academic freedom Culture Darwinism Intellectual freedom Intelligent Design

If ID is dead, why are some obsessed with shutting it down?

Spread the love

Do scientists think more about sex or ID? That was an Enter Laughing question at Evolution News and Science Today but it prompts reflection on why some people in science seem driven around the bend by the idea of design in nature. And others alter their message to avoid confronting the questions:

First, if the critics are right to say ID is “dead,” why devote so much time to it? Evolution News reported in 2014 that an article in the journal Nature admitted that scientists self-censor criticisms of neo-Darwinism to avoid lending credence to ID. As Laland et al. (2014) conceded: “Perhaps haunted by the spectre of intelligent design, evolutionary biologists wish to show a united front to those hostile to science.” In 2017 we observed how Laland followed his own advice, refusing to admit in a report published in Trends in Ecology and Evolution that the 2016 Royal Society meeting included strong critiques of the neo-Darwinian paradigm. Clearly, ID arguments are potent, and evolutionary biologists are aware of this — which is why they admit they don’t like to acknowledge problems in the evolutionary consensus.

Second, intelligent design’s supposed negative impact is hyped beyond reason. The notion that “financing of research” in the U.S. is being hurt by ID is laughable. ID research gets exactly zero dollars from the Federal Government. From other sources, the amount of money available to fund ID research, though not trivial, is minuscule compared to the amount of money available for evolutionary science. No evolutionary scientist has any right to complain.

Third, it’s a shame that “20 percent of their time and brain power” is going to ID because the trend in thought is now running toward government-backed censorship.

Evolution News, “Scientist Admits Biologists Are Obsessed with Intelligent Design” at Evolution News and Science Today

Ah yes. Mutterings about the need for censorship. When we don’t have a reasonable response to a troubling topic, first, we self-censor. Then we censor anyone who raises it. Sure, guys. That’ll work.

The questions are still there but only for those capable of addressing them.

162 Replies to “If ID is dead, why are some obsessed with shutting it down?

  1. 1
    asauber says:

    We can see this phenomenon right here at UD too:

    ID Is Dead But We Have To Perpetually Spam It And Oppose Everything About It.

    All with apparently complete unawareness they are doing it.

    And someone thinks a rational conversation can be had?

    Andrew

  2. 2
    bill cole says:

    Science should be thinking about ID because it is the right comparison for examining many of the events in evolutionary history.

  3. 3
    PaoloV says:

    Asauber @1:

    And someone thinks a rational conversation can be had?

    That’s a good question.

    A fool takes no pleasure in understanding, but only in expressing his opinion. Proverbs 18:2 (ESV)

     

    NIV Study Bible Notes

    18:2 airing their own opinions. See Ecc 10:3.

    NKJV MacArthur Study Bible, 2nd Edition

    18:2 Cf. Eccl. 10:12–14.

    Do not speak in the hearing of a fool, for he will despise the good sense of your words.  Proverbs 23:9 (ESV)

     

    NIV Study Bible Notes

    23:9 scorn your prudent words. Fools “despise wisdom” (1:7) and hate knowledge and correction (1:2212:1). They heap abuse on one who rebukes them (9:7).

    NKJV MacArthur Study Bible, 2nd Edition

    23:9 This is true because fools hate wisdom (cf. 1:229:812:1).

    Reformation Study Bible provided by Ligonier Ministries.

    23:9 This short instruction repeats the meaning of proverbs such as 9:7 that indicate that the fool is unteachable (cf. Matt. 7:6).

    Answer not a fool according to his folly, lest you be like him yourself.
    Answer a fool according to his folly, lest he be wise in his own eyes.   
    Proverbs 26:4-5 (ESV)

     

    NIV Study Bible Notes

    26:4 Do not answer a fool according to his folly. Do not stoop to his level (see 23:9Mt 7:6 and notes).

    26:5 Answer a fool according to his folly. Sometimes folly must be plainly exposed and denounced. Thus vv. 4–5 do not contradict each other, as often claimed.

    NKJV MacArthur Study Bible, 2nd Edition

    26:45 answer a fool. Taken together, these verses teach the appropriate way to answer a fool (e.g., an unbeliever who rejects truth). He should not be answered with agreement to his own ideas and presuppositions, or he will think he is right (v. 4), but rather he should be rebuked on the basis of his folly and shown the truth so he sees how foolish he is (v. 5).

    Reformation Study Bible

    26:45 Taken together these verses illustrate the point that no proverb is intended to cover every possible situation. The apparent contradiction in the two proverbs indicates that proverbs must be appropriately applied. One situation demands that we avoid playing the fool’s game by giving an answer, while another demands that we expose the folly so that the fool is not considered wise.

  4. 4
    Seversky says:

    If ID Is Dead, Why Are Some Obsessed With Shutting It Down?

    Perhaps they want it dead and buried?

  5. 5
    JClark says:

    Any good, useful, healthy theoretical pursuit is built around punching holes in one’s understanding. It’s the failures that are sought. In this, I can’t help but feel that ID is, in essence, the actual science, the actual empirical study of evolution, whereas that which is named as evolution is just a weird (and long obsolete) interpretation.

    Even if we were to assume, for the sake of argument, that evolution the metaphysic would emerge victorious, ID would at least be the work debt that evolutionary theory has thus far evaded. It’s going to come due; you can’t put it off forever.

  6. 6
    jawa says:

    Is @4 an example of what is said @3 ?
    😉

  7. 7
    jawa says:

    Alexa ranks…….top%…….top%
    EN:……. 235,528…….0.3%…….1%
    UD:……. 661,690…….0.7%…….1%
    TO:……. 672,565…….0.7%…….1%
    SW:……. 1,109,295…….1.2%…….2%
    PT:……. 1,470,590…….1.5%…….2%
    PS:……. 4,635,300…….4.7%…….5%
    TSZ:……. 6,755,069…….6.8%…….7%
    Based on 100M active websites.
    Comparable peers according to Alexa associations and inter contributions.

    Curiously SW was less than 100K behind UD very recently, but suddenly worsened. What happened?

  8. 8
    BobRyan says:

    Seversky

    Perhaps it has more to do with the complete lack of any evidence to support Darwinism. The scientific method is not complicated to understand. A hypothesis remains a hypothesis until such a time as it has been observed and the results replicated. No one has ever witnessed macro-evolution and the results have never been replicated. In other words, macro-evolution remains a hypothesis.

    A multiverse has never been witnessed and the results never replicated. Should we skip the steps and call the multiverse a scientific theory?

  9. 9
    OLV says:

    That’s a panic reaction.
    Are they anxious because the have to find a Darwin’s successor?

  10. 10
    asauber says:

    “Perhaps they want it dead and buried?”

    Sev,

    They sure do. Why? What is it about ID that motivates some to require an extreme Final Solution for it?

    Get your psychology notes out. 😉

    Andrew

  11. 11
    ET says:

    In order for ID to be dead, someone has to come up with a viable scientific alternative. And no one has. That says it all, really.

  12. 12
    chuckdarwin says:

    It is a good thing that scientists are obsessed with Intelligent Design for three reasons. First, although ID proponents have attempted to argue that ID is not religiously based (viz. biblically based), recent events show that it is not just implicitly Christian-based, but explicitly so. A few weeks back, on the podcast Unbelievable, James Tour, the ID chemist, went off on a five minute, pre-discussion rant about being a Christian, his strong faith, how religion informs science, etc. He was debating Lee Cronin, famed biochemist at the U of Glasgow, and even Justin Brierley seemed a bit uncomfortable and embarrassed by Tour’s tirade. Tour’s comments were completely inapposite and added nothing to the conversation except to demonstrate that Tour is a Christian zealot. Second, ID kingpin, Stephen Meyer was scheduled to publish his new opus this spring “Return of the God Hypothesis.” There is nothing even remotely ambiguous about the title of Meyer’s book. He is also a Christian zealot. For unexplained reasons, publication of the book has been delayed a year. Finally, even a superficial poll of the members of the Discovery Institutes so called Center for Science and Culture, demonstrates that every board member, scholar and staff member is an evangelical Christian or Catholic. The only exception is the always-annoying, David Berlinski who purports to be agnostic.

    The conservative, Christian pedigree of the ID movement has never been scientifically neutral, it has always been religiously motivated. The judge in the Dover trial quickly discovered that fact. If ID were to confine itself to operating within the scientific community (where it is universally ignored), it likely would not survive a couple more years. HOWEVER, the reason that it is important for scientists to stay obsessed with ID pertains to its continual attempts to invade the public schools, particularly high schools. State school boards in radicalized, evangelical dominated states continue to try and ban the teaching of evolution, at worst, or have it placed on par with ID, at best. These attempts, if successful would destroy science education in the US. According to PEW, “among the 35 members of the Organization for Economic Cooperation and Development, which sponsors the PISA [Program for International Student Assessment] initiative, the U.S. ranked 30th in math and 19th in science.” These scores are appalling for the richest and most technologically advanced country in the world.

    So I cheer the scientists that are ever vigilant about ID, they are doing what needs to be done to protect the integrity of science education in the US.

  13. 13
    ET says:

    ID is not religiously based. One can be an atheist and accept ID. One cannot be a materialist and accept ID, though.

    And there isn’t any scientist that argues against ID who can present a scientifically viable alternative. And that is very telling

    The US is ranked low in science due to the fact that the US teaches the unscientific evolutionism is science classrooms.

  14. 14
    asauber says:

    Chuckdarwin,

    Thank you for illustrating your position. You oppose Christianity. What a surprise.

    Andrew

  15. 15
    Ed George says:

    BR

    Perhaps it has more to do with the complete lack of any evidence to support Darwinism.

    Except for comparative anatomy, the fossil record, genomics, cladistics, proteomics, geology, stable isotopes analysis, antibiotic resistance, molecular biology, plate tectonics, ….

  16. 16
    JVL says:

    ET: One cannot be a materialist and accept ID, though.

    I think alien being can fit into a materialist world view nicely. Or are you saying ID is not about aliens?

  17. 17
    ET says:

    According to ID neither natural selection, drift nor any other materialistic, i.e. blind and mindless, process can produce living organisms. The same holds for the systems and subsystems that make up living organisms.

    But yes, ID is OK with an extraterrestrial OoL for the Earth.

  18. 18
    ET says:

    Acartia Eddie:

    Except for comparative anatomy, the fossil record, genomics, cladistics, proteomics, geology, stable isotopes analysis, antibiotic resistance, molecular biology, plate tectonics, ….

    None of which support Darwinism. Comparative anatomy doesn’t say anything about a mechanism. The fossil record doesn’t say anything about a mechanism. Genomics doesn’t say anything about a mechanism. Cladistics doesn’t say anything about a mechanism. Proteomics doesn’t say anything about a mechanism. Darwinism is all about the mechanism.

    The main evidence for macroevolution, over on talk origins, is absent a mechanism. Which is strange because their “evidence” is pattern based and patterns depend on mechanisms. But the point is their evidence does not support Darwinism.

    Clearly Acartia Eddie is just a clueless troll. Acartia Eddie is just a grand equivocator, oblivious to what is actually being debated. And clearly quite content with his willful ignorance.

  19. 19
    JClark says:

    Chuckdarwin @ 12

    The majority of the fathers of modern science were Christians who had no issue speaking up for Jesus. I don’t see the problem.

    In any case, appeal to motive is simply ad hominem. Hit me good with the predictive usefulness of evolutionary theory; something that doesn’t expound on arbitrary mythology outside of empiricism; make claims about entropy that are simply nonsense in any applied field; or reach for teleology that doesn’t even belong to it; and I, too, will fear for its loss.

  20. 20
    BobRyan says:

    ET @ 18

    Nice response to a Darwinist who fails to see the lack of evidence and points to everything as evidence where none exists.

  21. 21
    jawa says:

    Chuckdarwin @12:

    The problem with Dr Lee Cronin is that in his appearances at Unbelievable? he has not been able to show anything that gives at least a hint of how he could attempt to win the coveted Evo2.0 OOL $10M prize. James Tour’s main point was that every discovery in biology research is taking the finish line farther away from Dr Cronin. The hard problem he’s facing is getting harder with every discovery reported in the research literature these days. That’s what transpires from watching the Unbelievable? program. Dr Tour scored the slam dunks while Dr Cronin couldn’t even hold the ball in his hands. Regardless of the brand of the sneakers the players were wearing. That’s on the side. Dr Cronin got three strikes and was out. Pretty soon the game should be over.

  22. 22
    ET says:

    BobRyan- Their equivocation is pathetic. All alleged evidence for “evolution” is automatically also evidence for Darwinism, i.e. blind watchmaker evolution. “Ed George” is infamous for that sort of cowardly equivocation. It, along with lying and bluffing, are all they have. So they play them to the fullest.

  23. 23
    BrunoAr says:

    When ID proponents use the term “intelligent,” they simply seek to indicate that a structure has features requiring a mind capable of forethought to design the blueprint. But does intelligent design require perfect design?

  24. 24
    Silver Asiatic says:

    CD @ 12

    That was an interesting and concise overview of a popular anti-ID position. You brought together the key points, that have been made somewhat continually, since Dover, at least.
    1. Christians support ID and therefore it is biased and not scientific
    2. True (Darwinian) scientists are obsessed with ID because there are continual attempts for ID to enter schools.

    There are some contradictions, however.
    Point #1 above is not a scientific critique, but rather, a sociological one. ID is a scientific proposal, so what difference does it make if all its supporters are Christian? Most Darwinists are materialists, so is that enough to falsify it as a biased research project? It could be, but ID actually looks at the Darwinian claim of science and finds it lacking.
    ID is a non-materialist viewpoint, so why should it be troublesome that ID supporters are non-materialist (most are Christian)? David Klinghoffer who runs Evolution News is Jewish. But why not just say that most IDists are theistic? Isn’t that the same criticism? “ID is false because most of its scientists believe that God exists”. Ok, that’s a nonsensical argument.

    The other contradiction that I see all the time is that ID is “trying” to get into schools. However, thanks to vigilant Darwinists, this doesn’t happen. Dover made it illegal. There are no ID biology books being used in schools. ID has no standing in the scientific community (in your perspective.
    However, with all of that, you site statistics:

    “among the 35 members of the Organization for Economic Cooperation and Development, which sponsors the PISA [Program for International Student Assessment] initiative, the U.S. ranked 30th in math and 19th in science.” These scores are appalling for the richest and most technologically advanced country in the world.

    That’s the contradiction. Blame for the “appalling” results in science falls directly on the Darwinists (at least in biology). But the anti-ID argument is going to try to say that “because people are unsuccessfully trying to infiltrate science classrooms, the Darwinists who run things cannot teach properly”?
    No. Darwin rules unopposed in the classroom. The results are an appalling ignorance. ID has not been tested or measured in the classroom.

    So I cheer the scientists that are ever vigilant about ID, they are doing what needs to be done to protect the integrity of science education in the US.

    I think you can see that you just refuted yourself. What “integrity in science education” are you talking about? The “integrity” that caused a ranking of 19 out of 35 in science?
    You can’t have it both ways.

  25. 25
    OLV says:

    ID will be falsified the day somebody could show how to get -without the guidance of any conscious agent- biological systems that have things like this :

    Signal transmission through elements of the cytoskeleton form an optimized information network in eukaryotic cells

    Survival and proliferation of living systems require them to continuously acquire, process, and respond to information from the environment for threats, opportunities, or (in the case of multicellular organisms) instructions from local tissue

    eukaryotes use this mode of signal transmission [wire-like flow of electrons and ions along elements of the cytoskeleton] to convey spatial and temporal environmental information from the cell membrane to the nucleus. The cell membrane, as the interface between intra- and extra-cellular environments, is the site at which much external information is received.

    transmembrane ion gradients permit information acquisition when an environmental signal interacts with specialized protein gates in membrane ion channels and producing specific ions to flow into or out of the cell along concentration gradients. The resulting localized change in cytoplasmic ion concentrations and charge density can alter location and enzymatic function of peripheral membrane proteins. This allows the cell to process the information and rapidly deploy a local response.

    transmission of information received and processed in and around the cell membrane by elements of the cytoskeleton to the nucleus to alter gene expression.

    signal transmission by ion flow along the cytoskeleton is highly optimized.

    microtubules, with diameters of about 30?nm, carry coarse-grained Shannon information to the centrosome adjacent to the nucleus with minimum loss of input source information.

    microfilaments, with diameters of about 4?nm, transmit maximum Fisher (fine-grained) information to protein complexes in the nuclear membrane.

    These previously unrecognized information dynamics allow continuous integration of spatial and temporal environmental signals with inherited information in the genome.

    the elements of the cytoskeleton can interact in complex way with molecular transduction pathways.

     complex network for signal transmission and analysis that permits rich information dynamics that likely augments and modifies the more well-known and studied information found  molecular pathways (e.g. the MAPK pathway) that carry information following ligand binding to a membrane receptor to the nucelus.

    Or this:

    The cell-wide web coordinates cellular processes by directing site-specific Ca2+ flux across cytoplasmic nanocourses

    our observations point to the incredible signalling potential that may be afforded by modulating quantum Ca2+ flux on the nanoscale, in support of network activities within cells with the capacity to permit stimulus-dependent orchestration of the full panoply of diverse cellular processes. Perhaps more importantly, the cellular intranet conferred by the SR and its associated network activities are not hardwired, reconfiguring to deliver different outputs during phenotypic modulation on the path, for example, to cell proliferation. This in itself suggests that cytoplasmic nanocourses may be common to but vary in nature between different cell types. Supporting this, NE invaginations are a feature of many cell types while other junctional complexes of the S/ER vary by cell type and even between different smooth muscles.

     
    [emphasis added]

  26. 26
    jawa says:

    Any news from the OOL front lately?

    Have Dr Cronin and Dr Szostak made any progress in the pursue of the coveted Evo2.0 OOL $10M prize? There yet? 🙂

    Did Dr Cronin finally get the point of what Dr Tour told him at their “Unbelievable” chat?
    Did the penny drop yet?
    Or still struggling to understand it?
    🙂

  27. 27
    OLV says:

    ID could be falsified the day somebody would show how to get -without the guidance of any conscious agent- biological systems that have things like this :

    Choreography of molecular movements during ribosome progression along mRNA
     

    During translation elongation, ribosome translocation along an mRNA entails rotations of the ribosomal subunits, swiveling motions of the small subunit (SSU) head and stepwise movements of the tRNAs together with the mRNA. Here, we reconstructed the choreography of the collective motions of the Escherichia coli ribosome during translocation promoted by elongation factor EF-G, by recording the fluorescence signatures of nine different reporters placed on both ribosomal subunits, tRNA and mRNA. We captured an early forward swiveling of the SSU head taking place while the SSU body rotates in the opposite, clockwise direction. Backward swiveling of the SSU head starts upon tRNA translocation and continues until the post-translocation state is reached. This work places structures of translocation intermediates along a time axis and unravels principles of the motions of macromolecular machines.

  28. 28
    jawa says:

    Alexa ranks
    EN:……. 235,112
    TO:……. 654,740
    UD:……. 697,964
    SW:……. 949,491
    PT:……. 1,471,061
    PS:……. 2,593,807
    TSZ:….. 6,757,500

    PS has shown a substantial improvement

  29. 29
    BobRyan says:

    Intelligent Design explains the laws of physics, the existence of math, any origin of the universe which does include Big Bang, the uniqueness of man, the difference between the brain and the mind, the origin of life, the existence of every species that has ever existed and our ability to wonder about the heavens. Remove the intelligence and you have no explanation for any of it. Is it really difficult to believe something with far greater intelligence than man is responsible for everything?

  30. 30
    JVL says:

    BobRyan: the uniqueness of man

    Interesting thought: if we someday discover aliens just as intelligent as ourselves would you assume they were also intelligently designed? (You”d have to I think ’cause you believe there is an intelligence behind everything.) So, would man then still be unique?

  31. 31
    ET says:

    Yes, humans will still be remarkable, special, or unusual.

  32. 32
    OLV says:

    Here are some of the most recent attempts to figure out how water got into the coconuts:
    Circular Code Motifs in the Ribosome: A Missing Link in the Evolution of Translation?

    The origin of the genetic code remains enigmatic five decades after it was elucidated, although there is growing evidence that the code coevolved progressively with the ribosome. A number of primordial codes were proposed as ancestors of the modern genetic code, including comma-free codes such as the RRYRNY, or GNC codes (R = G or A, Y = C or T, N = any nucleotide), and the X circular code, an error-correcting code that also allows identification and maintenance of the reading frame. It was demonstrated previously that motifs of the X circular code are significantly enriched in the protein-coding genes of most organisms, from bacteria to eukaryotes. Here, we show that imprints of this code also exist in the ribosomal RNA (rRNA). In a large-scale study involving 133 organisms representative of the three domains of life, we identified 32 universal X motifs that are conserved in the rRNA of >90% of the organisms. Intriguingly, most of the universal X motifs are located in rRNA regions involved in important ribosome functions, notably in the peptidyl transferase center and the decoding center that form the original “proto-ribosome.” Building on the existing accretion models for ribosome evolution, we propose that error-correcting circular codes represented an important step in the emergence of the modern genetic code. Thus, circular codes would have allowed the simultaneous coding of amino acids and synchronization of the reading frame in primitive translation systems, prior to the emergence of more sophisticated start codon recognition and translation initiation mechanisms.

    The primordial tRNA acceptor stem code from theoretical minimal RNA ring clusters

    The aim is to understand what makes RNA rings such useful, and perhaps efficient, simulators of prebiotic evolution, independently of the possibility that RNA rings are the actual primordial sequences.

    theoretical RNA rings evolved along physicochemical constraints affecting nucleotide substitutions, apparently devoid of effects on their coding properties on amino acid sequences, in line with a pre-translational origin of diversification of RNA rings that would at a later stage become the population of primordial coding and decoding RNAs.

     
    Comparisons Between Small Ribosomal RNA and Theoretical Minimal RNA Ring Secondary Structures Confirm Phylogenetic and Structural Accretion Histories

    It is probable that the structural methods are more prone to errors due to evolutionary convergences than the phylogenetic method, though convergences remain the main difficulty in reconstructing evolution.

    Origin and Evolution of the Universal Genetic Code

    We propose an experimentally testable scenario for the evolution of the code that combines recognition of amino acids by unique sites on proto-tRNAs (distinct from the anticodons), expansion of the code via proto-tRNA duplication, and frozen accident.

    The problems of the nature, origin, and evolution of the genetic code appear to be unique in combining extreme outward simplicity with excruciating difficulty.

    In our view, theoretical study of the genetic code as a cryptographic problem has largely run its course. The best hope for further progress in understanding the origin and evolution of the code seems to lie with the technically challenging but conceptually clear experimentation aiming at recapitulation of the inferred steps in the translation system evolution.

    Evolution of Life on Earth: tRNA, Aminoacyl-tRNA Synthetases and the Genetic Code

    Life on Earth and the genetic code evolved around tRNA and the tRNA anticodon. We posit that the genetic code initially evolved to synthesize polyglycine as a cross-linking agent to stabilize protocells. We posit that the initial amino acids to enter the code occupied larger sectors of the code that were then invaded by incoming amino acids. Displacements of amino acids follow selection rules. The code sectored from a glycine code to a four amino acid code to an eight amino acid code to an ~16 amino acid code to the standard 20 amino acid code with stops. The proposed patterns of code sectoring are now most apparent from patterns of aminoacyl-tRNA synthetase evolution. The Elongation Factor-Tu GTPase anticodon-codon latch that checks the accuracy of translation appears to have evolved at about the eight amino acid to ~16 amino acid stage. Before evolution of the EF-Tu latch, we posit that both the 1st and 3rd anticodon positions were wobble positions. The genetic code evolved via tRNA charging errors and via enzymatic modifications of amino acids joined to tRNAs, followed by tRNA and aminoacyl-tRNA synthetase differentiation. Fidelity mechanisms froze the code by inhibiting further innovation.

     
     
    Hey, at least they’re trying hard.
    🙂

  33. 33
    JVL says:

    ET: Yes, humans will still be remarkable, special, or unusual.

    On what basis?

    What if an alien culture had a record of a saviour who died for their sins and was resurrected?

    Is it not possible for an alien culture to have equal standing as humans?

  34. 34
    Ed George says:

    JVL

    Is it not possible for an alien culture to have equal standing as humans?

    ID would not have a problem with this. 99% of ID proponents, however, would. Makes one wonder about the origin of ID.

  35. 35
    ET says:

    Acartia Eddie:

    ID would not have a problem with this. 99% of ID proponents, however, would.

    Liar. Does lying about other people make you feel better?

    Makes one wonder about the origin of ID.

    The two don’t have anything to do with each other. Obviously Acartia Eddie is proud to be a desperate fool

  36. 36
    ET says:

    JVL:

    On what basis?

    The diversity of life on Earth alone is enough.

    What if an alien culture had a record of a saviour who died for their sins and was resurrected?

    That wouldn’t make us any less remarkable, special or unusual. Our planet already hit that mark. It wouldn’t matter if a million earth like planets were found. Compared to the vastness of the universe, they would all still be remarkable, special and unusual.

    Is it not possible for an alien culture to have equal standing as humans?

    Of course it is. Perhaps you should buy a dictionary so you can understand what words mean.

  37. 37
    JVL says:

    ET: The diversity of life on Earth alone is enough.

    And if the diversity of life on another planet was the same?

    That wouldn’t make us any less remarkable, special or unusual. Our planet already hit that mark. It wouldn’t matter if a million earth like planets were found. Compared to the vastness of the universe, they would all still be remarkable, special and unusual.

    But then humans would not be so unique would they?

    Of course it is. Perhaps you should buy a dictionary so you can understand what words mean.

    I understand the definitions; I”m just trying to be sure you are applying them.

    Again, here is the question: If we found out that there was another whole bunch of alien beings who had the same orgin stories as us and the same saviour stories as us then could we say that humons are special in any way?

    Here’s another way of putting it: is it possible that the Christian saviour appeared to many different cultures and races and beings? So that there was no one chosen race or species or beings?

  38. 38
    ET says:

    JVL:

    And if the diversity of life on another planet was the same?

    That just makes my point. Humans and human-like aliens would be remarkable, special and unusual, when compared to the vast abundance of other life.

    But then humans would not be so unique would they?

    Gibberish. In the vastness of the universe all humans and human-like ETs would be remarkable, special and unusual.

    I understand the definitions; I”m just trying to be sure you are applying them.

    I don’t think you do understand the definitions.

  39. 39
    ET says:

    Now, if every planet in the universe had humans and human-like populations, then no, we humans on earth wouldn’t be unique at all.

  40. 40
    JVL says:

    ET: Now, if every planet in the universe had humans and human-like populations, then no, we humans on earth wouldn’t be unique at all.

    So, where is the line between unique and common?

    I think it’s easily possible that any alien beings we meet might have similar orgin stories and feel they are just as special as we are. So, where is the line?

  41. 41
    ET says:

    You’re a mathematician, figure it out. I would say that if humans make up 1% of all living organisms in the universe they would all still be remarkable, special and unusual. And 1% is very high, given what we know.

  42. 42
    JVL says:

    ET: I would say that if humans make up 1% of all living organisms in the universe they would all still be remarkable, special and unusual. And 1% is very high, given what we know.

    Would you say that any other intelligent alien species was also a product of design?

  43. 43
    ET says:

    JVL:

    Would you say that any other intelligent alien species was also a product of design?

    The odds favor it. But we have to wait and see.

  44. 44
    jawa says:

    Dr Tour and Dr Swamidass discuss OOL?

    https://youtu.be/yJgr38h_3H0

  45. 45
    JVL says:

    ET: The odds favor it. But we have to wait and see.

    Whoa! Hold the phone! You think fine-tuning says the universe was designed but you think it’s possible that complex life arose without being designed?

  46. 46
    jawa says:

    ET:

    You may want to read carefully what is said @3

  47. 47
    BobRyan says:

    JVL @ 40

    You state, “I think it’s easily possible that any alien beings we meet…” Does that mean you believe intelligent life exists in the universe? There is no evidence of their existence. What are you basing your belief on? I’m going to guess that it’s the vastness of the universe and there must be alien life out there somewhere.

  48. 48
    JVL says:

    BobRyan: Does that mean you believe intelligent life exists in the universe? There is no evidence of their existence. What are you basing your belief on? I’m going to guess that it’s the vastness of the universe and there must be alien life out there somewhere.

    I agree: there is ZERO evidence that there are any other highly intelligent beings in the universe except humans.

    I would be more surprised if there are not other intelligent beings than if there are because of the incredibly immense number of solars systems in the universe.

    What do you think?

  49. 49
    jawa says:

    Can someone explain how in the world the biological cells could have gotten these mechanisms established?
    Please note that the question is not how they got it but how it could be done. Thanks.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7104864/#!po=0.396825

  50. 50
    jawa says:

    BobRyan,

    You may want to read carefully what is said @3

  51. 51
    jawa says:

    Why do ID objectors usually refrain from engaging in scientific discussions (at technical level)? Is it lack of knowledge? Is it lack of humility? Is it lack of honesty? Is it something else?

  52. 52
    jawa says:

    Strong evidences that clearly support ID are popping up all over the map in research literature:

    Mechanistic insights into transcription factor cooperativity and its impact on protein-phenotype interactions

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949242/

  53. 53
    kairosfocus says:

    Folks, by now the issue, manifestly, is not weight or balance of evidence. That was settled once it was clear that alphanumerical algorithmic code was in the heart of the cell, complete with cases of interwoven code. The standard reaction as we saw in recent weeks? Obfuscation and denial. We are dealing with a mortally wounded dominant and domineering ideology lashing out even as it begins to bleed out. The willful unresponsiveness to manifest facts tells us all we need to know. KF

  54. 54
    ET says:

    JVL:

    You think fine-tuning says the universe was designed but you think it’s possible that complex life arose without being designed?

    LoL! We do NOT know, yet, if it is complex life, do we? That’s why I said what I did.

  55. 55
    ET says:

    JVL:

    there is ZERO evidence that there are any other highly intelligent beings in the universe except humans.

    That is pure nonsense.

    I would be more surprised if there are not other intelligent beings than if there are because of the incredibly immense number of solars systems in the universe.

    That has nothing to do with it.

  56. 56
    jawa says:

    KF @53:

    “ We are dealing with a mortally wounded dominant and domineering ideology lashing out even as it begins to bleed out. ”

    Spot on.

  57. 57
    jawa says:

    KF @53:

    “ by now the issue, manifestly, is not weight or balance of evidence. That was settled once it was clear that alphanumerical algorithmic code was in the heart of the cell, complete with cases of interwoven code. ”

    Spot on.

  58. 58
    JClark says:

    JVL @ 48:

    “I would be more surprised if there are not other intelligent beings than if there are because of the incredibly immense number of solars systems in the universe.”

    Letting the scenario be purely probabilistic and not worrying ourselves about deterministic exclusion, it reduces to a numerator over a denominator. The numerator is “incredibly immense”. How about the denominator?

    But isn’t this just headlining one term in Drake’s equation?

  59. 59
    ET says:

    Drake’s equation has been superseded by that of the Rare Earth hypothesis- rare earth equation. And the Rare Earth equation has been augmented by the Privileged Planet equation

  60. 60
    Ed George says:

    When we first started looking for exoplanets the technique used could only detect very large planets (eg Jupiter) in close orbits. If we stopped there, we would have concluded that solar systems with earth like planets are extremely rare. We now have techniques that can detect Solar systems with earth sized planets. Needless to say, we now have confirmed that earth sized planets are far more common than we could previously confirm.

  61. 61
    kairosfocus says:

    EG, the resources of the observable cosmos, stars and all are nowhere near enough to make alphanumeric code using life even remotely plausible on blind forces. KF

  62. 62
    ET says:

    LoL! @ Acartia Eddie- “Earth size” does not mean “Earth like”. Venus is “earth size”.

  63. 63
    OLV says:

    How secret conversations inside cells are transforming biology

    Organelles — the cell’s workhorses — mingle far more than scientists ever appreciated.

     
    ID evidence galore

  64. 64
    OLV says:

    ID evidence galore

    Here, there, and everywhere: The importance of ER membrane contact sites

    Some of the molecular machineries that regulate membrane tethering have now been identified, and thus MCSs can now be ascribed functions.
    In recent years, the involvement of MCSs in lipid and ion transport has been confirmed and some of the molecules and mechanisms involved in these processes have been pinpointed.

    Novel functions for MCSs, such as their crucial role in regulating organelle distribution and division, have also been identified.

    Moreover, it is becoming apparent that interorganelle communication is highly integrated in and subject to homeostatic regulation.

    For example, the establishment and regulation of ER-mitochondria and mitochondria-vacuole MCSs are interdependent and appear to respond to nutritional cues (22, 25, 27, 29).

    Notably, MCSs are linked to human diseases. Among the handful of proteins identified that specifically regulate MCS functions, a high proportion are mutated in a variety of diseases (127129).

    Footnote:
    ER: endoplasmic reticulum
    MCS: Membrane Contact Site

  65. 65
    OLV says:

    More ID evidences:

    Ribosome-associated vesicles: A dynamic subcompartment of the endoplasmic reticulum in secretory cells

    The endoplasmic reticulum (ER) is a highly dynamic network of membranes. Here, we combine live-cell microscopy with in situ cryo–electron tomography to directly visualize ER dynamics in several secretory cell types including pancreatic ?-cells and neurons under near-native conditions. Using these imaging approaches, we identify a novel, mobile form of ER, ribosome-associated vesicles (RAVs), found primarily in the cell periphery, which is conserved across different cell types and species. We show that RAVs exist as distinct, highly dynamic structures separate from the intact ER reticular architecture that interact with mitochondria via direct intermembrane contacts. These findings describe a new ER subcompartment within cells.

    The mechanisms by which RAVs emerge from the ER are unknown.

    the machinery for local translation of the protein products remains poorly defined

    RAVs may therefore represent a new mechanism for local translation, facilitating functional coupling between cell activity and protein synthesis at defined sites in the cell periphery. RAV-driven local translation in dendrites would require less time and energy than the traffic of mRNAs or translated products from conventional ER in the cell body.

    This work raises a number of important questions, including whether the ribosomes associated with RAVs translate a unique subset of proteins and whether these structures bear specific targeting machinery different from conventional ER for this translation.

    Future work will also define the mechanisms responsible for mRNA trafficking to specific sites of RAV-driven local translation as well for the membrane deformations producing RAV-mitochondrial membrane contact sites.

  66. 66
    OLV says:

    More ID-supporting evidences:

    Crosstalk between Mitochondria and Cytoskeleton in Cardiac Cells

    Elucidation of the mitochondrial regulatory mechanisms for the understanding of muscle bioenergetics and the role of mitochondria is a fundamental problem in cellular physiology and pathophysiology. The cytoskeleton (microtubules, intermediate filaments, microfilaments) plays a central role in the maintenance of mitochondrial shape, location, and motility. In addition, numerous interactions between cytoskeletal proteins and mitochondria can actively participate in the regulation of mitochondrial respiration and oxidative phosphorylation. In cardiac and skeletal muscles, mitochondrial positions are tightly fixed, providing their regular arrangement and numerous interactions with other cellular structures such as sarcoplasmic reticulum and cytoskeleton. This can involve association of cytoskeletal proteins with voltage-dependent anion channel (VDAC), thereby, governing the permeability of the outer mitochondrial membrane (OMM) to metabolites, and regulating cell energy metabolism. Cardiomyocytes and myocardial fibers demonstrate regular arrangement of tubulin beta-II isoform entirely co-localized with mitochondria, in contrast to other isoforms of tubulin. This observation suggests the participation of tubulin beta-II in the regulation of OMM permeability through interaction with VDAC. The OMM permeability is also regulated by the specific isoform of cytolinker protein plectin. This review summarizes and discusses previous studies on the role of cytoskeletal proteins in the regulation of energy metabolism and mitochondrial function, adenosine triphosphate (ATP) production, and energy transfer.

    Cells are highly organized units with multifaceted functional and structural interactions between various subcellular systems. A large number of studies provides strong evidence that elucidating individual organelles alone is not sufficient, and only systemic approaches must be applied for understanding intracellular signaling pathways and crosstalk between subcellular organelles. This may involve a “systems biology” approach and combinations of several most modern technologies such as genetic manipulations, live cell imaging, mathematical modelling, etc.

    Many structural and functional interactions were found to be involved in the integration of mitochondria with other cellular systems like the SR and cytoskeleton, connecting mitochondrial function, dynamics, and regulation with the entire cell physiology, in particular in the most energy consuming organ, the heart.

    The detailed characterization of molecular mechanisms implicated in mitochondrial–cytoskeleton interactions under normal and pathological conditions can be helpful for the development of new therapeutic approaches.

    many structural and functional aspects of mitochondria–cytoskeletal proteins interactions, as well as detailed molecular mechanisms of their formation, are not yet known, and the interactions of tubulin beta-II or plectin 1b with mitochondria (mitochondrial VDAC) have to be shown more directly, using the most modern methodologies

     

  67. 67
    OLV says:

    More discoveries supporting ID:

    Fission and fusion machineries converge at ER contact sites to regulate mitochondrial morphology

    The steady-state morphology of the mitochondrial network is maintained by a balance of constitutive fission and fusion reactions. Disruption of this steady-state morphology results in either a fragmented or elongated network, both of which are associated with altered metabolic states and disease. How the processes of fission and fusion are balanced by the cell is unclear.

     

     

  68. 68
    JClark says:

    KF @ 61:

    And this is with the generous assumption that it’s a nothing more than a matter of probability, i.e. we actually have states and sequences of states that map to the whole of the necessary set of gene sequences and could actually produce them with sufficient recombination; or, similarly, that physical processes will necessarily exhaustively search the genomic space rather than falling into some cyclic and/or deterministic output whose range likely excludes large portions of the genome.

    The need for evolution to appeal to undefined/undefinable distributions, magical “randomness”, is rather damning for anything that would be called a “theory”; after all, a theory is not a statement of truth; its value lies purely in its ability to make predictions.

  69. 69
    kairosfocus says:

    JC, yup, and they don’t even realise how generous the assumptions are. Start with, thermodynamics of highly endothermic molecules with bonds in a vulnerable energy range. Ask yourself how a viable abiotic soup could reasonably come about and be sustained, then how right molecules of right geometry — chirality! — would be assembled and protected. Notice, ATP and the enzyme that synthesises it, the one with the rotary mechanism. As a beginning. KF

  70. 70
    jawa says:

    KF,

    “they don’t even realise how generous the assumptions are.”

    Excessively generous.

    Imagine a person having to swim from Odessa (Ukraine) to any beach in Hawaii. No auxiliary boat going next to the swimmer.

    What Dr Cronin, Dr Szostak and other distinguished OOL scientists are trying to achieve seems like finding a way to getting a pair of fins, a mask and snorkel for the swimmer.

    The alternative models they present sound like determining whether the swim should start from Jaffa (Israel) instead. Quite a major improvement.

    Other discussions try to determine whether the swimmer should go (model a) through the Gibraltar strait to the Atlantic Ocean and the Panama Canal out to the Pacific Ocean or (model b) through the Suez Canal out to the Indian Ocean.

    In the model “a”, the ultimate breakthrough would be to find a way for the swimmer to start from Heraklion (Crete).

    In the model “b” the ultimate breakthrough would be to find a way for the swimmer to start from Ismailia (Egypt).

    They may have the swimmer wear a necklace with a shark tooth as a talisman.

    That’s it. Good luck. Cross your fingers. Knock on wood. Whatever.

    What are the odds?

    Low? Very low? Extremely low?

    Total nonsense.

    🙂

  71. 71
    jawa says:

    @70,
    But many could argue that we don’t understand, because it’s not about one swimmer, but a huge number of them attempting the same trick. And moreover, the experiment is repeated gazillion times. And the swimmers have to their disposition all the time they can use.
    That makes a difference, doesn’t it?
    Yeah, right.
    In their dreams.

  72. 72
    kairosfocus says:

    Jawa, even if they were to start from LA or from Singapore it would make no difference. The truth is, the debate over the design inference as best current and prospective explanation was decided once it became clear that Science was not fettered to a priori ideological evolutionary materialistic scientism AND — logic operator — we realised that there is complex, coded algorithmic alphanumeric information in the heart of the cell’s operations. There is just one serious explanation for such and once the ideological blinkers are removed, question begging is removed. Design is well warranted. The real onward issue is when the proud tower will crumble enough for its intimidation to lose power to suppress the manifest. Beyond, lies how can we reverse engineer as part of industrial civ 2.0. KF

    PS: The observed cosmos does not have enough search resources to plausibly discover FSCO/I beyond 1000 bits by blind forces.

  73. 73
    jawa says:

    KF:

    “The observed cosmos does not have enough search resources to plausibly discover FSCO/I beyond 1000 bits by blind forces.”

    Exactly.

    And yet some folks out there still believe that “somewhere, out there…” some evidences could be found that would support their wishful thinking.

    Who’s really worshiping some fictional gods of the gaps?

    The table has turned around.

    The first verse of the first chapter of the first book of the Christian Bible doesn’t say that in the beginning God created the things that are unknown.

    The first few verses of the first chapter of the fourth book in the NT confirm that Logos is God, who made the whole enchilada and the whole nine yards and their cousins. Everything. We worship the God of the entire show.

    God reveals His creation through the things that are known. The better we understand things, more of God’s work is revealed.

    Undoubtedly most scientific discoveries, specially in biology, increasingly point to our amazing Creator.

    Perhaps that’s a reason why most ID objectors refrain from engaging in any discussion that deals with recent biology research papers?

    Dunno.

  74. 74
    jawa says:

    KF,

    “even if they were to start from LA or from Singapore it would make no difference.”

    Good point. Agree 100%.

    However, if that were the case, then the pop-sci journals would gladly display large puffed up headlines affirming that they’re almost there! 🙂

  75. 75
    jawa says:

    Sonic Hedgehog is not a limb morphogen but acts as a trigger to specify all digits

    https://www.biorxiv.org/content/10.1101/2020.05.28.122119v1.full

    Limb patterning by Sonic hedgehog (Shh) is among the most highly touted and studied models of “morphogen” function1. Yet how Shh instructs distinct digit types (index to little finger) remains controversial.

  76. 76
    jawa says:

    What would make the ID objectors engage in a discussion in this thread?
    What is keeping them away?
    Is it the fact that recent research papers have been cited as evidence that supports ID?
    Don’t they have any argument against that affirmation?

  77. 77
    jawa says:

    The transcription factor E2A drives neural differentiation in pluripotent cells

    https://dev.biologists.org/content/early/2020/05/29/dev.184093

    The intrinsic mechanisms that link extracellular signalling to the onset of neural differentiation are not well understood.

    Our results suggest a crucial role for E2A in establishing neural lineage commitment in pluripotent cells.

  78. 78
    jawa says:

    A ubiquitin-based mechanism for the oligogenic inheritance of heterotaxy and heart defects

    https://www.biorxiv.org/content/10.1101/2020.05.25.113944v1.full

    developmental patterning events can be tightly regulated by mechanisms in target cells that function to precisely tune sensitivity to extracellular morphogens.

    left-right patterning (and cardiac and limb development) depend on a just-right “goldilocks” level of Hh signal amplitude or duration.

    The ubiquitination of receptors by membrane-tethered E3 ligases represents an attractive post-transcriptional mechanism to control the sensitivity of tissues to signaling ligands during development or tissue renewal.

    the MGRN1 family of RING E3 ligases can associate more generally across eukaryotes with single-pass TM proteins with conserved cytoplasmic motifs, each of which function as a substrate adaptor to target the ubiquitination of specific receptors or transporters

  79. 79
    jawa says:

    Hello!

    Any ID objector out there?

    Are they afraid of scientific discussions?

    Can they invite an academic objector to come and lecture us?

    🙂

  80. 80
  81. 81
    OLV says:

    @67:

    Fission and fusion machineries converge at ER contact sites to regulate mitochondrial morphology

    The steady-state morphology of the mitochondrial network is maintained by a balance of constitutive fission and fusion reactions. Disruption of this steady-state morphology results in either a fragmented or elongated network, both of which are associated with altered metabolic states and disease. How the processes of fission and fusion are balanced by the cell is unclear.

    ER MCSs define the interface between polarized and depolarized segments of mitochondria and can rescue the membrane potential of damaged mitochondria by ER-associated fusion.

    Mitochondrial morphology and dynamics are critical to normal cellular function. Mitochondrial morphology is maintained by a balance of constitutive fission and fusion reactions and by dynamic movements that occur along the cytoskeleton.

    How fission and fusion machineries are coordinatedto produce mitochondria of appropriatesize is a fundamentalquestionthat is still unresolved.

    the processes of fission and fusion are spatially coordinated and colocalized in a system of ER MCS nodes to regulate mitochondrial shape and health.

    The major question that remains is how do ER MCSs contribute to both the fission and fusion of mitochondria?

    Future studies will investigate whether the forward and reverse rates could be determined at the ER MCS by the relative recruitment and/or posttranslational modifications of fission and fusion machineries, by small signaling molecules like Ca2+, or by the recruitment of activators or inhibitors of these machineries.

    235

  82. 82
    OLV says:

    More evidences supporting ID:

    Mitochondria as intracellular signaling platforms in health and disease
     

    Mitochondria, long viewed solely in the context of bioenergetics, are increasingly emerging as critical hubs for intracellular signaling.

    mitochondria possess their own genome and carry unique lipid components that endow these organelles with specialized properties to help orchestrate multiple signaling cascades.

    Mitochondrial signaling modulates diverse pathways ranging from metabolism to redox homeostasis to cell fate determination.

    mitochondria serve as intracellular signaling platforms with a particular emphasis on lipid-mediated signaling, innate immune activation, and retrograde signaling.

    these signaling properties might potentially be exploited to develop new therapeutic strategies for a range of age-related conditions.

    Blending in and standing out, mitochondria are uniquely positioned to function as signaling hubs. Though expressed in hundreds of copies per cell, their unique composition and genome make them a complicated mix of the familiar and the distinct.

    key questions remain unanswered

    More research is needed… we look with much anticipation to reading future papers on new discoveries… it’s exciting.

     

     

  83. 83
    jawa says:

    KF @72:

    “The real onward issue is when the proud tower will crumble enough for its intimidation to lose power to suppress the manifest.”

    Spot on.

  84. 84
    jawa says:

    Apparently this thread got so technically boring that it’s practically shutdown. 🙁
    As we know we’ll, the ID objectors shun scientific discussions. They seem allergic to serious science.

  85. 85
    OLV says:

    More ID evidences:

    Gene network reverse engineering: The Next Generation
     
    Transcriptional Profiles and Regulatory Gene Networks
     
    Gene regulatory network inference resources: A practical overview
    Highlights

    Gene Regulatory Networks (GRNs) control all aspects of cellular behavior.


    Several approaches exist to infer GRNs. These can be broadly categorized based on the input data.


    GRN inference can stem from: coexpression, sequence motifs, ChIP-Seq, orthology, literature and Protein-Protein Interaction.


    We provide an extensive and commented list of >90 current GRN inference tools.


    Best Practices and Examples of GRN inference using multiple methods are described.

    Transcriptional regulation is a fundamental molecular mechanism involved in almost every aspect of life, from homeostasis to development, from metabolism to behavior, from reaction to stimuli to disease progression. In recent years, the concept of Gene Regulatory Networks (GRNs) has grown popular as an effective applied biology approach for describing the complex and highly dynamic set of transcriptional interactions, due to its easy-to-interpret features. Since cataloguing, predicting and understanding every GRN connection in all species and cellular contexts remains a great challenge for biology, researchers have developed numerous tools and methods to infer regulatory processes. In this review, we catalogue these methods in six major areas, based on the dominant underlying information leveraged to infer GRNs: Coexpression, Sequence Motifs, Chromatin Immunoprecipitation (ChIP), Orthology, Literature and Protein-Protein Interaction (PPI) specifically focused on transcriptional complexes. The methods described here cover a wide range of user-friendliness: from web tools that require no prior computational expertise to command line programs and algorithms for large scale GRN inferences. Each method for GRN inference described herein effectively illustrates a type of transcriptional relationship, with many methods being complementary to others. While a truly holistic approach for inferring and displaying GRNs remains one of the greatest challenges in the field of systems biology, we believe that the integration of multiple methods described herein provides an effective means with which experimental and computational biologists alike may obtain the most complete pictures of transcriptional relationships. This article is part of a Special Issue entitled: Transcriptional Profiles and Regulatory Gene Networks edited by Dr. Federico Manuel Giorgi and Dr. Shaun Mahony.

     
    Which came first, the transcriptional regulator or its target genes? An evolutionary perspective into the construction of eukaryotic regulons

    Eukaryotic regulons are regulatory units formed by a set of genes under the control of the same transcription factor (TF). Despite the functional plasticity, TFs are highly conserved and recognize the same DNA sequences in different organisms. One of the main factors that confer regulatory specificity is the distribution of the binding sites of the TFs along the genome, allowing the configuration of different transcriptional regulatory networks (TRNs) from the same regulator. A similar scenario occurs between tissues of the same organism, where a TRN can be rewired by epigenetic factors, modulating the accessibility of the TF to its binding sites. In this article we discuss concepts that can help to formulate testable hypotheses about the construction of regulons, exploring the presence and absence of the elements that form a TRN throughout the evolution of an ancestral lineage.

    This article is part of a Special Issue entitled: Transcriptional Profiles and Regulatory Gene Networks edited by Dr. Federico Manuel Giorgi and Dr. Shaun Mahony.

    Non-coding RNA regulatory networks
    Highlights

    Transcriptional regulatory networks regulate cell physiology and may determine pathologies.


    Network analyses could provide new insights on gene regulation and dysfunction mechanisms.


    Several ncRNAs (miRNAs, lncRNAs and circRNAs) have been shown to be involved in regulation.


    Integration of ncRNAs into regulatory networks is essential to identify molecular driver events.

    It is well established that the vast majority of human RNA transcripts do not encode for proteins and that non-coding RNAs regulate cell physiology and shape cellular functions. A subset of them is involved in gene regulation at different levels, from epigenetic gene silencing to post-transcriptional regulation of mRNA stability. Notably, the aberrant expression of many non-coding RNAs has been associated with aggressive pathologies. Rapid advances in network biology indicates that the robustness of cellular processes is the result of specific properties of biological networks such as scale-free degree distribution and hierarchical modularity, suggesting that regulatory network analyses could provide new insights on gene regulation and dysfunction mechanisms.
    In this study we present an overview of public repositories where non-coding RNA-regulatory interactions are collected and annotated, we discuss unresolved questions for data integration and we recall existing resources to build and analyse networks.

     

  86. 86
    jawa says:

    Here’s another evidence that supports ID:

    Cell fate decisions are orchestrated in large part by the concerted actions of transcription factors (TFs) and chromatin remodeling proteins.

    Cell fate decisions are governed by sequence-specific transcription factors (TFs) that act in small populations of cells within developing embryos.

    comprehensive maps of the binding sites of TFs and chromatin regulators are necessary to understand how gene expression patterns are rewired during cell fate changes.

    Profiling of Pluripotency Factors in Single Cells and Early Embryos

    https://www.cell.com/cell/fulltext/S0092-8674(19)30276-4

    Anybody dares to object?

  87. 87
    jawa says:

    Here’s another evidence that supports ID:

    The 3D genome

    The three-dimensional configuration of the genome is complex, dynamic and crucial for gene regulation.

    the organization of the genome is interconnected with nuclear architecture and can vary between cell types and during cell differentiation and development.

    genome organization and nuclear architecture regulate gene expression, cell fate and cell function

    https://www.nature.com/collections/rsxlmsyslk

    Any objections?

  88. 88
    jawa says:

    Another set of evidences supporting ID:

    Physical and data structure of 3D genome

    With the textbook view of chromatin folding based on the 30-nm fiber being challenged, it has been proposed that interphase DNA has an irregular 10-nm nucleosome polymer structure whose folding philosophy is unknown. Nevertheless, experimental advances suggest that this irregular packing is associated with many nontrivial physical properties that are puzzling from a polymer physics point of view. Here, we show that the reconciliation of these exotic properties necessitates modularizing three-dimensional genome into tree data structures on top of, and in striking contrast to, the linear topology of DNA double helix. These functional modules need to be connected and isolated by an open backbone that results in porous and heterogeneous packing in a quasi–self-similar manner, as revealed by our electron and optical imaging. Our multiscale theoretical and experimental results suggest the existence of higher-order universal folding principles for a disordered chromatin fiber to avoid entanglement and fulfill its biological functions.

    https://advances.sciencemag.org/content/6/2/eaay4055?rss=1

    Any objections?

  89. 89
    jawa says:

    @88:

    The intimate connection between three-dimensional (3D) interphase DNA structure and gene expression in eukaryotic cells has made chromatin folding a rapidly developing field. In the past decade, previously well-accepted concepts have been continuously challenged by new experimental discoveries.

    Haven’t we heard this before?

    “previously well-accepted concepts have been continuously challenged by new experimental discoveries”

  90. 90
    jawa says:

    @88:

    The non-Gaussian folding statistics and global coupling between chromatin properties suggest that interphase DNA explores the great genomic landscape as a complex network rather than a simple polymer. The possibility of chromatin having tree data structures and universal folding principles opens an exciting new paradigm to understand genomic organization and presents many new questions, the answering of which would require collaborations between experimentalists and theorists from different fields. We hope that our insights in this paper could inspire future interdisciplinary efforts on this grand challenge of life science.

    interphase DNA explores the great genomic landscape as a complex network rather than a simple polymer.

    opens an exciting new paradigm to understand genomic organization and presents many new questions

    grand challenge of life science

  91. 91
    jawa says:

    No ID objectors here yet?

    Where did they all go?

    Did they run for the hills?

    🙂

  92. 92
    jawa says:

    ID is the only empirically known cause for this:

    Ionic amplifying circuits inspired by electronics and biology

    Integrated circuits are present in all electronic devices, and enable signal amplification, modulation, and relay.

    Nature uses another type of circuits composed of channels in a cell membrane, which regulate and amplify transport of ions, not electrons and holes as is done in electronic systems.

    the physiological processes of living organisms rely on another type of circuit, which is entirely ionic and functions in an aqueous environment3,4. The key players in physiological processes are biological channels in a cell membrane that facilitate exchange of ions and molecules, for instance between the intracellular and extracellular spaces in cells and tissues. This transmembrane ionic transport is often the first step in a biological amplification process, which enables sensing external stimuli including light, sound, and odor. In the signal transduction of sound, for example, hair cells of the cochlea mechanically transduce sound waves into ion currents by opening cochlear ion channels to ionic transport; open channels allow millions of ions to pass through per second, which leads to signal generation (in the form of a change in transmembrane potential), and is ultimately detected and processed by the brain

  93. 93
    jawa says:

    @92:

    In principle ionic amplification is observed in the classic biological example of spatially and chemically complex ion transport that occurs in the synaptic cleft, where signaling molecules, driven by a propagating action potential, are released from the presynaptic terminal, diffuse across the synaptic cleft, and are taken up by receptors on the postsynaptic terminal14. This process—selective release (e.g., from vesicle fusion at the presynaptic terminal), confined transport of ions in space (in the synaptic cleft), and selective uptake (e.g., a specific ion channel receptor in the postsynaptic cleft), provides an ultimate example of what can be realized with gated and selective transport of ions. While abiotic systems cannot presently approach this level of sophistication, we can provide simplified, layered designs to construct synaptic cleft inspired devices.

    ID on steroids

  94. 94
    jawa says:

    @93:

    Undoubtedly ID

    In conclusion we demonstrated preparation of ionic circuits that were inspired by systems in biology and electronics.

    Any objector out there?

  95. 95
    jawa says:

    No objectors in this thread?

  96. 96
    jawa says:

    ID unleashed

    Deciphering eukaryotic gene-regulatory logic with 100 million random promoters

    https://www.nature.com/articles/s41587-019-0315-8

    How transcription factors (TFs) interpret cis-regulatory DNA sequence to control gene expression remains unclear, largely because past studies using native and engineered sequences had insufficient scale.

    TF activity depends on binding-site strand, position, DNA helical face and chromatin context.

  97. 97
    jawa says:

    ID unleashed

    Subcellular Spatial Transcriptomes: Emerging Frontier for Understanding Gene Regulation

    http://symposium.cshlp.org/con.....40352.long

  98. 98
    jawa says:

    ID unleashed

    “what sets the tempo and manages the order of developmental events? Are the order and tempo different between species? How is the sequence of multiple events coordinated?“

    https://dev.biologists.org/content/145/12/dev164368

  99. 99
    jawa says:

    ID unleashed

    “Robust organ size requires robust timing of initiation orchestrated by focused auxin and cytokinin signalling”

    https://www.nature.com/articles/s41477-020-0666-7

  100. 100
  101. 101
    jawa says:

    ID unleashed

    Ubiquitin chain-elongating enzyme UBE2S activates the RING E3 ligase APC/C for substrate priming

    https://www.nature.com/articles/s41594-020-0424-6

    The interplay between E2 and E3 enzymes regulates the polyubiquitination of substrates in eukaryotes. Among the several RING-domain E3 ligases in humans, many utilize two distinct E2s for polyubiquitination.

    However, the potential coordination between these steps in ubiquitin chain formation remains undefined.

    Our work reveals an unexpected model for the mechanisms of RING E3–dependent ubiquitination and for the diverse and complex interrelationship between components of the ubiquitination cascade.

    “unexpected model for the mechanisms”?

    There they go again.

    What else did they expect?

  102. 102
    jawa says:

    @101:

    ID unopposedly unleashed

    The conjugation of Ub onto proteins is a key cellular process that mediates eukaryotic protein regulation. Polyubiquitination of targeted substrates (the linkage of several ubiquitins onto a single target) can induce changes to subcellular localization, alter protein function or lead to proteasomal degradation, an important aspect of cell cycle control.

    As severe consequences result from the dysregulation of polyubiquitination, namely several cancers and developmental dis-orders, this process must be tightly controlled.

    tightly controlled?

    Hmm…

  103. 103
    jawa says:

    I’ve been criticized for taking advantage of the scientific weaknesses of the ID objectors because it’s well known they lack valid arguments to engage in a serious discussion here.
    Sorry for making that impression, but I’m just offering a friendly invitation to present objections.

    They could invite the distinguished scientists Dr Art Hunt and Dr Larry Moran to come back and present their counter arguments. They know they’re always welcome here. It’s not my fault that they can’t stand the heat and run for the hills.

    🙂

  104. 104
    BobRyan says:

    Jawa @ 103

    Don’t you know challenging their beliefs are verboten. There is nothing scientific about Darwinists worldview. Cult members never like to be called out for being part of a cult. They believe the universe magically came into existence, since the universe created itself out of nothing. They believe life originated by magic. They believe macro-evolution to be fact, when there are no facts in science. Since science is based on what is observable at any given time, future generations may observer something that contradicts existing hypothesis and theories. They cannot even bring themselves to admit this simple truth regarding science.

  105. 105
    jawa says:

    @102:

    RING E3 ligases switch between active and inactive states through precise regulatory control that ensures the specificity and timing of polyubiquitination events.

    Activators, inhibitors and posttranslational modifications of RING E3s coordinate to control accurate cell cycle timing.

    precise regulatory control?

    ensures the specificity and timing?

    coordinate to control accurate cell cycle timing?

    How?

  106. 106
    jawa says:

    BobRyan @104:

    I agree. Very interesting point. Thanks!

    We’ve had professors Art Hunt (u Kentucky) and Larry Moran (u Toronto) engaged in discussions here in UD, but for some reason they quit when the discussion gets too technical. What kind of science professors are they?

  107. 107
    BobRyan says:

    Jawa:

    You’re welcome. Darwinists throw out logic and reason, which is the reason for the birth of the whole WOKE nonsense.

  108. 108
    jawa says:

    BobRyan @107:

    Wow! That’s a really interesting association I didn’t realize. Thanks!

  109. 109
    jawa says:

    We’ve had professors Art Hunt (u Kentucky) and Larry Moran (u Toronto) engaged in discussions here in UD, but for some reason they quit when the discussion gets too technical. What kind of science professors are they?
    How can they still rule academics while being so scientifically weak?
    Does anybody understand it?

  110. 110
    jawa says:

    Did somebody notice the trend in biology research discoveries lately? It seems increasingly to be in the area of controls. Is this a correct perception?
    If this is the case, what does it mean for whatever is left of the Darwinian micro-2-macro extrapolation?

  111. 111
    BobRyan says:

    Jawa:

    If truth and fact are removed, you can replace it with anything you wish. Socialists do not value either, since neither supports their belief in the idea of Marx over the reality of what has been tried. Men and women are biologically different. Men have more gray matter, women have more white matter. Testosterone produce more calcium then estrogen, which leads to stronger and denser bones in men. Men have a lung capacity 50% greater than women.

    There is a Rabbinical saying that goes along the lines of the following, God did not choose to take a bone from Adam’s foot, since he did not want man to trample on a woman. God did not choose to take a bone from Adam’s head, since he did not want woman to lead man. God chose the rib from Adam so man and woman can stand side by side. Men and women balance each other out.

    A boy who is taught there is no difference between boys and girls does not learn the important lesson of not hitting girls. They are not told that women are physically weaker than men due to biology and men should respect women. We are seeing an increase in domestic abuse by these same boys who grew up in a world without differentiation between the two sexes.

  112. 112
    jawa says:

    BobRyan @111:

    Very well stated. Again. Thanks!

  113. 113
    OLV says:

    Evidences that support ID keep coming out of research:

    Discovery of genes required for body axis and limb formation by global identification of retinoic acid–regulated epigenetic marks

    Identification of target genes that mediate required functions downstream of transcription factors is hampered by the large number of genes whose expression changes when the factor is removed from a specific tissue and the numerous binding sites for the factor in the genome. Retinoic acid (RA) regulates transcription via RA receptors bound to RA response elements (RAREs) of which there are thousands in vertebrate genomes. Here, we combined chromatin immunoprecipitation sequencing (ChIP-seq) for epigenetic marks and RNA-seq on trunk tissue from wild-type and Aldh1a2-/- embryos lacking RA synthesis that exhibit body axis and forelimb defects. We identified a relatively small number of genes with altered expression when RA is missing that also have nearby RA-regulated deposition of histone H3 K27 acetylation (H3K27ac) (gene activation mark) or histone H3 K27 trimethylation (H3K27me3) (gene repression mark) associated with conserved RAREs, suggesting these genes function downstream of RA. RA-regulated epigenetic marks were identified near RA target genes already known to be required for body axis and limb formation, thus validating our approach; plus, many other candidate RA target genes were found. Nuclear receptor 2f1 (Nr2f1) and nuclear receptor 2f2 (Nr2f2) in addition to Meis homeobox 1 (Meis1) and Meis homeobox 2 (Meis2) gene family members were identified by our approach, and double knockouts of each family demonstrated previously unknown requirements for body axis and/or limb formation. A similar epigenetic approach can be used to determine the target genes for any transcriptional regulator for which a knockout is available.

    In addition to H3K27ac and H3K27me3 epigenetic marks that are quite commonly observed near genes during activation or repression, respectively, it is likely that further ChIP-seq studies that identify RA-regulated binding sites for coactivators and corepressors will provide additional insight into RA target genes and transcriptional pathways. Such knowledge is essential for determining the mechanisms through which RA controls developmental pathways and should be useful to address RA function in adult organs. A similar epigenetic approach can be used to determine the target genes for any transcriptional regulator for which a knockout is available, thus accelerating the ability to understand gene regulatory networks in general.

  114. 114
    OLV says:

    There are many direct or indirect ID evidences in this paper:

    Strategies and prospects of effective neural circuits reconstruction after spinal cord injury

    Spinal cord injury (SCI) is a severely disabling disease that leads to loss of sensation, motor, and autonomic function

    Due to the disconnection of surviving neural elements after spinal cord injury (SCI), such patients had to suffer irreversible loss of motor or sensory function, and thereafter enormous economic and emotional burdens were brought to society and family.

    The pathophysiology of SCI is complex and multifaceted, and its mechanisms and processes are incompletely understood.

    In this review, we summarize the recent progress in biological and engineering strategies for reconstructing neural circuits and promoting functional recovery after SCI, and emphasize current challenges and future directions.

    It is believed that in the future we can analyze and record the nerve signals, and regulate the nerve signals through cell transplantation and molecular regulation after SCI. By stimulating local nerve circuits related to sensorimotor control and spinal cord autonomy, the protection, maintenance and even re-bridging of nerve circuits can be achieved. The relevant nerve circuits are fine-tuned, and then the corresponding nerve circuits are trained and strengthened by various rehabilitation methods. It can help the individual with SCI to resume autonomous movement as soon as possible, and ultimately promote the research and treatment of SCI to achieve more enormous breakthroughs in many fields.

  115. 115
    jawa says:

    @44:

    Dr Swamidass would require that ID doesn’t limit to pointing to design but rather explains how the design was done. I respect his opinion, but that’s just his opinion. When I open the hood of a 2020 RAV4 XLE AWD Hybrid and someone explains to me very roughly how that engine works, I must conclude that what I’m looking at must have been designed. However, I still don’t have to know much, or anything at all, about how the design was done or the identity of the designer.
    Actually, given the average Joe’s poor knowledge of mechanical engineering, chemical engineering and electrical engineering, which are disciplines I assume associated with designing such a car, a rough technical explanation of how the design was done could easily blow Joe’s mind.
    In the case of biology, the problem increases in complexity by orders of magnitude.
    If we see how some complex object functions, we may imply design even without understanding who designed it or how it was designed.

  116. 116
    jawa says:

    AiG:…….47,223…….
    EN:…….296,884…….
    TO:…….769,013…….
    UD:…….805,441…….
    SW:…….1,367,722…….
    PT:…….1,419,233…….
    PS:…….2,651,165…….

    What happened to TSZ? Fell off the Alexa radar?

  117. 117
    OLV says:

    Game over! ID wins by KO!

    Studying DNA Double-Strand Break Repair: An Ever-Growing Toolbox
     

    To ward off against the catastrophic consequences of persistent DNA double-strand breaks (DSBs), eukaryotic cells have developed a set of complex signaling networks that detect these DNA lesions, orchestrate cell cycle checkpoints and ultimately lead to their repair. Collectively, these signaling networks comprise the DNA damage response (DDR).

    Our capacity to create DSBs in a programed manner and in such a way that is compatible with a set of diverse methodologies to investigate the events that follow DNA damage, has led to our current deep understanding of the DDR. The induction of DSBs at random locations using different sources of radiation or genotoxic compounds, provides the easiest approach to analyze the recruitment kinetics of proteins to sites of DNA damage and is a powerful strategy to temporally resolve the sequence of DNA repair events. The development of methods to induce annotated DNA breaks at transgenic loci inserted in the genome, or at endogenous loci (restriction enzymes, CRISPR/Cas9) allowed the analysis of the DDR at molecular resolution and were instrumental in disclosing functional links between the DDR and processes such as transcriptional, chromatin dynamics, and DNA replication. Yet all the tools described here display significant drawbacks. For instance, nucleases-induced DSBs undergo consecutive cycles of repair/cleavage until these have been mutated, calling for caution when investigating DNA repair using these tools. A major challenge is now to refine these DSB-inducible systems and the subsequent methodologies to analyze repair in order to overcome these limitations.

  118. 118
    OLV says:

    More evidences favoring ID

    Enhancer transcription identifies cis-regulatory elements for photoreceptor cell types

    Identification of cell type-specific cis-regulatory elements (CREs) is crucial for understanding development and disease, although identification of functional regulatory elements remains challenging. We hypothesized that context-specific CREs could be identified by context-specific non-coding RNA (ncRNA) profiling, based on the observation that active CREs produce ncRNAs. We applied ncRNA profiling to identify rod and cone photoreceptor CREs from wild-type and mutant mouse retinas, defined by presence or absence, respectively, of the rod-specific transcription factor (TF) NrlNrl-dependent ncRNA expression strongly correlated with epigenetic profiles of rod and cone photoreceptors, identified thousands of candidate rod- and cone-specific CREs, and identified motifs for rod- and cone-specific TFs. Colocalization of NRL and the retinal TF CRX correlated with rod-specific ncRNA expression, whereas CRX alone favored cone-specific ncRNA expression, providing quantitative evidence that heterotypic TF interactions distinguish cell type-specific CRE activity. We validated the activity of novel Nrl-dependent ncRNA-defined CREs in developing cones. This work supports differential ncRNA profiling as a platform for the identification of cell type-specific CREs and the discovery of molecular mechanisms underlying TF-dependent CRE activity.

     

  119. 119
    OLV says:

    More support for ID

    Mapping the cis-regulatory architecture of the human retina reveals noncoding genetic variation in disease

    Regulation of gene expression is critical for all complex biological processes including vision. Mutations within cis-regulatory elements (CREs) can disrupt gene expression and contribute to human diseases. However, it is challenging to screen for mutations within CREs that affect vision because the genomic locations and mechanisms of action of these elements are largely unknown. Here, we take advantage of advances in epigenomic and transcriptomic profiling techniques to identify and characterize CREs in three regions of the human eye commonly affected in visual disorders. Our data identify shared and unique CREs in each region, reveal the combinatorial binding of TFs, and provide a resource for understanding the role of noncoding genetic variation in visual disorders.

    The interplay of transcription factors and cis-regulatory elements (CREs) orchestrates the dynamic and diverse genetic programs that assemble the human central nervous system (CNS) during development and maintain its function throughout life. Genetic variation within CREs plays a central role in phenotypic variation in complex traits including the risk of developing disease. We took advantage of the retina, a well-characterized region of the CNS known to be affected by pathogenic variants in CREs, to establish a roadmap for characterizing regulatory variation in the human CNS. This comprehensive analysis of tissue-specific regulatory elements, transcription factor binding, and gene expression programs in three regions of the human visual system (retina, macula, and retinal pigment epithelium/choroid) reveals features of regulatory element evolution that shape tissue-specific gene expression programs and defines regulatory elements with the potential to contribute to Mendelian and complex disorders of human vision.

  120. 120
    OLV says:

    More ID evidences

    OTX2 represses sister cell fate choices in the developing retina to promote photoreceptor specification

    During vertebrate retinal development, subsets of progenitor cells generate progeny in a non-stochastic manner, suggesting that these decisions are tightly regulated. However, the gene-regulatory network components that are functionally important in these progenitor cells are largely unknown.

    OTX2 is required for the generation of photoreceptors, but also for repression of specific retinal fates and alternative gene regulatory networks. These include specific subtypes of retinal ganglion and horizontal cells, suggesting that in this context, OTX2 functions to repress sister cell fate choices.

    Taken together, the current study proposes a model in which OTX2 serves as a key positive regulator of photoreceptor genesis from restricted RPCs, while repressing specific subtypes of other retinal fates (Figure 7M). At the gene regulatory network level, OTX2 represses key transcription factors involved in non-photoreceptor cell types (Figure 7N). Further combined use of the single cell sequencing/CRISPR gene editing approach with variation of time, targeted genes, and labeled cell populations will provide a powerful genetic strategy to examine developmental gene regulatory networks.

  121. 121
    OLV says:

    ID is the only empirically reasonable explanation for this:

    Neurogenesis and Specification of Retinal Ganglion Cells

    Across all species, retinal ganglion cells (RGCs) are the first retinal neurons generated during development, followed by the other retinal cell types.

    How are retinal progenitor cells (RPCs) able to produce these cell types in a specific and timely order? 

    the ciliary marginal zone is a new stem cell niche in mice contributing to retinal neurogenesis, especially to the generation of ipsilateral RGCs.

    RGCs are composed of many different subtypes that are anatomically, physiologically, functionally, and molecularly defined.

    Retinal ganglion cells (RGCs) are the sole output neurons from the retina and thus integrate and transmit all visual information to the brain.

    How are these RGCs generated during development?

    Over recent decades, much progress has been made to improve the understanding of RGC neurogenesis and differentiation. The current view is that retinal progenitor cells in vertebrates can generate different retinal types in a stochastic manner but with a probabilistic bias for some cell types that change during development. This model could explain why all retinal cell types can be generated at any given developmental time but with a different probability, ending up with RGCs generated mostly early on and rod photoreceptors later.

    The extrinsic and intrinsic factors that regulate the cell fate determination are being isolated, with compelling evolutionary conserved factors initially identified in the more deterministic neurogenesis of the drosophila eye.

    However, two aspects remain to be established:

    (1) how the developmental expression of these factors is regulated, and

    (2) how the change in cell fate probabilities occur over time.

    The transcription factors that regulate RGC neurogenesis are identified: Atoh7 and Pou4f2 appear as the key regulators with several transcription factors in between.

    As RGCs are not a homogeneous population, several studies have tried to identify the molecular determinants and/or markers of RGC subtypes.

    This characterization was done initially by combinatorial expression of various transcription factors or markers for different types of RGCs.

    However, the recent emergence of single-cell RNA sequencing technology will hopefully allow the identification of new markers for RGC subtypes but also to determine their specification pathways during development.

    In the future, studies will undoubtedly link molecular specification of RGC subtypes with their brain connectivity to decipher the molecular mechanisms that are at hand.

    Finally, understanding the developmental mechanisms determining the specification of retinal cells is crucial for the efficient, targeted generation of retinal cells from induced pluripotent stem cells of patients for research on the human retinal neurogenesis and also potential therapeutic strategies.

  122. 122
    jawa says:

    Alexa ranks in global internet engagement

    AIG:………..47,242……CMI, ICR
    CMI:………151,923…….AIG, BL, EN
    ICR:……..200,369…….CMI, AIG, TO
    EN:………..302,714…….TO, UD, BL
    BL:…………319,667…….EN, IGH, AIG
    RTB:…….335,069……IGH
    UD:………..745,610…….EN, TSZ
    TO:………..763,600…….EN, ICR, CMI
    IGH:…….1,223,524…….RTB, BL
    SW:…….1,379,954…….UD
    PS:………..1,395,116…….TSZ
    PT:……….1,431,438…….UD
    TSZ:…….[no rank]…….UD, PS

    PS has shown a tremendous increase in internet traffic lately.
    TSZ has done so poorly that it’s off the Alexa radar.

    AIG: Answers in Genesis
    BL: Biologos
    CMI: Creation Ministries International
    EN: Evolution News
    ICR: Institute for Creation Research
    IGH: Is Genesis History?
    PS: Peaceful Science
    PT: Panda’s Thumb
    RTB: Reasons to Believe
    SW: Sandwalk (Dr Larry Moran)
    TO: Talk Origins
    TSZ: The Skeptical Zone
    UD: Uncommon Descent

  123. 123
    jawa says:

    @122:

    Another way to see the relations according to Alexa stats:

    ——-AIG—BL—CMI—EN—ICR—IGH—PS—PT—RTB—SW—TO—TSZ—UD
    AIG:———O——X————-X———————————————————–
    BL: —-X————O——X————-X—————————————————
    CMI:—X—–X————-X—–O——————————————O—————
    EN:———–X—–O———————————————————X————-X-
    ICR:—-X————X———————————————————X—————
    IGH:———-X————————————————X——————————-
    PS:————————————————————————————-X——–
    PT:——————————————————————————————–X-
    RTB:—————————————-X—————————————————
    SW:——————————————————————————————-X-
    TO:——————-X——X——X———————————————————-
    TSZ:————————————————X—————————————–X-
    UD:————————–X—————————-O————O————X——–
    ——-AIG—BL—CMI—EN—ICR—IGH—PS—PT—RTB—SW—TO—TSZ—UD

  124. 124
    jawa says:

    @123:
    Another way to see the relations according to Alexa stats:

    AIG————BL——————-IGH——————-RTB
    |……\………………|………………………………|………………………………/
    |……….\…………..|………………………………|……………………………./
    |…………..\……….|………………………………|…………………………../
    |………………\…. |……………………………….|…………………………/
    |…………………\. |……………………………….|………………………./
    |…………………CMI…………………………….|……………………../
    |…………………./..|..\……………………………|……………………/
    |………………../….|……\………………………..|…………………./
    |………………/……|……….\……………………..|………………./
    |……………./……..|………….\…………………..|……………../
    |…………../……….|……………..\……………….|……………/
    |…………/…………|………………..\…………….|…………./
    |………./…………..|…………………..\………….|………../
    |……../…………….|………………………\………|………/
    |……/………………|…………………………\……|……/
    |…/…………………|……………………………\…|…/
    ICR———-TO———————-EN
    …………………………………………………………..|
    ……………………………………………PT——UD——SW
    ……………………………………………………………|
    ………………………………………………………….TSZ
    …………………………………………………………….|
    …………………………………………………………..PS

  125. 125
    jawa says:

    Alexa ranks in global internet engagement

    Web………….rank…………….tsli*
    AIG:………..46,750………….4,136
    CMI:………161,817…………….1,884
    ICR:……..207,115…………….2,329
    EN:………..311,392…………….999
    RTB:………316,803………….1,018
    BL:…………330,966…………789
    UD:………..706,183………….804
    TO:………..827,407…………3,013
    IGH:…….1,119,605……….72
    SW:…….1,379,237………..501
    PS:………..1,394,344………16
    PT:……….1,502,748………..1,175
    TSZ:…….[no rank]………57

    tsli: total sites linking in

  126. 126
    jawa says:

    For the first time PS has ranked higher than SW and PT!
    Dr Swamidass is getting more online traffic in his website.
    But TSZ sank so deep that got off Alexa radar – what happened?

    AIG:……. 46,947
    RTB:……. 292,858
    EN:……. 309,663
    MM:……. 532,604
    UD:……. 707,799
    TO:……. 825,582
    PS:……. 1,397,637
    SW:……. 1,450,061
    PT:…… 1,506,678

  127. 127
    jawa says:

    Updated list of acronyms:

    AIG: Answers in Genesis
    BL: Biologos
    CMI: Creation Ministries International
    EN: Evolution News
    ICR: Institute for Creation Research
    IGH: Is Genesis History?
    MM: Mind Matters
    PS: Peaceful Science
    PT: Panda’s Thumb
    RTB: Reasons to Believe
    SW: Sandwalk (Dr Larry Moran)
    TO: Talk Origins
    TSZ: The Skeptical Zone
    UD: Uncommon Descent

  128. 128
    jawa says:

    Alexa Internet ranks
    AIG:…….47,336
    CMI:…….157,446
    ICR:…….207,705
    RTB:…….289,060
    EN:…….319,159
    BL:…….333,297
    MM:…….534,166
    UD:…….714,898
    TO:…….890,997
    IGH:…….1,203,371
    PS:…….1,402,140
    SW:…….1,454,927
    PT:…….1,512,057

  129. 129
    jawa says:

    Alexa Internet ranks

    AIG:……. 48,115
    CMI:……. 157,759
    ICR:……. 204,627
    RTB:……. 285,515
    EN:……. 318,883

    BL:……. 346,506
    MM:……. 521,238
    UD:……. 716,976

    TO:……. 919,958
    PS:……. 1,406,582
    IGH:……. 1,457,809

    SW:……. 1,459,858
    PT:……. 1,517,080
    TSZ…….[internet traffic dropped too low – off the radar]

  130. 130
    kairosfocus says:

    Jawa, such results are doubtless heavily biased by the censoring impact of biased search engine algorithms. We have a major war being waged by ideologues against truth. KF

  131. 131
    jawa says:

    KF, I see your point. It makes sense. Still it’s interesting to see Answer in Genesis, and other creationist websites (CMI, ICR) having relatively much higher volume of internet engagement than anti-ID websites like TO, SW, PT, despite the he censoring impact of biased search engine algorithms.

    Also, it’s interesting to see how those numbers fluctuate so often in all directions. Perhaps this confirms what you wrote about the censoring impact of biased search engine algorithms.

    Lastly, it’s interesting to see TSZ having so little traffic that it’s out of Alexa’s radar. Not long ago PS was in that situation, but it has gone up quite rapidly lately.

  132. 132
    OLV says:

    More ID on display here:

     
    The acquisition of positional information in the developing cochlea

    The sensory epithelium of the mammalian murine auditory organ, the organ of Corti, is an exquisite example of how specialized asymmetry dictates auditory function. Across the radial axis, the organ consists of three rows of outer hair cells to one row of inner hair cells, which are innervated by efferent and afferent neurons. The mechanosensory inner hair cells that reside in the neural compartment detect sound whereas the outer hair cells in the abneural compartment modulate sound levels. A complex combination of spatiotemporal signaling inputs across the radial axis endows cells with positional information to take on specific cell fates.

    The Wnt and Bmp pathways are two potential signaling mechanisms that influence this radial asymmetry in an opposing manner. We analyzed the requirement of the Bmp pathway for setting up cochlear patterning. Smad4 cKOs showed a loss of the abneural compartment. Prolonged Bmp inhibition decreased the formation of the abneural compartment and outer hair cells. Bmp was required for determining the abneural boundary of the sensory domain. Immediately after hair cell differentiation, Bmp signaling was no longer required. Bmp is necessary, but not sufficient for patterning the entire epithelium. Activation of the Wnt pathway leads to a selective expansion of the neural compartment and inner hair cells. This selective neural expansion was also conserved in the chicken cochlea. Signaling crosstalk of these pathways in a spatiotemporal manner is necessary for proper patterning of the organ of Corti.

  133. 133
    OLV says:

    More ID displayed here:

    Evaluation of BMP-mediated patterning in a 3D mathematical model of the zebrafish blastula embryo
     

    Bone Morphogenetic Proteins (BMPs) play an important role in dorsal–ventral (DV) patterning of the early zebrafish embryo. BMP signaling is regulated by a network of extracellular and intracellular factors that impact the range and signaling of BMP ligands. Recent advances in understanding the mechanism of pattern formation support a source-sink mechanism, however it is not clear how the source-sink mechanism shapes patterns in 3D, nor how sensitive the pattern is to biophysical rates and boundary conditions along both the anteroposterior (AP) and DV axes of the embryo. We propose a new three-dimensional growing Partial Differential Equation (PDE)-based model to simulate the BMP patterning process during the blastula stage. This model provides a starting point to elucidate how different mechanisms and components work together in 3D to create and maintain the BMP gradient in the embryo. We also show how the 3D model fits the BMP signaling gradient data at multiple time points along both axes. Furthermore, sensitivity analysis of the model suggests that the spatiotemporal patterns of Chordin and BMP ligand gene expression are dominant drivers of shape in 3D and more work is needed to quantify the spatiotemporal profiles of gene and protein expression to further refine the models.

     

  134. 134
    OLV says:

    …….

  135. 135
    OLV says:

    Reverse engineering biological processes? Huh? 🙂

    Engineering in Development and Aging

    Chemical Engineering plays a role in how we understand and modify human development and aging. This session will cover the applications of biological and chemical engineering principles to reverse engineer the biological processes associated with development and aging, including but not limited to cell signaling, biomechanics, patterning and organogenesis. Also relevant is the application of systems and synthetic biology approaches toward engineering multicellular systems.

     

     

     

  136. 136
    OLV says:

    Obvious ID on display here:

    BMP Signaling Gradient Scaling in the Zebrafish Pectoral Fin
     

    Secreted growth factors can act as morphogens that form spatial concentration gradients in developing organs, thereby controlling growth and patterning. For some morphogens, adaptation of the gradients to tissue size allows morphological patterns to remain proportioned as the organs grow. In the zebrafish pectoral fin, we found that BMP signaling forms a two-dimensional gradient. The length of the gradient scales with tissue length and its amplitude increases with fin size according to a power-law. Gradient scaling and amplitude power-laws are signatures of growth control by time derivatives of morphogenetic signaling: cell division correlates with the fold change over time of the cellular signaling levels. We show that Smoc1 regulates BMP gradient scaling and growth in the fin. Smoc1 scales the gradient by means of a feedback loop: Smoc1 is a BMP agonist and BMP signaling represses Smoc1 expression. Our work uncovers a layer of morphogen regulation during vertebrate appendage development.

    Taken together, our data suggest a scenario where the fin contains a proximal BMP source that generates a single gradient deployed along the proximo-distal axis, while signaling, as revealed by the BRE reporter, is only seen in the ROI. This is consistent with the presence of BMP signaling antagonists in the endoskeletal disc (Bauer et al., 1998, Fürthauer et al., 1999), which could decrease the signaling levels in the center of the endoskeletal disc. This could generate an effective scenario where two signaling gradients are deployed in the fin.

    Further exploration into the specific properties of a fold change detection system during the embryonic growth of the pectoral fin will provide a general framework to understand growth and patterning of vertebrate appendages.

     

  137. 137
    jawa says:

    Alexa Internet ranks

    AIG:……. 52,021
    CMI:……. 152,656
    ICR:……. 226,008
    RTB:……. 271,555
    EN:……. 306,383
    BL:……. 356,068
    MM:……. 480,673
    TO:……. 842,175
    UD:……. 902,119
    SW:……. 1,404,957
    PS:……. 1,684,357
    IGH:……. 1,885,604
    PT:……. 2,084,078
    TSZ…….[internet traffic dropped too low – off the radar]

    Updated list of acronyms:

    AIG: Answers in Genesis
    BL: Biologos
    CMI: Creation Ministries International
    EN: Evolution News
    ICR: Institute for Creation Research
    IGH: Is Genesis History?
    MM: Mind Matters
    PS: Peaceful Science
    PT: Panda’s Thumb
    RTB: Reasons to Believe
    SW: Sandwalk (Dr Larry Moran)
    TO: Talk Origins
    TSZ: The Skeptical Zone
    UD: Uncommon Descent

    Note:
    it’s interesting to see Answer in Genesis, and other creationist websites (CMI, ICR) having relatively much higher volume of internet engagement than anti-ID websites like TO, SW, PT, despite the censoring impact of biased search engine algorithms.

    Also, it’s interesting to see how those numbers fluctuate so often in all directions. Perhaps this confirms what KF wrote @130 about the censoring impact of biased search engine algorithms, but could there be other factors involved here too?

    Lastly, it’s interesting to see TSZ having so little traffic that it’s out of Alexa’s radar. Not long ago PS was in that situation, but it has gone up quite rapidly lately.

    Here’s a interesting observation about a website that perhaps does not exactly qualify to be in the above list, but shows that their internet traffic increased substantially around the time their founder passed away. Over two months after that event, the traffic hasn’t decreased.

    https://www.alexa.com/siteinfo/rzim.org

  138. 138
    OLV says:

    An old paper that shows abundant evidences for ID:

    Alternative pre-mRNA splicing: the logic of combinatorial control
    (published 20 years ago)

    Alternative splicing of mRNA precursors is a versatile mechanism of gene expression regulation that accounts for a considerable proportion of proteomic complexity in higher eukaryotes. Its modulation is achieved through the combinatorial interplay of positive and negative regulatory signals present in the RNA, which are recognized by complexes composed of members of the hnRNP and SR protein families.

     

     

  139. 139
    kairosfocus says:

    Jawa there are a few big Creationist orgs. which antedate the web. They built their own platforms, and their web engagement is really secondary. KF

  140. 140
    jawa says:

    KF,
    Yes, that seems to be the case.

  141. 141
    jawa says:

    Alexa ranks:

    AiG:……. 54,612
    CMI:……. 152,722
    RTB:……. 243,699
    ICR:……. 246,139
    EN:……. 318,123
    BL:……. 388,769
    MM:……. 474,500
    UD:……. 823,033
    TO:……. 1,085,205
    SW:……. 1,677,682
    PS:……. 1,729,263
    IGH:……. 2,284,628
    PT:……. 3,227,929

  142. 142
    jawa says:

    After noticing that TSZ hasn’t been ranked by Alexa, I looked into it and found that they haven’t had a new article posted for over 1.5 month.
    Why?

  143. 143
    jawa says:

    @141:

    Apparently PT sank so deep after having server problems that kept them off for a long time. They’re back on and their Alexa stats could improve soon.

  144. 144
    jawa says:

    ID all over
    🙂

    Clock-controlled rhythmic transcription: is the clock enough and how does it work?

    Circadian clocks regulate the rhythmic expression of thousands of genes underlying the daily oscillations of biological functions. Here, we discuss recent findings showing that circadian clock rhythmic transcriptional outputs rely on additional mechanisms than just clock gene DNA binding, which may ultimately contribute to the plasticity of circadian transcriptional programs.

    https://www.tandfonline.com/doi/full/10.1080/21541264.2019.1673636

  145. 145
    jawa says:

    ID on steroids:

    Chromatin information content landscapes inform transcription factor and DNA interactions

    Interactions between transcription factors (TFs) and chromatin are fundamental to genome organization and regulation and, ultimately, cell state.

    variations in the information content of chromatin architecture reflect functional biological variation, with implications for cell state dynamics and memory.

    application of information theory methods to chromatin profiles captures a dynamic landscape of TF-chromatin interactions, with implications for cell state memory and gene regulation.

    local chromatin architecture encodes rich signatures of TF interactions

    TF-chromatin interaction patterns are driven by TF residence time, resulting in distinct CIE signatures.

    directional binding is an intrinsic property of TF-chromatin interactions.

    the landscape of TF-chromatin interactions varies across tissues and reflects protein domain-level TF properties.

    high f-VICE TFs are more likely to mediate genetic effects on gene expression, but not their magnitude.

    TFs with potential pioneer-like properties bookmark regions of the genome to allow binding of other migrant-like TFs

    Obviously, all that functional information was the result of unguided processes, random variations and natural selection.

  146. 146
  147. 147
    jawa says:

    The sequence of nucleotides in DNA could serve as a code for amino acids (used later at the tRNA-aaRS/ribosome level) or a code for regulatory ncRNA or a code for pre-mRNA (before post-transcriptional modifications) or a code for transcriptional regulation (TF binding sites, promoter, enhancer and the whole nine yards). Then apart we have the epigenetic marks, including the ones associated with the nucleosomes, and so on and so forth. Then we have the splicing code. Then the post-translational modification code. What else?

    But the most important thing is that all of the above came to be as result of undirected processes. How?

  148. 148
    jawa says:

    Reverse engineering directed gene regulatory networks from transcriptomics and proteomics data of biomining bacterial communities with approximate Bayesian computation and steady-state signalling simulations
    https://bmcbioinformatics.biomedcentral.com/articles/10.1186/s12859-019-3337-9

    I thought you could reverse-engineer what has been engineered first. Where did I get this wrong? Did I miss something?

  149. 149
    jawa says:

    A paradigm shift in medicine: A comprehensive review of network-based approaches

    https://www.sciencedirect.com/science/article/pii/S1874939919302500?via%3Dihub

    Network medicine is a rapidly evolving new field of medical research, which combines principles and approaches of systems biology and network science, holding the promise to uncovering the causes and to revolutionize the diagnosis and treatments of human diseases. This new paradigm reflects the fact that human diseases are not caused by single molecular defects, but driven by complex interactions among a variety of molecular mediators. The complexity of these interactions embraces different types of information: from the cellular-molecular level of protein-protein interactions to correlational studies of gene expression and regulation, to metabolic and disease pathways up to drug-disease relationships. The analysis of these complex networks can reveal new disease genes and/or disease pathways and identify possible targets for new drug development, as well as new uses for existing drugs. In this review, we offer a comprehensive overview of network types and algorithms used in the framework of network medicine.

    Another confirmation of ID

  150. 150
  151. 151
    jawa says:

    Truthfreedom,
    Interesting article.

  152. 152
    jawa says:

    Alexa ranks (update):

    Top 0.1%
    AiG:……. 57,240

    Top 1%
    CMI:……. 174,850
    RTB:……. 231,021
    ICR:……. 295,589
    EN:……. 297,307
    BL:……. 363,848
    MM:……. 388,600
    UD:……. 662,559

    Top 2%
    TO:……. 1,060,561
    SW:……. 1,663,253
    PS:……. 1,947,079

    Top 8%
    PT:……. 7,485,326

    TSZ:……. [insignificant traffic]

    Why has PT lost so much traffic recently? Their server was down but has been restored. Any thoughts?

    The situation of TSZ is quite puzzling too. They lost so much traffic.

    PS has gone up significantly from the bottom of the ranks (at one point was off like TSZ is now).

    TO and SW have been within the 1% range but have lately sunk into the 2% level recently. It could be temporary.

    Note that the % refers to the top 100 million active websites.

  153. 153
    jawa says:

    Hyperacetylated chromatin domains mark cell type-specific genes and suggest distinct modes of enhancer function

    https://www.nature.com/articles/s41467-020-18303-0

  154. 154
    jawa says:

    @152:
    Correction:
    TO and SW have been within the 1% range before, but have lately dropped to the 2% level recently. It could be temporary.

  155. 155
    jawa says:

    @153:

    That recent paper shows that the plot thickens and the bad news for the Darwinian (macroevolutionary) ideas keep getting worse. 🙂

    Fundamental issues regarding enhancer function, however, remain unclear. For example, the dominant model for how enhancers communicate with their cognate gene promoters, termed looping, involves direct interactions between factors bound to enhancers and factors bound near promoters. Evidence for such interactions, however, has provided little insight into how a distal enhancer finds a gene promoter, or how it distinguishes among potential promoters in gene-dense regions. Moreover, some evidence suggests that mechanisms of enhancer-promoter communication may be more varied

  156. 156
    jawa says:

    Why don’t ID objectors post their strong counter arguments here?
    Simply because they lack what it takes to engage in serious scientific discussions. That’s all.
    Their case is doomed.

  157. 157
    jawa says:

    @153, 155:

    “the super-enhancer concept tends to oversimplify more complex patterns of gene regulation.”

    Isn’t that what we see in many cases?

    🙂

  158. 158
    jawa says:

    Here it goes again:

    ENCODE discovers many new transcription-factor-binding-site motifs and explores their properties

    https://www.nature.com/articles/nature28170

  159. 159
    jawa says:


    Video on YouTube


    Dr Sue Biggins interviews Dr Leland Hartwell.


    Video published 2019-02-19


    2020-09-16 only 2,340 views and one comment


    Cell Division Cycle (CDC)


    2001 Nobel Prize in Physiology or Medicine


    Define Cell Cycle Checkpoints:

    Well, we tried to define it relatively clearly, as something which is needed to arrest division when something goes wrong We certainly wondered that. And I think over the years, a lot more has been discovered.And so… you know, one of the, I think, really fundamental principles about biology, that fascinates me, is the tremendous accuracy of biological processes. So, yeast cells lose a chromosome about once in 100,000 divisions. That’s remarkably precise and reproducible, especially when you watch mitosis and see the chromosomes jiggling around and everything. You wonder how they keep track of them. And I suspect that’s true for all kinds of cellular processes, that normally we can’t measure the accuracy because it is so accurate. And… and so the extent to which evolution has driven the accuracy of biological processes is really enormous. And it… I think it must mean that for most things that go on in biology, there’s the basic machinery, there are things which repair the basic machinery when it gets in trouble, and there are things that coordinate that repair with everything else that’s going on. And we probably only know the tip of the iceberg yet in terms of cell biology.

  160. 160
    jawa says:

    @159:

    What did Dr Hartwell mean by
    “ the extent to which evolution has driven the accuracy of biological processes is really enormous. ”
    ???

    How could that have happened?
    Any clues?

  161. 161
    jawa says:

    What is this for:

    “Approval Ready Consulting –
    Dissertation Writing Service”

    ???

  162. 162
    jawa says:

    ID on steroids?

    Cellular Dialogues: Cell-Cell Communication through Diffusible Molecules Yields Dynamic Spatial Patterns

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6975168/

    Cells form spatial patterns by coordinating their gene expressions. How a group of mesoscopic numbers (hundreds to thousands) of cells, without pre-existing morphogen gradients and spatial organization, self-organizes spatial patterns remains poorly understood.

Leave a Reply