a “speciation event” by pointing out that the LTEE was not designed to isolate citrate-using mutants or to deal with speciation since in their 2008 paper they said “that becoming Cit+ was only a first step on the road to possible speciation”, and thus did not propose that the Cit+ mutants were a different species, but that speciation might be an eventual consequence of the trait’s evolution.[46] Lenski acknowledges that scientists, including him and his team, often use short hand and jargon when discussing speciation, instead of writing more carefully and precisely on the matter, and this can cause issues.[46] However, he notes that speciation is generally considered by evolutionary biologists to be a process, and not an event.[46] He also criticizes Van Hofwegen et al. and Roth and Maisnier-Patin for positing “false dichotomies” regarding the complex concept of historical contingency. He argues that historical contingency means that history matters, and that their 2008 paper presented data that showed that the evolution of Cit+ in the LTEE was contingent upon mutations that had accumulated earlier. He concludes that “…historical contingency was invoked and demonstrated in a specific context, namely that of the emergence of Cit+ in the LTEE—it does not mean that the emergence of Cit+ is historically contingent in other experimental contexts, nor for that matter that other changes in the LTEE are historically contingent—in fact, some other evolved changes in the LTEE have been highly predictable and not (or at least not obviously) contingent on prior mutations in the populations.”[46]

  208. 208
    gpuccio says:

    bill:

    By the way, at present my favourite option for the origin of de novo genes is: design of pre-existing non coding sequences by guided transposon activity.

  209. 209
    gpuccio says:

    Just a little oddity:

    There are more comment about my OP in the TSZ thread (223) than here (209 including this one).

    I suppose I must really be thankful to my “friends” there for the kind attention! 🙂

  210. 210
    Dionisio says:

    gpuccio @205

    […] they are still using that paper for their propaganda. They are shameless!

    In terms of biology research these days that paper is kind of old (2001?), isn’t it?
    Can’t they pull out something newer?
    They need more fresh food for thoughts.
    Biology research* is very dynamic in the sense that ‘surprising’ and ‘unexpected’ discoveries are happening almost daily these days. The old dogmas** are being shaken by some of those discoveries. Over 15-year old publication in biology seems outdated, doesn’t it?

    (*)There are certain fields of knowledge where the old documents remain as valid as they were at the time they were written originally, because what they say does not change with time, although people’s interpretation may change daily.

    (**) http://plato.stanford.edu/entr.....iological/
    http://arxiv.org/abs/1606.07184v1

  211. 211
    Dionisio says:

    gpuccio @209

    There are more comment about my OP in the TSZ thread (223) than here […]

    Wow! they like you there too!
    Have you considered running for a public office in the next elections? Maybe UN General Secretary?
    🙂

  212. 212
    Dionisio says:

    @205

    “Why son’t we ass the 10^70 starting sequences computed to be necessary to get the wildtype sequence in the rugged landscape paper?”

  213. 213
    Dionisio says:

    gpuccio @205

    By the way, have you noticed that the total functional information content of the beta chain of ATP synthase as conserved from E. coli to humans (about 6oo bits), while huge and amazing, is still much lower than the mean functional information jump of the six proteins in my OP?

    Interesting observation indeed.

  214. 214
    Dionisio says:

    Hierarchy and extremes in selections from pools of randomized proteins.

    Boyer S1, Biswas D1, Kumar Soshee A1, Scaramozzino N1, Nizak C2, Rivoire O3.

    Proc Natl Acad Sci U S A.
    2016 Mar 29;113(13):3482-7.
    doi: 10.1073/pnas.1517813113.
    Epub 2016 Mar 11.

  215. 215
    gpuccio says:

    bill:

    By the way, another “small” point about those numbers (be them Keefe & Szostak’s, Axe’s, or Ayashi’s: right or wrong that they may be, they are all about rather “short” protein sequences, about 100 AAs.

    Astrotactin 2 is a 1339 AAs protein. 889 of them are identical in sharks and humans.The positives are 1048.

    I would really appreciate if our friends at TSZ could comment about this very simple fact.

  216. 216
    gpuccio says:

    Dionisio #212:

    Corrected!

    But “Why son’t we ass” was picturesque, wasn’it? RV at its best! 🙂

  217. 217
    gpuccio says:

    Dionisio at #214:

    I did not know that one, seems interesting. I will take the time to read it carefully, thank you.

  218. 218
    Dionisio says:

    gpuccio @216

    Yes, it was picturesque, like RV at its best. But it could affect the sequence functionality (i.e. the statement meaning), specially in the cases of folks who tend to misinterpret -sometimes apparently intentionally- most of what you write so clearly.
    The mind is so amazing that it automatically corrects those misspelled words for us to understand the whole context. But if some folks have a priori decided not to understand your point, they could use any misspelling as a cheap excuse to justify their attitude. 🙂

  219. 219
    Dionisio says:

    Are we closer to match the number of posts related to this OP in the other blog?

    🙂

  220. 220
    gpuccio says:

    Dionisio:

    Us – them: 219 – 229.

    It’s a beautiful match! 🙂

  221. 221
    gpuccio says:

    bill:

    This is very interesting:

    “Deep mutational scanning of an RRM domain of the Saccharomyces cerevisiae poly(A)-binding protein”

    http://www.ncbi.nlm.nih.gov/pm.....MC3851721/

    Just a couple of quotes (the paper is rather complex, and really rich of facts):

    While the enrichment scores of the single amino acid substitutions indicate that most mutations were deleterious for RRM2 function, a few mutations had enrichment scores that were greater than that of the wild type. In particular, the enrichment score for Q194C was 2.9. However, we measured the growth rate of yeast cells carrying Q194C and found that it was the same as those carrying the wild-type version (data not shown). This observation agrees with our finding that enriched variants follow the distribution of synonymous mutants and therefore are likely to be neutral

    And:

    By assaying variants of the RRM2 domain of the yeast Pab1 in high throughput, we scored most (83%) of the possible 1500 single amino acid substitutions (including stop codons), and more than 100,000 variants with multiple substitution events, in a 75-residue-long sequence. The results highlight the RNA-binding surface of RRM2 as the most important element for its function, although each position in the RRM2 shows a nearly unique pattern of mutational sensitivity. We clustered the data to reveal other residues highly sensitive to mutation, as well as core hydrophobic residues that tolerated substitution only by other hydrophobic amino acids. By comparing the evolutionary conservation of RRM residues with their ability to function in the context of the yeast Pab1 protein, we could implicate some residues in yeast-specific functions. Finally, we used epistasis analysis to identify interacting residues in Pab1.

    This techinque of Deep mutational scanning seems specially appropriate to study the protein functional space.

  222. 222
    gpuccio says:

    bill:

    I have looked at a couple of other papers using Deep mutational scanning . The idea is the same: mutations are either deleterious or neutral, usually with some bimodal distribution.

    Interestingly, there is good correlation between evolutionary conservation and experimental fitness results, but with distinct differences. Obviously, conservation is an “experiment of nature”, and lab conditions are not really the same thing as natural conservation. However, both metrics are measuring the same thing (functional restraints), with different methodology. The strong similarity of the results is important. But also the differences can reveal important aspects of protein function specificity, as suggested by the authors in their final remarks.

  223. 223
    gpuccio says:

    Rumraket, at TSZ, goes wild with the old “deck of cards” idiocy.

    “The posterior probability fallacy is the quintessential fallacy of creationism.” he says.

    “It’s like rolling 100 dice and then calculating the odds of that particular arrangement coming up. It will be 1 in 6^100. So an event with a probabiliy of 6^-100 just happened. So every roll of 100 dice is a miracle, or what? ” he says.

    He has really understood everything!

    So, I suppose that we can easily observe the molecules in a gas assuming ordered states, like for example being all in the right half of some volume at the same time.

    Of course, it is perfectly possible! After all, the probabilities of that configuration are exactly the same as those of any other configuration which is commonly observed!

    Only stupid creationists could believe that the laws of probabilistic mechanics, as applied to gases, have any value!

  224. 224
    gpuccio says:

    Allan Miller at TSZ:

    It is clearly an observed fact that many folds are not obviously related to other folds within extant life. This, however, does not prove them isolated islands of function in itself. Because if evolution and common descent were true, one would expect loss of relationship information over time. In an evolutionary scenario, many configurations are passed through then lost. It is wrong – the same mistake as Durston’s – to regard extant life as a representative sample of all sequence space. It is also wrong to regard the lack of detectable ‘lateral’ connection to be conclusive of a lack of coalescent connection when adding the dimension of lineage. It seems to be a molecular version of the ‘dogs giving birth to cats’ trope – you can’t get to modern sequence A from modern sequence B.

    My rather clear question was:

    “Maybe Alan Fox thinks that there are a lot of completely different sequences, with a near constant distribution across sequence space (whatever that means), which could easily work in ATP synthase in the place of the alpha and beta chain. But why should that be true? Has he any reason to believe such a weird thing, beyond simple imagination?

    Allan Miller’s response can represent a clear answer: none.

    Allan, must I remind you that those “configurations” which “are passed through then lost” must be. to be of any relevance, increasingly functional configurations?

    You see, we are again at the myth of lost intermediates.

    So, I ask to you, too: Have you any reason to believe such a weird thing, beyond simple imagination?

    And beyond your dogmas?

  225. 225
    gpuccio says:

    As expected, my comments about Keefe and Szostak have evoked a chorus of complaints at TSZ! I should have known. Never criticize sacred monsters with skeptics! 🙂

    I have discussed Keefe and Szostak’s paper ad nauseam. I cannot always repeat the same things.

    Very briefly. The lies are those about what that paper means.

    The paper only shows that in a big enough random library of proteins there are a few molecules with some weak binding of ATP.

    And that it is possible to select those molecule in the lab, by artificial selection, and to use a procedure of rounds of mutation and further selection for ATP binding, and guess what? They obtain a molecule which strongly binds ATP. And which has some folding. And which is absolutely non naturally selectable,, exactly like its precursors in the original library!

    Amazing! So, protein engineering works (up to a point). Who would have suspected such a thing.

    Important points:

    1) Neither the weakly binding proteins, nor the artificially engineered final protein, have been shown to be even vaguely naturally selectable, Indeed, the final protein has been shown to be deleterious, in the right environment.

    2) Some folding has been shown for the engineered protein, not for the “natural” sequences in the original library.

    3) You can like the paper as you want, but it is a fact that it tells absolutely nothing about the occurrence of naturally selectable protein sequences in random libraries. Least of all quantifies it.

  226. 226
    Mung says:

    hi gpuccio,

    There is an article at ENV that you may find interesting and of some relevance to vertebrate origins.

    In Current Biology, Thibaut Brunet and Detlev Arendt appear excited about the possibility of solving the “hard problem of cartilage origins.”

    http://www.evolutionnews.org/2.....03032.html

    They give no explanation for the emergence of 3 sets of genes that code for collagen. “The ancestral soxD+ soxE+ colA+ ventral mesentery is assumed to have given rise to both the chordate sclerotome and the chelicerate endosternite,” they say, ‘assuming’ that six transcription factor genes and the collagenase gene conspired to create the first hard parts.

  227. 227
    bill cole says:

    gpuccio

    As expected, my comments about Keefe and Szostak have evoked a chorus of complaints at TSZ! I should have known. Never criticize sacred monsters with skeptics! 🙂

    I think you are addressing the fundamental argument in evolutionary biology today.
    If we assume that Szostak’s numbers are correct we still have still have to look at additional functions of evolved proteins. My research is in the nuclear protein area where proteins have multiple binding sites.

    My argument would be that these proteins approach and even surpass Axe’s numbers that are just dealing with binding penicillin.

    Rumraket’s (Mikkel’s) argument is that a protein does not need to bind to anything specific when it evolves so the odds are closer to Szostak’s numbers.

    I think he may be right for the first protein of the flagellum but protein 2 thru 40 then approach Axe’s numbers because they now have to bind to specific proteins inside the cell.

  228. 228
    bill cole says:

    Gpuccio

    per Rumracket

    “It’s like rolling 100 dice and then calculating the odds of that particular arrangement coming up. It will be 1 in 6^100. So an event with a probabiliy of 6^-100 just happened. So every roll of 100 dice is a miracle, or what? ” he says.

    My question.

    Rumraket July 30, 2016 at 9:07 pm
    colewd: If we roll the dice and a very improbable outcome came up 10 times in a row, at the time we observed it the probability of the out come is indeed 100%.

    The next question might be, what is the chance the result we are observing is the result of a stochastic process?

    His answer 🙂

    What is the probability of another sequence of 10 particular but dissimilar rolls, coming up? The same as 10 of the same in a row.

  229. 229
    gpuccio says:

    Mung:

    Always a pleasure to hear from you. 🙂

    It seems interesting. I will look at it as soon as possible.

  230. 230
    gpuccio says:

    bill cole at #228:

    Rumracket is beyond hope. I would suggest that you don’t waste your time with him.

    The “deck of cards” argument is probably the most stupid and irritating statement ever made by neo darwinists (not all of them, luckily, I suppose that the more intelligent ones, or those who simply are familiar with statistics, understand what it is, and strictly avoid to comment).

    The deck of card argument goes more or less so:

    1) If we shuffle a deck of cards, each single permutation is highly improbable. True. The probability of each permutation is 1:52!, that is about 1:8*10^67.

    2) Therefore, IDists could say that each result is a miracle! Wrong. Only the fools who make the deck of cards argument can think so. Each result, after having happened, has happened, There is no more any problem of probability of a result which is already there.

    Now, where is the problem? The problem is simply in how we define the probability of a set of results.

    So, a specific result, defined in advance, is completely unlikely.

    The repetition of a specific result, already observed, is completely unlikely.

    The occurrence of a specific ordered result, like all the cards in ordered sequence, is completely unlikely.

    So, what kind of result is very likely?

    It’s simple: the occurrence of some sequence which has no specific order, and is not defined in any special way independently from the observation of the sequence itself after it has occurred.

    Indeed, that’s what happens. We obtain a disordered sequence. We never, never obtain a completely ordered sequence.

    For the same reason that the molecules of a gas never stay in the right half of the container.

    Now, the ordered sequence has a probability of 1:8*10^67. It will never happen.

    But a generic, disordered sequence has a probability of almost 1.

    If Rumracket had to bet his own money, what do you think he would do?

    Of course, here he is only betting his intellectual dignity, and so it’s easy to make the wrong choice.

  231. 231
    gpuccio says:

    bill cole at #227:

    I agree with you, except when you say:

    “If we assume that Szostak’s numbers are correct”

    No. I cannot even assume that. They are not correct, period.

    The sequence which was in the initial library, the only one about which they should be saying anything and giving numbers, was simply some sequence with a weak affinity for ATP.

    I think we can find some sequence with a weak affinity for anything, in a modestly big library like that.

    So, what did they do? Didi they just study the sequence which was in the library, and say: Hey, we can find this kind of sequence once in 10^11?

    No. Why? Because nobody would have cared.

    That sequence is simply insignificant.

    So, they did change it. By rounds of intelligent selection.

    But that means that the final result is not what can be found in a random library. The final result is what intelligent protein engineering (and not natural selection) can derive from a random library.

    This is the only honest way of putting it. The numbers are wrong, and completely non pertinent to any discussion about evolution. They cannot be used in any way to antagonize other numbers, like Axe’s. Because they are wholly non pertinent.

    I agree with all the rest that you say. I can only start to think what the numbers would be for astrotactin 2, if someone were fool enough to try to derive it, or a functional equivalent, from a random library. Without any protein engineering, of course.

  232. 232
    Dionisio says:

    gpuccio @220

    Us – them: 219 – 229.
    It’s a beautiful match! 🙂

    Oh, no, we’re still behind…
    Let’s encourage more UD folks to post comments in this thread so this OP can win the match!
    🙂

    Jokes aside, obviously your OP has won the debate already, since your politely-dissenting interlocutors haven’t produced any serious argument against the central message of your OP.
    🙂

    Actually some of them look as though they have not understood your OP yet. But let’s hope eventually they will get it. Just don’t hold your breath while waiting for that to happen. 🙂

  233. 233
    gpuccio says:

    bill:

    By the way, have you seen my posts 221 and 222?

    This technique of Deep mutational scanning seems a very good way to explore protein space. It is a high throughput technique, and it seems very powerful.

    Maybe we will soon have the answers we are waiting. Maybe all the functions expected by our hopeful neo darwinist friends will be found! 🙂

    And it’s good to see that someone is using a metrics based on evolutionary conservation in scientific papers, comparing it to the results of another metrics. Maybe they are crypto-creationists, after all?

  234. 234
    Dionisio says:

    Update:

    The scores have changed:

    Us – them: 233 – 229.

    Now we’re ahead!

    🙂

    BTW, this “us – them” thing reminds me of an old song by Pink Floyd in their “Dark side of the moon” album. 🙂

  235. 235
    gpuccio says:

    Dionisio:

    What I am really happy of is that the debate has revealed many interesting aspects which were not obvious at first sight, as it always happens when people discuss with a minimum of intelligence and respect. Yes, I am very happy of that.

    Even if I had to witness a revival of the deck of cards argument (in dice form), which has always specially irritated me, and to pick up again the never ending story of Keefe and Szostak!

  236. 236
    gpuccio says:

    Dionisio:

    “Now we’re ahead!”

    OK, let’s enjoy our moment of glory! 🙂

    It will probably not last very much, like all good (and bad) things in this world…

  237. 237
    Mung says:

    Typical nonsense coming from Rumraket.

    What is the probability that after having thoroughly shuffled a deck of cards the cards will appear in the exact same order they were in before they were shuffled?

    If you actually saw them appear in the exact same order with your own eyes, would you believe you had witnessed a miracle or would you believe you had somehow been deceived?

    If you actually saw them appear in the exact same order with your own eyes and denied the evidence of your own eyes would you be self-deceived, or would you blame your lying eyes?

  238. 238
    bill cole says:

    gpuccio

    “Deep mutational scanning of an RRM domain of the Saccharomyces cerevisiae poly(A)-binding protein”

    http://www.ncbi.nlm.nih.gov/pm…..MC3851721/
    Just a couple of quotes (the paper is rather complex, and really rich of facts):

    Thank you for this very interesting paper. I think it supports my hypothesis that the more ways a specific protein functions i.e. binding to small molecules other proteins etc the more critical its sequence is.

    When we get to nuclear proteins that may interact with dozens of other proteins most mutations will be problematic.

    This is where we approach the equation that 1/total possible sequences=probability of finding the required function by random search.

  239. 239
    gpuccio says:

    bill:

    “Thank you for this very interesting paper. I think it supports my hypothesis that the more ways a specific protein functions i.e. binding to small molecules other proteins etc the more critical its sequence is.

    When we get to nuclear proteins that may interact with dozens of other proteins most mutations will be problematic.”

    Absolutely!

    And that becomes even more true for complex long regulatory proteins, like the six I have considered in my OP.

    And it is not necessary to have “1/total possible sequences=probability of finding the required function by random search”, which is probably never true for any protein: it’s enough to have a huge functional information, as measured, for example, by the conservation based methodology I have used in the OP.

    And the longer the protein, the more the search space becomes so huge that any functional target space, however big, can be considered as trivial in comparison (that is exactly the reason why we never get ordered states in gas molecules).

    And finally, let’s remember that my conservation based method can only underestimate functional information, because it cannot see all the functional information in a sequence that is taxonomically restricted, or even species specific: see for example my considerations about Prickle protein here:

    http://www.uncommondescent.com.....ted-genes/

    and the interesting conclusion of the authors of the quoted paper:

    By comparing the evolutionary conservation of RRM residues with their ability to function in the context of the yeast Pab1 protein, we could implicate some residues in yeast-specific functions.

    (emphasis mine)

    IOWs, the results of their metrics, based on direct measure of function in the lab, compared with the results of a conservation based metrics (like the one I have used in the OP) can help detect that important part of functional information which is species specific.

    That is certainly a relevant part of the total functional information, especially in regulatory molecules, like TFs, which act multi-combinatorially, as you very correctly say.

    IOWs, my estimate of 1531 bits of specific functional information in astrotactin 2 based on its specific conservation in vertebrates is certainly a big underestimate! There is certainly a part of functional information, specific for example to fish, or to snakes, or to birds, or to mammals, that my methodology cannot see!

    But 1531 bits are common to all vertebrates, and that part my conservation based methodology sees all too well. 🙂

  240. 240
    Dionisio says:

    gpuccio:

    Have you seen this paper?

    The fitness landscape of a tRNA gene
    Chuan Li, Wenfeng Qian, Calum J. Maclean, and Jianzhi Zhang
    Science. 352(6287): 837–840.
    doi: 10.1126/science.aae0568

    Not sure if it relates to the discussed topics, though.

  241. 241
    gpuccio says:

    Dionisio:

    Well, this is about a tRNA gene, so the scenario is a little different. However, the results seem quite similar, according to the abstract:

    Fitness landscapes describe the genotype-fitness relationship and represent major determinants of evolutionary trajectories. However, the vast genotype space, coupled with the difficulty of measuring fitness, has hindered the empirical determination of fitness landscapes. Combining precise gene replacement and next-generation sequencing, we quantify Darwinian fitness under a high-temperature challenge for over 65,000 yeast strains each carrying a unique variant of the single-copy Embedded Image gene at its native genomic location. Approximately 1% of single point mutations in the gene are beneficial, while 42% are deleterious. Almost half of all mutation pairs exhibit significant epistasis, which has a strong negative bias except when the mutations occur at Watson-Crick paired sites. Fitness is broadly correlated with the predicted fraction of correctly folded tRNA molecules, revealing a biophysical basis of the fitness landscape.

  242. 242
    gpuccio says:

    Mung at #237:

    The correct probabilities in the deck of cards scenario:

    1) Probability of a new occurrence of a sequence which we has just occurred: 1:8*10^67. Miracle or design.

    2) Probability of the occurrence of the perfectly ordered sequence, independently defined: 1:8*10^67. Miracle or design.

    3) Probability of the occurrence of some non specific, non ordered sequence: almost 1. What always happens.

  243. 243
    gpuccio says:

    Mung at #237:

    Just for a comparison:

    The correct probabilities in the case of “gas molecules in a container” scenario:

    1) Probability of a state with all the molecules in the right half of the molecule, and void in the left half: practically zero. Miracle or design.

    2) Probability of a state with all the molecules in the left half of the molecule, and void in the right half: practically zero. Miracle or design.

    3) Probability of a state with all the molecules distributed non specifically and without any recognizable order in all the volume of the container: practically 1. What always happens.

  244. 244
    gpuccio says:

    Dionisio:

    We also have to consider that a tRNA gene is about 70 – 90 nucleotides, for a total maximum search space of 180 bits: big, but not huge.

    As a general rule, the lower the search space, the higher the target space/search space ratio will be, in average. In language, for example, it’s easy to verify that the search space grows much more rapidly than the target space. See here:

    http://www.uncommondescent.com.....-language/

  245. 245
    gpuccio says:

    Dioniso:

    Us – them: 245 -255.

    Life is cruel! 🙂

  246. 246
    gpuccio says:

    Flint, at TSZ, reiterates the errors about the deck of cards arguments (always in the dice form):

    This always seems to confuse some people. If the dice are fair, then ANY sequence of 10 rolls is going to be highly improbable, and all will be equally improbable. I think people tend to find ordered sequences (according to some ordering scheme in their minds) as being somehow inherently less likely. For example, they might consider a lottery number selection of 1-2-3-4-5-6 as being less likely than a more “random-looking” sequence.

    What would be suspicious is if the same sequence were rolled twice.

    Emphasis mine.

    And I ask:

    Flint, why would that be suspicious? According to your reasoning, the first occurrence has the same probability as any other sequence. Correct.

    Well, but after the sequence has occurred, what is its probability of occurring a second time? The answer is simple: exactly the same.

    So, what is the probability of having the same sequence occurring twice in a row? Exactly the same as the probability of having any couple of sequences occur (the product of the individual probabilities).

    This is absolutely correct: any couple of sequences (with repetition) has the same probability to occur.

    So, why do you find that scenario “suspicious”? Is it because people tend to find recurring sequences (according to some scheme in their minds) as being somehow inherently less likely?

    No, the answer is more simple. It’s because people, correctly, compute probabilities for specified sets of results.

    A set of ordered results is small and highly unlikely. A set of non specific, disordered results is highly likely.

    The same sequence twice in a row is simply a form of order. Like the ordered sequence of the cards. Like all gas molecules in half the space. Like function.

    Small specified sets are extremely unlikely in a big search space. Which is exactly the concept of ID.

    I hope that, if your anti-ID dogma allows it, you can recognize your error.

  247. 247
    Dionisio says:

    #240, #241 & #244 follow-up

    1. tRNA regulation:

    1.1 Are the tRNA genes expressed straightforwardly as per the central dogma, i.e. without any post-transcriptional or post-translational modifications?

    1.2 Are their expressions triggered by some kind of signaling pathways associated with specific spatiotemporal conditions?

    2. aminoacyl tRNA synthetase (aaRS) regulation:

    2.1 Are the aaRS genes expressed straightforwardly as per the central dogma, i.e. without any post-transcriptional or post-translational modifications?

    2.2 Are their expressions triggered by some kind of signaling pathways associated with specific spatiotemporal conditions?

    3. Is there any known spatiotemporal/quantitative relation between the above processes (1) and (2)?

  248. 248
    Dionisio says:

    Sorry for the off topic digression @247.
    Should move it out to another thread:
    http://www.uncommondescent.com.....ent-614196

  249. 249
    gpuccio says:

    OMagain at TSZ:

    “Hahaha! This is funny. I’m quite sure gpuccio will not appreciate how funny that is. ‘Deleterious in the right environment’ indeed.”

    Why is it funny? I am referring to a paper where they tried to introduce the protein in a bacterial system, and it proved to be deleterious. It’s the only experimental living system where it was tested, as far as I am aware.

    What is the funny part? Just to know.

  250. 250
    gpuccio says:

    Allan Miller at TSZ:

    “Random peptides have, incidentally, been shown to successfully replace knockouts for multiple functions in vivo, with absolutely no connection between the algorithm used to subset peptide space and the peptide replaced. But I guess, unless one releases them into the wild and gets a brand new pathogenic strain out of it, it’s inconclusive on the ‘selectable’ question!”

    I am well aware of those experiments. However, apart from the question that you correctly mention of selectability in the wild, there are a couple of other problems with those scenarios:

    1) Function is only partially retrieved. Like in Ayashi’s rugged landscape experiment.

    2) The mechanism for that partial retrieval of function, as far as I am aware, is not elucidated.

    One problem with function retrieval experiments is that they rely on some functions which persists, although impaired. Moreover, function retrieval can be due to indirect events, implying other existing functions. Ayashi’s experiment, IMO, is the only one where function retrieval has been directly connected to the RV in substituted sequences. And it is also the one that gives the best insight of the function landscape.

    As I have said, Deep mutational scanning techniques will help us understand things better. I am very confident! 🙂

  251. 251
    gpuccio says:

    keiths (an old “friend”) makes an unusual statement at TSZ:

    Since I typically disagree with gpuccio, it’s good when I occasionally find something to agree with him about.

    I think his criticism of Flint’s statement is valid.

    Thank you Keiths. I hoped that someone at TSZ would be honest enough to admit what is obvious, but I must confess that I was not betting on that.

    This is appreciated. 🙂

  252. 252
    Dionisio says:

    @249

    What is the funny part? Just to know.

    We lack neo-Darwinian sense of humor.

  253. 253
    gpuccio says:

    OMagain at TSZ demonstrates again that he does not understand my arguments. Good.

    gpuccio destroys the core of his own argument and does not seem to notice:

    I think we can find some sequence with a weak affinity for anything, in a modestly big library [Szostak’s] like that.

    The core of my own argument? !!!

    And that would be?

    I quote my true argument, with some emphasis added just to help OMagain to understand it! (OK, one can always dream…):

    The paper only shows that in a big enough random library of proteins there are a few molecules with some weak binding of ATP.

    And that it is possible to select those molecule in the lab, by artificial selection, and to use a procedure of rounds of mutation and further selection for ATP binding, and guess what? They obtain a molecule which strongly binds ATP. And which has some folding. And which is absolutely non naturally selectable, exactly like its precursors in the original library!

    Amazing! So, protein engineering works (up to a point). Who would have suspected such a thing.

    Important points:

    1) Neither the weakly binding proteins, nor the artificially engineered final protein, have been shown to be even vaguely naturally selectable. Indeed, the final protein has been shown to be deleterious, in the right environment.

    2) Some folding has been shown for the engineered protein, not for the “natural” sequences in the original library.

    3) You can like the paper as you want, but it is a fact that it tells absolutely nothing about the occurrence of naturally selectable protein sequences in random libraries. Least of all quantifies it.

    And from post #231:

    I think we can find some sequence with a weak affinity for anything, in a modestly big library like that.

    So, what did they do? Did they just study the sequence which was in the library, and say: Hey, we can find this kind of sequence once in 10^11?

    No. Why? Because nobody would have cared.

    That sequence is simply insignificant.

    So, they did change it. By rounds of intelligent selection.

    But that means that the final result is not what can be found in a random library. The final result is what intelligent protein engineering (and not natural selection) can derive from a random library.

    This is the only honest way of putting it.

    Maybe I should remind OMagain that, in his theory (neo darwinism), naturally slectable functions are the only functions that count. Any other “function” is insignificant, because it cannot be “seen” by the NS process.

    IOWs, any function which does not confer any reproductive advantage is not a function, in a neo darwinian context.

    Is that so difficult to understand? I suppose that one who embraces a scientific theory should at least try to understand it.

    In the meantime, I would suggest that OMagain (and a few others) read carefully this OP of mine:

    http://www.uncommondescent.com.....selection/

    If they want, of course. This is a free world.

  254. 254
    Dionisio says:

    Maybe this was referred here before?

    Epistasis in protein evolution.
    Starr TN1, Thornton JW2.
    Protein Sci. ;25(7):1204-18.
    doi: 10.1002/pro.2897.

    How mutational epistasis impairs predictability in protein evolution and design.
    Miton CM1, Tokuriki N1.
    Protein Sci. 25(7):1260-72.
    doi: 10.1002/pro.2876.

    Evolving Methanococcoides burtonii archaeal Rubisco for improved photosynthesis and plant growth.
    Wilson RH1, Alonso H1, Whitney SM1.
    Sci Rep. ;6:22284.
    doi: 10.1038/srep22284.

    Selection on different genes with equivalent functions: the convergence story told by Hox genes along the evolution of aquatic mammalian lineages.
    Nery MF1, Borges B2, Dragalzew AC2, Kohlsdorf T3.
    BMC Evol Biol. ;16(1):113.
    doi: 10.1186/s12862-016-0682-4.

    Hundreds of Genes Experienced Convergent Shifts in Selective Pressure in Marine Mammals.
    Chikina M1, Robinson JD2, Clark NL1.
    Mol Biol Evol. pii: msw112.
    doi: 10.1093/molbev/msw112

    Not sure if it relates to the discussed topics, though.

  255. 255
    gpuccio says:

    Dionisio:

    This is very interesting. I think Berlinski would love it! 🙂

    Hundreds of Genes Experienced Convergent Shifts in Selective Pressure in Marine Mammals.

    Mammal species have made the transition to the marine environment several times, and their lineages represent one of the classical examples of convergent evolution in morphological and physiological traits. Nevertheless, the genetic mechanisms of their phenotypic transition are poorly understood, and investigations into convergence at the molecular level have been inconclusive. While past studies have searched for convergent changes at specific amino acid sites, we propose an alternative strategy to identify those genes that experienced convergent changes in their selective pressures, visible as changes in evolutionary rate specifically in the marine lineages. We present evidence of widespread convergence at the gene level by identifying parallel shifts in evolutionary rate during three independent episodes of mammalian adaptation to the marine environment. Hundreds of genes accelerated their evolutionary rates in all three marine mammal lineages during their transition to aquatic life. These marine-accelerated genes are highly enriched for pathways that control recognized functional adaptations in marine mammals, including muscle physiology, lipid-metabolism, sensory systems, and skin and connective tissue. The accelerations resulted from both adaptive evolution as seen in skin and lung genes, and loss of function as in gustatory and olfactory genes. In regard to sensory systems, this finding provides further evidence that reduced senses of taste and smell are ubiquitous in marine mammals. Our analysis demonstrates the feasibility of identifying genes underlying convergent organism-level characteristics on a genome-wide scale and without prior knowledge of adaptations, and provides a powerful approach for investigating the physiological functions of mammalian genes.

  256. 256
    Dionisio says:

    gpuccio:

    Regardless of our opinions on the subject, we should admit that their “half full cup” optimistic view of how much is currently understood is encouraging:

    […] the genetic mechanisms of their phenotypic transition are poorly understood […]

    How much is “poorly” – 75%, 50%, 25%, 5%, 1%, 0.1%? 🙂

    That’s why we’ve got to do more research in biology.

    Emphasis mine.

  257. 257
    gpuccio says:

    Allan Miller at TSZ:

    Yes, gpuccio, rounds of intelligent selection are only possible in a peptide space that is connected – where weak function can be tuned by [some kind of] selection to improve. Why is this possible in an experimental setup, yet not in nature? It’s not as if the people are picking the sequences most likely to improve. They are simply assaying for the chosen function, then subsetting the peptide library on that basis, mutating and repeating.

    In this case, the only connection is between an existing affinity and a refined affinity, IOWs, a tweaking if the same function in the same functional island. That tells us absolutely nothing about “connections” between different, isolated functional islands, like protein superfamilies. I am sure that you understand that.

    You ask:

    “Why is this possible in an experimental setup, yet not in nature?”

    It’s simple. Because here you have a function which can only be selected by us because we recognize it, and we set up the lab to select for that desired function. That’s called intelligent selection, and is a form of design.

    In “nature”, nothing like that could happen: the weak binding to ATP that was present in the original library cannot give any reproductive advantage, and therefore is not naturally selectable. Indeed, as I have said many times, not even the engineered protein is naturally selectable.

    Therefore, the experiment tells absolutely nothing about neo darwinist evolution. When will you people admit it?

    Never, I suppose.

  258. 258
    gpuccio says:

    OMagain, lacking other “arguments”, becomes if possible even more trivial:

    “gpuccio, you obviously have the time to comment on my posts rather than the more specific more technical rebuttals others have made. Why is that?”

    Maybe I am fascinated by your personality.

    By the way, which “more technical rebuttals”?

    Does my answer to Allan Miller at #257 count?

    I will answer for the moment your very technical question:

    “For example, are all functional proteins designed?”

    OK. I tend to believe that they are, but what I believe is of no importance.

    The correct question is: for what functional proteins can we reasonably infer design?

    And I have given the answer many times:

    For all proteins which exhibit a total functional information (or an informational transition) higher than an appropriate threshold (150 bits are good, for me), and for which there is no trace of a detailed naturally selectable pathway that can lower the probabilistic barriers (that is easy: there is no such trace at all for any complex protein).

  259. 259
    gpuccio says:

    Rumracket at TSZ reaches new peaks of his favourite quality:

    “A human being being within a few meters of the test tube isn’t going to make ATP binding suddenly appear where it would not be if the human stepped further away. Gpuccio’s excuse couldn’t be any more ridiculous even if he tried.”

    Obviously, the fact that the human being has set up columns which can bind proteins with ATP affinity, and performs mutational PCR followed by further column selection, is not relevant. The important thing is that the human being is within a few meters of the test tube. This is magic, after all.

    And of course nature is completely able to do the same. As OMagain has demonstrated many times, we can believe anything, if we try hard.

  260. 260
    gpuccio says:

    Rumracket tries again:

    (we can criticize these guys as much as we like, but they are really obstinate!).

    “ATP binding is a naturally selectable function. Countless critical regulatory elements and core metabolic enzymes have ATP binding pockets necessary for their current function. If tomorrow all the ATP binding capacity of Gpuccio’s cells disappeared, he’d die in less than a minute (and if he doesn’t have children already, his reproductive success would go to zero).”

    It is tiresome to explain neo darwinism to neo darwinists, but OK:

    The problem is simply: is the weak ATP binding in the protein which was present in the original library naturally selectable?

    IOWs (please, put your full attention on it, maybe you will understand): if such a sequence arose by chance in some living being, did it give some reproductive advantage, which allowed for its selection and fixation?

    If the answer is no, then the sequence is not naturally selectable.

    As I have said, there is no trace of demonstration the either the original sequence or the final engineered protein can confer some reproductive advantage in a living system.

    Are you aware of any evidence that I am not aware of?

  261. 261
    gpuccio says:

    Rumrackest adds:

    “But as I wrote already earlier, we can forget about Keefe and Szostak if it makes Gpuccio feel better, and start talking about other similar types of experiments, such as Hayashi et al 2006, where the selection criterion was the capacity of a bacteriophage to infect a bacterium, using a randomized ~140 amino acid protein subdomain. So the reproductive success here was that of a bacteriophage. That’s textbook natural selection. What’s Gpuccio’s excuse going to be now?”

    No excuse. I am a great fan of the Ayashi paper, as everybody who reads my posts should know.

    It is one of the few experiments which deal really with NS.

    The result show clearly that, while some low level rescue of function (in a system where the function is already present and organized, but has been partially knocked out) is possible, but that the rugged nature of the functional landscape makes it practically impossible to reach the wildtype, or any comparable functionality: indeed, none of the selected sequences has any sequence homology with the wildtype. (So much for connected spaces!) And the authors compute that an initial library of 10^70 would be necessary to reach the wildtype.

    You see, even if you darwinists seem not to understand it, the rugged landscape is the death of any possible connected space.

  262. 262
    gpuccio says:

    Allan Miller:

    So the peptide space is grudgingly accepted to be rich in ‘function’ – defined as showing up in some assay for that function – but poor in ‘naturally selectable function’? How has that been determined? You can’t just look at the space and declare it so. It renders all the ooga-booga probability calculations (and all effort spent addressing them) a waste of time, since selection is entirely context dependent. There is no information regarding it anywhere in protein space.

    If you read my OP about functional information:

    http://www.uncommondescent.com.....n-defined/

    you will see that “function” is a very generic concept, unless it is linked to precise definitions and context.

    In ID, for example, function in itself is of no importance. What is important is only the quantity of information connected to some defined function. Complex functional information points to design, not function in itself.

    In neo darwinisms, the only function that counts is naturally selectable function. So, it is the burden of neo darwinists to show that naturally selectable functions exist with some relevant frequency in random libraries.

    That’s what Keefe and Szostak’s paper is supposed to do.

    It’s not what it does. It simply uses a very generic concept of function, and then gives the illusion that the results can apply to naturally selectable function.

    And you neo darwinists fall for it! So much for skepticism.

    So your position becomes that NS of new complex functions arising from RV cannot be detected, but can exist, like the missing intermediates, and like all the myths of neo darwinism.

    Have you ever thought that science should be based on facts, and not only on conjectures (and rather unreasonable conjectures, for that!)

  263. 263
    Mung says:

    And you neo darwinists fall for it! So much for skepticism.

    Hanging out at a blog called “The Skeptical Zone” doesn’t make one a skeptic.

  264. 264
    Mung says:

    Therefore, the experiment tells absolutely nothing about neo darwinist evolution. When will you people admit it?

    My guess is at about the same time they admit a program designed to find a target phrase has nothing to do with neo darwinist evolution.

  265. 265
    gpuccio says:

    Mung:

    Evolutionary times, I suppose. 🙂

  266. 266
    gpuccio says:

    What a pity. The comments at TSZ have gone completely wild.

    No more arguments, no more reason.

    I will just answer this brief question from Allan Miller, who remains after all one of the most “normal” people there:

    “Good grief! ID of organismal proteins – how non-conjectural is that? Or is gpuccio of the “ID is not a science” school?”

    ID explains facts, and is motivated by facts. Functional information in proteins is a fact. My OP here is about facts.

    I copy here my question at #215. About a fact:

    “Astrotactin 2 is a 1339 AAs protein. 889 of them are identical in sharks and humans.The positives are 1048.

    I would really appreciate if our friends at TSZ could comment about this very simple fact.”

    On the other hand, missing intermediates, imaginary pathways, connections in proteins space, are all conjectures without a trace of support from facts, and against any rationale.

    So yes, ID is not conjectural, and neo darwinism is.

    And no, I am not of the “ID is not a science” school. ID is science. Completely empirical science.

  267. 267
    bill cole says:

    gpuccio

    OMagain: For all proteins which exhibit a total functional information (or an informational transition) higher than an appropriate threshold (150 bits are good, for me), and for which there is no trace of a detailed naturally selectable pathway that can lower the probabilistic barriers (that is easy: there is no such trace at all for any complex protein)

    pre Rumracket
    This is hilarious. Gpuccio is making a designer of the gaps-argument. Where we lack a sufficiently detailed phylogeny, that’s where the designer acted.

    The TSZ guys are bringing designer of the gaps arguments out. The use of straw-man arguments appears to signal the end of a viable challenge to your arguments at this point.

    The fact that the genome is a sequence appears to be a very difficult problem for Neo-darwinism and modern evolutionary theory including universal common descent.

  268. 268
    Mung says:

    The Ideologue Zone.

    Richardthughes suggested I should form my own blog. I think it will be a satire.

  269. 269
    gpuccio says:

    bill:

    “The TSZ guys are bringing designer of the gaps arguments out. The use of straw-man arguments appears to signal the end of a viable challenge to your arguments at this point.”

    I agree.

    We are going back to the beginning. CLAVDIVS started with a God of the gaps argument at #44.

    After having discussed that point in detail (see especially #86) I hoped that was that, but here we are again: our friends at TSZ, having no more arguments, are back to “designer of the gaps”.

    Well, at least they must have noticed that I have never made any reference to God. I should consider that progress, but I don’t know why, I am not so sure.

    The discouraging truth is: these people are well ready to pretend to discuss as far as they think they have obvious confutations of the opponent’s position. But, when their confutations meet explicit answers, they simple avoid any recognition of those answers. Which does not mean to agree, but simply to admit that some answer has been given.

    But no, one who gives answers becomes immediately a fool, a crypto-creationist, you name it, and arguments are abandoned to leave room to name calling, or other trivialities.

    The discussion at TSZ started about my mention of a plan. I have clarified what plan I meant. I have answered the stupid objections about considering humans the purpose of the plan (which had never been part of my reasoning). I have explained why I was using human molecules, answering the objections about that.

    We have discussed the infamous desk of cards argument. We have discussed Keefe and Szostak. We have discussed natural selection and intelligent selection. And many other important points.

    We have discussed my metrics based on conservation. Any kind of objections have been made. I have answered them.

    I have even presented a paper which uses a conservation based metrics.

    Has anyone considered my points, even to refute them? No. Each time I give a reasonable explanation, they go back to other old “arguments”, and in the end to name calling.

    Well, they may think that they are open minded, skeptics, capable of respectful discussion.

    Well, they are not.

    Of course, each of them is different, and I should make some acknowledgments of partial goodwill, occasionally. Even keiths has agreed with me on one point.

    But the general trend is discouraging. With all respect, due or not.

  270. 270
    gpuccio says:

    Mung:

    See previous post.

    However, when you open your Zone, please let me know. 🙂

  271. 271
    Dionisio says:

    gpuccio @266

    On the other hand, missing intermediates, imaginary pathways, connections in proteins space, are all conjectures without a trace of support from facts, and against any rationale.

    What about the powerful multi-domain “co-option” mechanisms that help to explain so many biology issues?
    🙂

  272. 272
    gpuccio says:

    Dionisio:

    And convergent evolution of hundreds of genes! 🙂

    But why do we call those natural ideas “conjectures”? We must really be the bad guys…

  273. 273
    Dionisio says:

    Definitely we have to humbly admit that the neo-Darwinian folks have more creative imagination than anyone else.
    They all could have made profitable careers writing “fascinating” pseudoscience nonsense fiction books for the numerous gullible readers out there.
    Actually some folks have become famous doing exactly that. Some of them have been mentioned in this site before.
    🙂
    However, with such prolific imaginations, it is difficult to understand why they get surprised by what they call intriguingly “unexpected” discoveries these days?
    It’s kind of an ironic contradiction that the same folks that on one hand impute to nature powerful (almost unrestricted) “quasi-magic” attributes, are surprised by so-called intriguingly “unexpected” discoveries made by researchers lately.
    Go figure! 🙂

  274. 274
    Dionisio says:

    gpuccio @272

    But why do we call those natural ideas “conjectures”?

    Simply because we don’t understand biology. Yes, that’s an embarrassing situation, but we have to face it and do something about it.
    We have been told many times to take basic biology courses so we can at least start to understand the clever neo-Darwinian literature, which is loaded with fascinating stories that we’re missing.
    🙂
    Now, jokes aside, for a number of years I was on the opposite side of this important debate.
    This means that I must be compassionate to those folks, because -as professor Tour said- they don’t know what they’re talking about.
    Actually, none of us know many things we’re seeing in biology these days.

  275. 275
    Dionisio says:

    gpuccio:

    You may want to look at this:

    http://www.uncommondescent.com.....ent-614293

  276. 276
    Dionisio says:

    gpuccio:

    You may like to read this too.

    Paper referenced @1773-1775 in this link:

    http://www.uncommondescent.com.....ent-614300

  277. 277
    gpuccio says:

    Dionisio at #275 and #276:

    Thank you.

    Both papers seem very pertinent to my OP indeed, because the 6 proteins I considered, with their functional novelty in vertebrates, are probably important actors in the geometry of the vertebrate brain, being implied in the regulation of neuronal migration.

    The central nervous system works as a whole (Figure ?(Figure1),1), and it is well established that the principles of structural design (spatial distribution, number and types of neurons, and synapses per volume, etc.) differ considerably in the different parts of the nervous system, as well as between species and strains.

    And:

    Both the concepts of homology and convergence can be united for a common aim: that of identifying the ‘geometry of life’ [41] whose algorithms, if uncovered, would enable an explanation […]

    […] what might be the laws of nature that can lead to nervous system centralization and the formation of brains, or their evolved reduction and loss several times during the course of evolution?

    It is becoming clear that more than genes, genomes and morphologies are needed to elucidate the origin and evolution of the nervous system, although a start has been made.

  278. 278
    Dionisio says:

    gpuccio:

    They wrote:

    It is becoming clear that more than genes, genomes and morphologies are needed to elucidate the origin and evolution of the nervous system, […]

    Why is taking them so long to arrive at such an obvious conclusion?

    Perhaps the expression:

    It is becoming clear that more than […] are needed to elucidate […]

    will become a standard template in future biology research papers. Just fill in the […] to complete the sentence in any given biology-related context. 🙂

  279. 279
    Dionisio says:

    gpuccio:

    You may want to look at the papers referenced @1047-1055 in this link:

    http://www.uncommondescent.com.....ent-614345

  280. 280
    gpuccio says:

    Dionisio:

    “Coevolution Theory of the Genetic Code at Age Forty: Pathway to Translation and Synthetic Life”

    Wow!!!!!!!

    I was not aware of the level of abstracted imagination that OOL theories can achieve. Here, we are beyond even the best and most creative science fiction writers of the good old times.

    Seriously, this paper is really interesting as a catalogue of the thousands of logical impossibilities of a non design theory of OOL (the authors are well aware of most of them) and of the extremes to which human imagination can go to explain what cannot be explained!

    Really, I am amazed. I suppose this is considered science, and published in a scientific journal after peer review, while our discussions here are conjectural. 🙂

    I really liked their frequent use of the term “prescriptive information”. These guys must have learned a lot from ID and Abel.

    The “peptidated RNA world” is fun, but what about these other examples?

    Aminoacyl-tRNA synthetases and the evolution of coded peptide synthesis: the Thioester World.

    Jakubowski H

    Coded peptide synthesis must have been preceded by a prebiotic stage, in which thioesters played key roles. Fossils of the Thioester World are found in extant aminoacyl-tRNA synthetases (AARSs). Indeed, studies of the editing function reveal that AARSs have a thiol-binding site in their catalytic modules. The thiol-binding site confers the ability to catalyze aminoacyl~coenzyme A thioester synthesis and peptide bond formation. Genomic comparisons show that AARSs are structurally related to proteins involved in sulfur and coenzyme A metabolisms and peptide bond synthesis. These findings point to the origin of the amino acid activation and peptide bond synthesis functions in the Thioester World and suggest that the present-day AARSs had originated from ancestral forms that were involved in noncoded thioester-dependent peptide synthesis.

    And:

    The evolution of Class II Aminoacyl-tRNA synthetases and the first code.

    Smith TF, Hartman H.

    Class II Aminoacyl-tRNA synthetases are a set of very ancient multi domain proteins. The evolution of the catalytic domain of Class II synthetases can be reconstructed from three peptidyl-hairpins. Further evolution from this primordial catalytic core leads to a split of the Class II synthetases into two divisions potentially associated with the operational code. The earliest form of this code likely coded predominantly Glycine (Gly), Proline (Pro), Alanine (Ala) and “Lysine”/Aspartic acid (Lys/Asp). There is a paradox in these synthetases beginning with a hairpin structure before the Genetic Code existed. A resolution is found in the suggestion that the primordial Aminoacyl synthetases formed in a transition from a Thioester world to a Phosphate ester world.

    Worlds seem to abound in the world of OOL theories.

    Seriously, and obviously out of personal ignorance, I ask a simple question: in the peptidated RNA world, or in any other imaginary world where ancestors of aaRNA synthetases seemed to exist (according to these authors), where was the information for these peptides and proteins? How was it genetically transmitted, in the absence of a code and a translation system? Were the proteins immortal, and simply passed from cell to cell? Were they assembled by luck? By complex specific biochemical systems? Whose information arose from?

    Just to understand. Not OOL, of course, I don’t believe that any of this can help understand OOL, but rather the possible internal “logic” of OOL theories imagination.

  281. 281
    gpuccio says:

    Dionisio:

    When I read stuff like that, I am reminded of the famous Sherlock Holmes quote:

    “How often have I said to you that when you have eliminated the impossible, whatever remains, however improbable, must be the truth?”

    The impossible, of course, is design.

    OK, at least we have found some epistemological support to OOL theories: Conan Doyle is better than nothing! 🙂

  282. 282
    Dionisio says:

    gpuccio

    Excellent comments. Thank you.
    Refreshing sense of humor too. 🙂

  283. 283
    Dionisio says:

    gpuccio @266:

    What a pity. The comments at TSZ have gone completely wild.
    No more arguments, no more reason.

    Couldn’t they do better than that?

    🙂

  284. 284
    Dionisio says:

    gpuccio @280

    “Worlds seem to abound in the world of OOL theories.”

    Well, in the multiverse theory everything is possible, isn’t it?

    🙂

  285. 285
    Dionisio says:

    gpuccio:

    Someone might need help to translate Mina’s song from Italian to English:

    http://www.uncommondescent.com.....ent-614429

    🙂

  286. 286
    gpuccio says:

    Dionisio:

    Here is the main (and simple) concept:

    “Parole, parole, parole
    Parole parole, parole
    Parole, parole, parole
    Parole, parole, parole, parole
    Parole, soltanto parole
    Parole tra noi”

    “Words, words, words
    Words, words, words
    Words, words, words
    Words, words, words, words
    Words, only words
    Words between us”

    Ah, Mina! 🙂

  287. 287
    Dionisio says:

    gpuccio:

    Thank you for the translation @286.

    Apparently the person referred to @285 hasn’t come back to continue ‘chatting’.

    I have a simple question:

    In the abstract of this paper:

    http://journal.frontiersin.org.....00067/full

    is there (d) between (c) and (e)?

    Just curious to know if this is right.

    Thank you.

  288. 288
    Dionisio says:

    gpuccio:

    I’d like to know your opinion on this:

    What do you think of the comments posted @1804-1805 in the following link?

    http://www.uncommondescent.com.....ent-614578

    BTW, this is in reference to the concluding remarks in the same paper referenced @287.

    Thank you.

  289. 289
    Dionisio says:

    gpuccio:

    The long title of the paper referenced @287 reminds me of the long title of a song they played on the radio before I went to high school. The original English title was long:
    “Sgt. Pepper’s Lonely Hearts Club Band”,
    but the Spanish translation was even longer:
    “La Banda del Club de Corazones Solitarios del Sargento Pimienta”. That was longer than the entire lyrics of many songs. 🙂

  290. 290
    gpuccio says:

    Dionisio:

    Sorry, I was away for a couple of weeks.

    OK, the abstract:

    (a) the duration of the proliferative phase of the neuroepithelium, (b) the relative duration of symmetric (expansive) versus asymmetric (neuronogenic) sub phases, ( c) the spatial organization of each kind of cell division, (e) the time of determination and cell cycle exit and (f) the time of onset of the post-mitotic neuronal migration and (g) the time of onset of the neuronal structural and functional differentiation.

    And the text:

    (a) the duration of the proliferative phase of the OT neuroepithelium, (b) the relative duration of symmetric (expansive) versus asymmetric (neuronogenic) subphases, ( c) the dynamics and (d) the spatial organization of each kind of cell division, (e) the time of determination and cell cycle exit and (f) the time of onset of the post-mitotic neuronal migration and (g) the time of onset of neuronal function.

    So, it seems that in the abstract they just forgot to include “the dynamics”.

  291. 291
    gpuccio says:

    Dionisio:

    “It is presumed that the modern neurosciences will accumulate enough information as to describe the human mind in terms of the function of interconnecting cortical and subcortical neuronal circuit networks.”

    Wrong presumption. No description of subjective experiences “in terms of” neuronal or other objective configurations will ever be achieved.

    It is certainly possible, however, to describe how subjective experiences are linked to objective configurations of the brain, and vice versa. We are describing an interface, and that is not an explanation “in terms of”.

    “While this could be a long-range goal, a less ambitious objective could be the description of the behaviors of lower species in terms of defined patterns of activity of the above mentioned neuronal circuits.”

    Less ambitious is better! 🙂

    However, here again, we are simply describing a relation between behaviors and neuronal patterns. Behaviours are objective observations too, so a relationship is easier to be made, but again it is just a connection between objective observations which are connected through an interface which reasonably implies subjective experiences, and not an explanation “in terms of”.

  292. 292
    gpuccio says:

    Dionisio:

    “The peer-review publications should stand firmly against the consumption of any hallucinogenic drugs by the authors before their papers get published. 🙂 ”

    Who are we to judge scientists’ lifestyles? 🙂

    “BTW, is psychology a science?”

    Big question. I would say it is, if it is treated scientifically.

  293. 293
    gpuccio says:

    Dionisio:

    “Sgt. Pepper’s Lonely Hearts Club Band”

    Ah, what beautiful memories of the old times!

    I don’t believe that anyone has ever even tried to translate that into italian! 🙂

    It would be:

    “La banda del club dei cuori solitari del Sergente Pepper”

    (I would definitely leave “Pepper” untranslated).

  294. 294
    Dionisio says:

    gpuccio

    Thank you for your comments.

    No description of subjective experiences “in terms of” neuronal or other objective configurations will ever be achieved.

    It is certainly possible, however, to describe how subjective experiences are linked to objective configurations of the brain, and vice versa. We are describing an interface, and that is not an explanation “in terms of”.

    Behaviours are objective observations too, so a relationship is easier to be made, but again it is just a connection between objective observations which are connected through an interface which reasonably implies subjective experiences, and not an explanation “in terms of”.

    That’s clear. No additional comments required.

  295. 295
    Axel says:

    ‘There are, in natural history, a few fundamental transitions which scream design more than anything else.’

    The design throughout nature is unambiguous and indisputable, and is most certainly not unintelligent design.

    Random is, as random does, effectively creating unintelligibility in very principle ; in practice, a jumble.

    Unintelligent design ? No. Because such would be an oxymoron, never mind that it is the hegemonic oxymoronic paradigm of the atheists’ scientism cult. Might is no more right in the intellectual sphere than it is in the moral sphere, is it ?

  296. 296
    Axel says:

    ‘“BTW, is psychology a science?”

    Big question. I would say it is, if it is treated scientifically.’

    Just trying to piggy-back on empirical science, which needed to strip away consideration of everything else of value, indeed, of greater value than that of brute matter, to achieve such notable success within its own competence.

    His opening paragraph certainly dates Aldous Huxley’s essay at the back of HarperCollins’ publication of his work, The Perennial Philosophy :

    ‘No account of the scientific picture of the world and its history would be complete unless it contained a reminder of the fact, frequently forgotten by scientists themselves, that this picture does not even claim to be comprehensive . From the world we actually live in, the world that is given by our senses, our intuitions of beauty and goodness, our emotions and impulses, our moods and sentiments, the man of science extracts a simplified private universe of things possesing only those qualities which used to be called ‘primary’. Arbitrarily, because it happens to be convenient, because his methods do not allow him to deal with the immense complexity of reality, he selects from the whole of experience only those elements which can be weighed, measured, numbered, or which lend themselves in any other way to mathematical treatment. By using this technique of simplification and abstraction, the scientist has succeeded to an astonishing degree in understanding and dominating the physical environment. The success was intoxicating*, and with an illogicality which, in the circumstances, was doubtless pardonable, many scientists and philosophers came to imagine that this useful abstraction from reality was reality, itself.’

    He goes on to say that the meaninglessness that is the product of this grotesque over-simplification of reality ‘lends itself very effectively to furthering the ends of erotic or political passion ; in part to a genuine intellectual error – the error of identifying the world of science. a world from which all meaning and value has been deliberately excluded, with ulitmate reality.

    (This latter puts me in mind of the aptness of the application by someone to Lady Cardboard (Thatcher) of Oscar Wilde’s ‘bon mot : ‘She knows the price of everything and the value of nothing.’)

    And so it goes on. I need to reread it though, as its almost sixty years since I first read it.

  297. 297
    Axel says:

    I meant to add in a footnote, what a euphemistic, though customary, sense the word ‘intoxicating’ conveys here, in relation to its etymology :

    ‘The success was intoxicating, and with an illogicality which, in the circumstances, was doubtless pardonable, many scientists and philosophers came to imagine that this useful abstraction from reality was reality, itself.’

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