Behe on LYST

A second highly selected gene, LYST, is associated with pigmentation, and changes in it are probably responsible for the blanching of the ancestors’ brown fur. Computer analysis for the multiple mutations of the gene showed that they too were almost certainly damaging to its function.

In fact, of all the mutations in the seventeen genes that were most highly selected, about half were predicted to damage the function of the respective coded proteins. Furthermore, since most altered genes bore several mutations, only three to six (depending on the method of estimation) out of seventeen genes were free of degrading changes [fn 2]. Put differently, 65 to 83 percent of helpful, positively selected genes are estimated to have suffered at least one damaging mutation.

  • Darwin Devolves p. 21

fn 2 is Table S7 of Liu et al.

Can we work through this one item at a time to see what people agree with or disagree with?

228 thoughts on “Behe on LYST

  1. Alan Fox:
    CharlieM,

    Don’t know if anyone has mentioned exaptation to you. This talk of “damaging” mutations is based on an analysis intended to spot possibly pre-cancerous mutations. So a change resulting a loss of function is not necessarily damaging to the organism if there is the possibility of a new use for a protein (or system) that no longer functions in its original role. Melanin loss in body haircausing bears to be less visible to potential prey is such an exaptation, an advantage when bears encountered the new niche of the arctic.

    ETA exaptation

    And this is basically what Behe is saying. It is beneficial to polar bears that their hair lacks melanin. If a gene is mutated so that it prevents the appearance of melanin in the hair by whatever means then it is advantageous. And it is much easier for mutations to prevent processes from happening than it is to build new structures. It is much easier to alter the function of a TV set by flicking a switch that cuts its power supply than it is to alter it by inserting a novel component into its circuit.

    Do we have any examples of exaptation where we have a clear idea of the genetic changes involved?

  2. CharlieM,

    I like the example wikipedia (biased skeptic website) uses for exaptation-bird feathers. They speculate that once they were for warmth, and then later got used for flight.

    But I much prefer the neutral theory idea. First the feathers were for nothing, then they just so happened to be good for flight.

    Hahahahaha….Go Swamidass!

  3. Corneel: Let me stir the pot a little.

    Complete loss of LYST gene function in humans results in Chediak-Higashi syndrome, a heritable disease associated with decreased pigmentation of hair (hey surprise!) but also partial albinism, immunodeficiency, coagulation defects, varying neurologic problems and peculiar malignant lymphoma. Death often occurs before the age of 7 years. Assuming LYST serves a similar function in polar bears as in humans, it is apparent that it has not completely lost all of its former gene functions.

    The reason for this pleiotropic behaviour is that LYST is not only expressed in melanocytes of hair follicles, but ubiquitously expressed to regulate vesicular transport. Therefore, it is also required for e.g. the proper function of cytotoxic lymphocytes, in particular natural killer cells. Now, this is all speculation of course, but it seems to me that since polar bears are not suffering en masse from Chediak-Higashi syndrome that LYST must still capable of performing its ancestral molecular function, despite it having accumulated several “harmful” mutations. It thus appears that LYST function was selectively decreased in follicular melanocytes, because of its adaptive value. How smart of blind non-intelligent natural selection.

    Thanks, this is actually relevant information, because this implies LYST is actually likely to be a “modification of FCT” in the polar bear, as opposed to a “loss of FCT”, going by Behe’s 2010 paper parlance.

    And he actually does appear to use these terms in his new book, if you look on Amazon page, some parts of the book are visible, and he uses the term on page 294 there:

    The research results tell a different story, one that showcases the First Rule of Adaptive Evolution. It turns out that the system was switched back on by loss-of-FCT mutations.

    It is likely Behe introduces and defines these terms earlier in his book.

    Another funny little gem on that visible page:

    Almost all work on the evolution of flagella consists in comparing sequences, a method that-although it can support interesting conjectures about who descended from whom-says nothing about the mechanism of evolution. The very little work that has been done that’s relevant to the mechanism strongly supports the arguments of this book.

    That is Behe’s attempt to infer modes and patterns of evolution from phylogenetics. Notice the inherent irony in that statement. How does Behe know that the genes in polar bear are “strongly selected” and “damaging”, and therefore is inferred by him to support his first rule of adaptive evolution? BY SEQUENCE COMPARISONS. Inferences made on the basis of the existence of gene sequences with differences in them between different species and different individuals. That’s how it is inferred that they evolved under selection. The very concept Behe now rejects when put to analysis of flagellum proteins.

    Hypocritical, selective, double standard.

  4. phoodoo: I like the example wikipedia (biased skeptic website) uses for exaptation-bird feathers. They speculate that once they were for warmth, and then later got used for flight.

    But I much prefer the neutral theory idea. First the feathers were for nothing, then they just so happened to be good for flight.

    Hahahahaha….Go Swamidass!

    I see you’ve failed to understand the distinction between the neutral theory of molecular evolution, and phenotypic evolution. In essence, you don’t get the genotype vs phenotype distinction.

    Nobody claims the macroscopic physiological attributes of organisms, such as feathers, are neutral or just evolved for no reason at all.

  5. CharlieM: Do we have any examples of exaptation where we have a clear idea of the genetic changes involved?

    Yes, the cit+ function in Richard Lenski’s LTEE is an example of exaptation. Exaptation between distinct genomic entities have been observed to happen, to create functional associations between previously disparate genetic elements.

    A genomic locus (the citrate transporter protein) was duplicated into another part of the genome, and it just so happened to end up under control of a promoter that was active under aerobic conditions, and the translocated gene just so happened to be a citrate transporter that could take up citrate, which just so happened to be present in the growth medium.

    So in this instance, it is actaully the promoter, normally involved in regulating a different set of genes, that is exapted to regulate the citrate transporter to create the novel function of aerobic citrate transport.

  6. Rumraket: Nobody claims the macroscopic physiological attributes of organisms, such as feathers, are neutral or just evolved for no reason at all.

    Really, nobody?

    Maybe you better read some more evolutionists websites. Care to bet?

  7. Rumraket: I see you’ve failed to understand the distinction between the neutral theory of molecular evolution, and phenotypic evolution.

    Isn’t that the mistake that Swamidass makes? You’re free to say so here. 🙂

  8. Mung: Part IV: Solution

    dazz: How long is part IV? Can you please summarize it in a few sentences?

    No response, Mung? Do you realise how big of a paradigm change it would be to have a new mechanism for evolutionary innovation? Why would the ID camp not boast about this awesome scientific milestone?

    I know why, there’s nothing there in chapter IV worth shit. Otherwise that would be the main point of the book instead of the ubiquitous, IDiotic, negative argument

  9. Mung: Isn’t that the mistake that Swamidass makes? You’re free to say so here.

    Its pretty funny, if we were only talking about molecular evolution, and not changes to the phenotype, HOW could you have anything but neutral mutations? How is a phenotype that isn’t changed any going to be selected over another phenotype that is the same?

    Does Rumraket know what selection means do you think?

  10. phoodoo: Really, nobody?

    Maybe you better read some more evolutionists websites. Care to bet?

    You can probably find some crackpot random internet nobody who says it. You can also find people who think a snake can talk, and that a man once resurrected himself after being dead for three whole days. Go figure.

  11. Mung: Isn’t that the mistake that Swamidass makes? You’re free to say so here.

    I haven’t seen him make this mistake. Point it out to me.

  12. phoodoo: Its pretty funny, if we were only talking about molecular evolution, and not changes to the phenotype, HOW could you have anything but neutral mutations? How is a phenotype that isn’t changed any going to be selected over another phenotype that is the same?

    Is there anyone here who can make sense of this latest gibberish of phoodoo’s?

    Does Rumraket know what selection means do you think?

    Do you understand written english, at all?

  13. phoodoo:
    dazz,

    Its in a book.I think its by Futamamamia.Go read it, you will find the answers.

    You can bet your sweet life that not a single cent of mine will ever go to the scumbags of the DiscoTute. Your refusal to tell us about this supposedly huge discovery speaks volumes anyway

  14. Rumraket: Yes, the cit+ function in Richard Lenski’s LTEE is an example of exaptation. Exaptation between distinct genomic entities have been observed to happen, to create functional associations between previously disparate genetic elements.

    A genomic locus (the citrate transporter protein) was duplicated into another part of the genome, and it just so happened to end up under control of a promoter that was active under aerobic conditions, and the translocated gene just so happened to be a citrate transporter that could take up citrate, which just so happened to be present in the growth medium.

    So in this instance, it is actaully the promoter, normally involved in regulating a different set of genes, that is exapted to regulate the citrate transporter to create the novel function of aerobic citrate transport.

    Is that not the same one that Behe discusses in his new book?

  15. CharlieM: Is that not the same one that Behe discusses in his new book?

    I’m sure he’s got some sort of spin about it. In his view it probably only counts as a modification of function.

  16. dazz: No response, Mung?

    That’s correct. I’m trying to stay on topic. Feel free to get the book and read Part IV and start your own OP on it.

  17. Mung: That’s correct. I’m trying to stay on topic. Feel free to get the book and read Part IV and start your own OP on it.

    Oh, bummer. I guess we’ll never know about it. Almost as if it didn’t exist. Very godlike BTW

  18. phoodoo: Maybe you better read some more evolutionists websites. Care to bet?

    Sure. What’s the bet precisely? State the entire bet.

  19. OMagain: State the entire bet.

    I bet that if there is a lottery that is guaranteed to have a winner that there will be a winner no matter how improbable it is. Therefore IDists don’t understand probability.

  20. Mung: I bet that if there is a lottery that is guaranteed to have a winner that there will be a winner no matter how improbable it is. Therefore IDists don’t understand probability.

    And you would still be wrong. Can you see why?

  21. DNA_Jock: P.S. You ran away from our conversation on the Three Musketeers thread:

    Still reading the book. Should I shortcut and just do a search for selection, mutation or gene? Perhaps.

    ETA: I didn’t “run away” from anything.

  22. DNA_Jock: Do you really mean mutations, rather than genes?

    I’ll go with genes.

    The examples just discussed show how common are beneficial degradative mutations, but don’t link them directly to speciation. The example with which we started the book—the polar bear—does. Recall that the most highly selected genes in its pathway of descent from the brown bear were mostly damaged ones, including those involved in fur color and fat metabolism.

  23. And as we have seen, it is likely the LYST example discussed in this thread is actually just a case of “modification of FCT” by Behe’s own definition, rather than “loss”. So that’s one potential misrepresentation by Behe about LYST.

    Should we proceed to the next gene?

  24. Only if it is the “most highly selected”, Rumraket.
    Mung has clarified that this

    Now, in his book, Behe explicitly states that he is talking about the mutations under the strongest selection. That has to be taken into account if we want to understand him.
    Any disagreement on that?

    refers to the most highly selected genes, not mutations. [‘Mutations’ really made no sense…]
    So let’s take that into account, and ask: “Are the genes under the strongest selection more likely to have a majority of non-‘benign’ mutations?
    Here goes:
    Liu et al used three criteria to identify genes under strong selection in the polar bear since divergence.
    1) The homogeneity test statistic (HTS) (which looks for a low polymorphism and high divergence)
    2) The HKA test to detect selection that was specific to the polar bear branch, and not the brown bear branch of the tree.
    3) The estimated fixation index, Fst (think of it as how little variation there is within a population, as compared with the variation between populations…)
    Which metrics might Behe use to zero in on the genes under strongest selection?
    Wanna use the HTS? Okay, TTN is the winner and 60 – 80% of mutations in TTN are ‘benign’.
    Wanna use the HKA? Well, OR5D13 is the winner and 100% of mutations are ‘benign’.
    Wanna use Fst? Oh, TTN is still the winner. Let’s not always see the same hands shall we? The runner-up is AIM1 and 67 – 100% of mutations are ‘benign’.

    Even if you accept Behe’s interpretation and use of Liu’s data (and you should not), then Behe’s thesis is not holding up.

  25. DNA_Jock: Even if you accept Behe’s interpretation and use of Liu’s data (and you should not), then Behe’s thesis is not holding up.

    You’re cherry picking and you know it. Stop it.

  26. Mung: You’re cherry picking and you know it.

    That’s a bold claim! (Might be a bald assertion too, especially the “and you know it” bit). Are you saying DNA-Jock selected examples from data, some of which does not agree with the question “Are the genes under the strongest selection more likely to have a majority of non-‘benign’ mutations?” Can you point to the cherry-missed data?

  27. It is true; I cannot tell a lie. I picked a cherry. Allow me to explain.
    Mung pointed out that we must ‘take into account’ that Behe is explicit that he is talking about the genes under the strongest selection.
    Liu used three criteria. I listed all three. By each criterion, there was one gene that was the most selected. I listed those genes. Furthermore, I listed the % benign mutations under BOTH predictive algorithms.
    Zero cherry picking so far.
    However, when I saw that TTN was the winner in two categories, I decided to offer the tiara to the second place finisher in the Fst category, and not to the second place finisher in the HTS category, because it was funnier that way. (Second place in HTS was APOB, which had already been discussed somewhat…)
    I was guilty of cherry-picking there. I am sorry.
    Now, about the statement

    Put differently, 65%-83% of helpful, positively-selected genes are estimated to have suffered at least one damaging mutation.

    or

    Below is the relevant information from Liu et al.’s Table S7. Those who can understand the table will see that it supports every actual, undistorted claim I made about the polar bear.

    or

    It seems, then, that the magnificent Ursus maritimus has adjusted to its harsh environment mainly by degrading genes that its ancestors already possessed.

    The first Behe quote here is cherry-picking. The others are good old-fashioned false.
    But that’s just hunky dory, and begs for a charitable reading? As you wish.

  28. Alan Fox: That’s a bold claim! (Might be a bald assertion too, especially the “and you know it” bit).

    Given that it was a past event the probability was 1. But really, I just flipped a
    coin. Either he was cherry picking or he wasn’t. Either he knew it or he didn’t. The odds were really quite good!

  29. Mung: Given that it was a past event the probability was 1. But really, I just flipped acoin. Either he was cherry picking or he wasn’t. Either he knew it or he didn’t. The odds were really quite good!

    On the scale of cherry picking, how do you rate Behe and DNA-Jock?

  30. Alan Fox: On the scale of cherry picking, how do you rate Behe and DNA-Jock?

    “Darwin does devolve. Sometimes. So what?”
    “…A minority of the changes correspond to loss of function, including most obviously loss of pigmentation, yet by extreme cherry picking Behe presents the loss of function as dominant…”

    Really?

    Darwin does devolve. Sometimes. So what?

    Darwinian science is sh**ty. Most of the times. So what?

    Nothing, no evidence, will change someone’s mind if he doesn’t want to change it. Always. So why continue to bother to try???

  31. J-Mac: Nothing, no evidence, will change someone’s mind if he doesn’t want to change it. Always. So why continue to bother to try???

    At least some of us try, perhaps sometimes not as hard as we could, to see and comprehend an alternative point of view. You, however, seem to avoid clarifying or supporting your apparent disdain for evolutionary biology. It’s not a hugely effective technique.

  32. Behe:

    In fact, about half of the mutations in the 17 most highly selected polar bear genes were predicted to be damaging.

    Is there any disagreement about which genes belong in the list of 17 “most highly selected polar bear genes”?

  33. Alan Fox: Good article, thanks for the link.

    I have to disagree… I think this article is bad, for Darwinists, of course…

    If I were a Darwinist, I would seriously reconsider my support for this ideology…
    No matter what mechanism Darwinists would like to include in their ideology, it really looks bad when the main mechanism of the theory is exposed as the devourer, rather than builder, of new genes and functions and the author dismisses it with: “So what?”

    It proves my many points that Darwinism is not about evidence but rather about philosophy and ideology…

  34. Mung: Is there any disagreement about which genes belong in the list of 17 “most highly selected polar bear genes”?

    Yes, yes there is.

    By the way, what did Behe have to say about Farese et al. 1995 in “Darwin Devolves”?

    [that’s PNAS 92(5):1774-8]
    Thanks.

  35. Mung:
    Behe:

    Is there any disagreement about which genes belong in the list of 17 “most highly selected polar bear genes”?

    I’m sure Jock will find something he doesn’t like…

  36. Alan Fox: At least some of us try, perhaps sometimes not as hard as we could, to see and comprehend an alternative point of view.

    What’s that? Are you suggesting there is a third-way-view?

  37. Mung:
    https://evolutionnews.org/2019/03/lessons-from-polar-bear-studies/

    My favorite part of Behe’s response is this:
    “Professor Lenski is perhaps the most qualified scientist in the world to analyze the arguments of the book.”
    and
    “…Echoing blogged arguments by his lesser-known co-authors of the appalling review of my book in Science, Professor Lenski points out …”
    He doesn’t even mention Lents and Swamidass by their names…

    I think it is because both of them embarrassed themselves so much, especially recently, that he doesn’t want the critic of his book to lose credibility…That’s why he calls Lenski “…the most qualified scientist in the world to analyze the arguments of the book…” lol

  38. J-Mac,

    I think it is because both of them embarrassed themselves so much, especially recently, that he doesn’t want the critic of his book to lose credibility…That’s why he calls Lenski “…the most qualified scientist in the world to analyze the arguments of the book…” lol

    The embarrassment is not only these guys but also L Moran and K Miller in the past. They publicly used straw man arguments to try and neutralize Behe. A straw man that would minimize their burden of proof.

  39. J-Mac,

    If I were a Darwinist, I would seriously reconsider my support for this ideology…

    What’s a Darwinist?

  40. colewd:
    J-Mac,

    The embarrassment is not only these guys but also L Moran and K Miller in the past.They publicly used straw man arguments to try and neutralize Behe.A straw man that would minimize their burden of proof.

    This is just the beginning…
    Wait until embryo development becomes mainstream, including spatial anisotropies…an such… 😉

  41. J-Mac: I think it is because both of them embarrassed themselves

    Ah you think that do you? That’s cute.

  42. After 10 seconds of searching OMIM

    Familial Hypercholesterolemia Type B

    Familial hypercholesterolemia can be caused not only by defects in the LDL receptor (LDLR; 606945) but also by mutations in apolipoprotein B causing decreased LDLR binding affinity, so-called familial ligand-defective apolipoprotein B (144010). The first mutation of this sort was described by Soria et al. (1989); see 107730.0009. A second was described by Pullinger et al. (1995); see 107730.0017.

    emphasis mine.

    Sorry to burst your bubble, but I would advise some caution. Chances are that it is Behe that is going to be embarassed. Pulling a single favorable publication from the hundreds of papers on hypercholesterolemia and APOB function does not look all that impressive to me.

  43. Who knows. I’m a Darwinist, in the sense that I think natural selection is important and is a significant part in the explanation for the diversity of life and it’s ability to adapt to environmental challenges.

Leave a Reply