Nested Hierarchies (Tree of life)

Moderator’s remark: this post is long enough to need a “more” tag.  But the wordpress editor will only allow me to add that at the very beginning or the very end.  So here it is at the very beginning.

Do you want to be my cousin?
Sure. If not me, then who?

  1. “Nested hierarchies” or “cladistic analysis” or “consilience of independent phylogenies” is often offered as support for Darwinist evolution. This is the idea that the “tree of life” classification of organisms is somehow objective despite being a creation of very zealous “evolution” advocates. The three basic assumptions of cladistics models are: a) Any group of organisms are related by descent from a common ancestor (UCD – universal common descent); b) There is a bifurcating pattern of cladogenesis; c) Change in characteristics occurs in lineages over time. Although not explicit, UCD (“descent from a common ancestor”) here means by a Darwinian “natural selection mechanism” and not by a process generated by a designer that also happens to make use of biologic reproduction.
  2. No assumption can be tested by the model that uses them. That is why they’re called ‘assumptions’ and not ‘conclusions’. Instead, assumptions have to be tested independently through an entirely separated method or be accepted as axioms. An UCD “mechanism” has never been observed or proved elsewhere and is not “self-evidently true”, therefore not a valid axiom. Because UCD is an assumption in “cladistic analysis”, it cannot be logically also a conclusion of any such analysis. Furthermore the conclusions of any “cladistic analysis” will always and trivially be compatible with the UCD assumption in that model.
  3. Hypothesis testing requires an alternative (null) hypothesis and a procedure that demonstrates how the data available is compatible with the successful hypothesis and at the same time is statistically incompatible with the alternative hypothesis. In the “cladistic analysis” case, the alternative hypothesis to UCD is “common design”, and of course UCD cannot be an assumption of such an analysis. However this rule is violated twice, first by the use of an assumption also presented as conclusion, and second by the prejudiced rejection of the alternative “common design” hypothesis before analysis. This clearly demonstrates that “cladistic analysis” can never be logically used as proof of UCD. What “cladistic analysis” is instead is ‘curve fitting’ where the cladistics model is best fitted to certain (conveniently selected!) morphologic/biochemical/genetic biologic data points.
  4. The ‘designer’ hypothesis cannot fail against the ‘no designer’ (Darwinist evolution) alternative in a biologic comparative analysis as designers have maximum flexibility. This is not surprising as designers are free to incorporate whatever mechanism they want, including intelligent “selection” (human breeders do!) and “common descent” (human breeders do!) if they so desire.
  5. The claim that cars and other entities cannot be uniquely and objectively classified (“nested hierarchy”), while organisms can, is false. On one hand, we do know the history of the automobile, so a proper classification must be able to reconstruct their unique “evolution”. Yes, vehicle share parts, so to get to the actual development tree, we must group them differently than organisms since mass production works differently than biologic reproduction. On the other hand, organisms may not be uniquely classified as demonstrated by the numerous revisions and exceptions to the “tree of life”, and in any case, “uniquely classified” is an absolute claim that can never be proven since it is impossible to compare the infinity of possible organism classifications.
  6. The claim that the “tree of life” based on anatomy is validated by the match with the tree based on biochemistry fails. Anatomy is not independent of biochemistry. Also, the oldest DNA ever found was 700k years old therefore any match between the independent trees is limited. This is not to say that the fossil record is complete, or that fossils can be positively linked to one another and the living without – once again – presupposing UCD. The claim that “there is no known biological reason, besides common descent, to suppose that similar morphologies must have similar biochemistry” is false as the ‘designer’ hypothesis produces the same result when one designer creates all morphologies, and furthermore “I cannot think of an alternative reason why…” is not a valid argument.
  7. A “tree of life” is an artificial human construct as organisms do not come labeled with their position in a cladistics hierarchical structure. To decide the position of a certain organism, the human creators of the “tree” have to decide which morphologic/biochemical/genetic characteristics to include and what weight to attach to each of those measures. This further supports the claim that “cladistic analysis” is ‘curve fitting’ rather than ‘hypothesis testing’ – if a tree must be built, a tree will be built as in this example: “The close relationship between animals and fungi was suggested by Thomas Cavalier-Smith in 1987, […] and was supported by later genetic studies. Early phylogenies placed fungi near the plants and other groups that have mitochondria with flat cristae, but this character varies. More recently, it has been said that holozoa (animals) and holomycota (fungi) are much more closely related to each other than either is to plants […].”

 

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1,059 thoughts on “Nested Hierarchies (Tree of life)

  1. Nonlin.org: I don’t know that variations are strictly genetical. Do you? Can you prove? Who cares anyway?

    Just trying to get some things clear. Somewhat higher up the thread you claim that “man births man” and “duck births duck”. Would you please extend that to include “ocelot births ocelot”, ” serval births serval”, “tiger births tiger”, etc. That would satisfy my first request.

    Nonlin.org: What’s “an originally created group”?

    This is the first time I have been asked by a creationist to define this. I was referring to a “created kind”, sometimes called a “baramin”. You know what those are, right?

    Following the logic given above (“duck births duck”), I would guess that you think Felidae can NOT be a created kind, because there cannot have been speciation within created kinds. But since your logic works a bit differently from mine, I won’t be placing any bets on that. Will you please satisfy my second request and take a clear position on this?

    Nonlin.org: Your problem is that you are stuck in the wrong frame of mind and can’t get out therefore keep asking senseless questions.

    Just because you have a hard time answering my questions doesn’t make them senseless.

    Nonlin.org: And let me ASK YOU a question this time: Say one of these days humans get a cat born from a dog. Would that be proof of Intelligent Design? Darwinian evolution? Both? Neither?

    Now that’s a senseless question. As far as I know, nobody is claiming than cats were ever born from dogs, or ever will be. So it won’t count as proof for anything.

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  2. Nonlin.org: Why ONE SINGLE LUCA and not more?

    Keiths and Dazz have been trying to tell you, but you haven’t caught on yet, it seems:

    If there are multiple ancestors to all life, they are not universal, and therefore none of them is the LUCA. By definition, there is either one (1) LUCA or there is none.

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  3. 7/7

    Not for Nonlin. well of course Nonlin is welcome to read the whole thing (if she was able), I could stop her (if she was able). I’m just not directing these to her because she’s shown as astounding inability to understand the most obvious of her mistakes.

    A “tree of life” is an artificial human construct as organisms do not come labeled with their position in a cladistics hierarchical structure.

    1. Of course it’s an “artificial human” construct, just like any other conceptual framework we build to try and understand natural phenomena. Planets don’t come labeled with their positions in orbit. Yet, orbits, those “artificial human” constructs, help us understand the movements of those planets.

    2. Labels are “artificial human” constructs. If organisms came labeled with their positions in a phylogenetic tree, then I’d start considering the possibility of a magical being in the sky. Poor Nonlin shot herself in the foot … yet again.

    To decide the position of a certain organism, the human creators of the “tree” have to decide which morphologic/biochemical/genetic characteristics to include and what weight to attach to each of those measures.

    They have to be able to justify their choices, otherwise they would get their articles rejected.

    This further supports the claim that “cladistic analysis” is ‘curve fitting’ rather than ‘hypothesis testing’

    This further supports that Nonlin has no idea what she’s talking about, but we already clarified this bullshit.

    – if a tree must be built, a tree will be built

    Sure. That doesn’t mean that any tree will be accepted unless it comes with the proper statistical support.

    as in this example: “The close relationship between animals and fungi was suggested by Thomas Cavalier-Smith in 1987, […] and was supported by later genetic studies. Early phylogenies placed fungi near the plants and other groups that have mitochondria with flat cristae, but this character varies. More recently, it has been said that holozoa (animals) and holomycota (fungi) are much more closely related to each other than either is to plants […].”

    It’s always amusing that an ignorant creationist would quote an example where scientists figure things out and correct mistakes as more data, and better statistical procedures, become available, as “support” for the creationist’s claim that trees do not test hypotheses (yet those evil scientists are rejecting earlier hypotheses in favour of newer ones), and that trees are manipulated to tell whatever story evil “Darwinistas” want the tree to tell (yet mistakes were corrected).

    But Nonlin thinks that the universe follows her decrees. Therefore, there’s no way that she can understand any of the many mistakes she’s made. It’s all in her head, she commands it. Therefore it must be so.

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  4. keiths, to Entropy:

    I notice that you use “she” and “her” to refer to Nonlin. Has Nonlin actually self-identified as female?

    I’d like to use the correct pronouns when referring to him/her.

    Entropy:

    Nope. Not that I know. I was trying to be neutral using a generic “she her.” Any suggestion? Maybe “they / them” like some poet, whose name escapes me, used to do?

    English doesn’t really have a good solution. “They/them” is used informally and is catching on in formal use, but it can create some awkwardness. “A person in debt should reconsider their spending habits” works pretty well, since we’re talking about a generic person. “Nonlin should reconsider their spending habits” feels awkward to me, because “they/them/their” doesn’t fit well with a reference to a specific named person.

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  5. keiths,

    Yep. Looks awkward when referring to a specific person. I’m too lazy for the “(s)he – him/her.” So I might keep using she/her for now.

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  6. “I could stop her”

    I meant “I could not stop her.”

    So, is should read

    Not for Nonlin. well of course Nonlin would be welcome to read the whole thing (if she was able), I could not stop her (if she was able). I’m just not directing these to her because she’s shown as astounding inability to understand the most obvious of her mistakes.

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  7. Entropy: I meant “I could not stop her.”

    So, is should read

    Oh dear, you seem to be caught in an endless typo loop 😀

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  8. John Harshman,

    In chart number 9 a gene family of around 100 genes appears in chimps and rats but not mice and humans. The same gene set had to have been lost at least twice which seems like an exceeding rare event. Thoughts?

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  9. colewd:
    John Harshman,

    In chart number 9 a gene family of around 100 genes appears in chimps and rats but not mice and humans.The same gene set had to have been lost at least twice which seems like an exceeding rare event.Thoughts?

    Three thoughts:

    1) That may or may not be true. Gene annotations may be incomplete or incorrect. The proper test is to locate the flanking sequences and assure yourself that no homologous fragments are present in the taxa that supposedly lack the genes. You might also inquire whether the various members of the family are orthologous between chimps and rats. It may not be as simple as you claim. One should also look at lots of species of rodents and primates to check their conditions. Lists of gene families in a few widely separated taxa are not very reliable data. Comparative sequences are better.

    2) Two losses may be rare but is also not out of the question. After all, if losses are independent events, the probability of two losses is just the square of the probability of one loss.

    3) I would also like to point out that you are confused. There is no chart 9. Table 9 doesn’t mention any mammals. Figure 9 doesn’t mention the sizes of any gene families, just the number of families. And you have the number wrong too: it’s 50, not 100. Do better.

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  10. John Harshman,

    Thanks.

    Figure 9: Subset of the dependency graph inferred from the HomoloGene database The graph only shows modules with at least 100 GENES,

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  11. colewd: Figure 9: Subset of the dependency graph inferred from the HomoloGene database The graph only shows modules with at least 100 GENES,

    You have misunderstood again. But I will agree that what you quote is confusing, so you can’t really be blamed. It isn’t the families that have at least 100 genes, it’s the modules. The number of genes per family in the module is not given, though the number of families in the module is (roughly). Still, you have twice failed to comprehend the same bit of the same figure. Should that suggest anything to you?

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  12. colewd,

    What that means is that modules with less than 100 genes were not displayed. So, say, if one “module” had 100 genes in mice, but 99 in humans, the human one would not be displayed.

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  13. John, to Bill:

    3) I would also like to point out that you are confused. There is no chart 9. Table 9 doesn’t mention any mammals. Figure 9 doesn’t mention the sizes of any gene families, just the number of families. And you have the number wrong too: it’s 50, not 100. Do better.

    Divers inanities flowed forth from the rock, like water, and John was sorely vexed. He spake to the rock, saying “Do thou better!”, but the rock was unmoved, and inanities continued to pour forth. John seized his rod and smote the rock thrice, and cursed it. Lo, even then did the inanities rain forth from it.

    John rent his robe and anointed his forehead with ashes. To this day that place is known as Dum Bol-der, or “the place of the stupid rock”.

    Thus were the words of the prophets fulfilled, who said: “Thou canst teach a dumb rock new tricks.”

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  14. Oops — that should be “Thou canst not teach a dumb rock new tricks.”

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  15. Entropy,

    What that means is that modules with less than 100 genes were not displayed. So, say, if one “module” had 100 genes in mice, but 99 in humans, the human one would not be displayed.

    Thanks for trying to clarify. The circles on the graph were actually referred to as families although I agree this is probably interchangeable with modules

    Per the right side group on Figure 9 the circles of the graph were labeled as gene families.
    50 Gene Families
    100 Gene Families
    500 Gene Families
    1000 Gene Families

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  16. John Harshman,

    Two losses may be rare but is also not out of the question. After all, if losses are independent events, the probability of two losses is just the square of the probability of one loss.

    Each gene that is lost in gene organism A and then in organism B is an individual event as you stated previously unless you are proposing that all the genes disappeared in each lineage at once which in itself would be exceedingly rare.

    Either way randomly generated gene loss seems like a poor explanation for the observation.

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  17. colewd:
    Entropy,

    Thanks for trying to clarify.The circles on the graph were actually referred to as families although I agree this is probably interchangeable with modules

    Per the right side group on Figure 9 the circles of the graph were labeled as gene families.
    50 Gene Families
    100 Gene Families
    500 Gene Families
    1000 Gene Families

    No, no, no! The circles are not labeled as gene families. Gene families and modules are not interchangeable. The size of a circle represents the number of gene families (which is not the number of genes) in a module. This is your third consecutive misunderstanding of a simple figure. Ask yourself what this signifies for your ability to read.

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  18. colewd:
    John Harshman,

    Each gene that is lost in gene organism A and then in organism B is an individual event as you stated previously unless you are proposing that all the genes disappeared in each lineage at once which in itself would be exceedingly rare.

    Either way randomly generated gene loss seems like a poor explanation for the observation.

    I can’t respond until this is translated into English.

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  19. John Harshman,

    What does this mean to you?

    Every gene family is introduced in a single module and inherited by all modules that depend on that module.

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  20. John Harshman,

    I can’t respond until this is translated into English.

    Gene loss does not look like a reasonable explanation for the pattern.

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  21. colewd:
    Thanks for trying to clarify.The circles on the graph were actually referred to as families although I agree this is probably interchangeable with modules

    The thing on the side indicates the number of gene families in each module. So, no. Modules and families are not interchangeable. I haven’t read that piece of crap, so I don’t know if the authors used a special language. Normally, gene families means sets of genes that are homologous to each other. Modules normally means a set of genes whose products perform some function. In this piece of crap they might mean something else, but I don’t know if that’s so.

    Anyway, since they don’t display modules with less than 100 genes, that means that a module with 50 gene families contains several genes of the same family. Again, if they’re using common terms.

    Maybe it’s a good idea to read the article very, but very, carefully (a good idea for you, I really don’t care for creationist “literature”).

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  22. colewd:
    Gene loss does not look like a reasonable explanation for the pattern.

    Eukaryotic genomes contains loads and loads of repetitive elements that make it relatively easy for large regions to recombine and thus cause large expansions and losses. So, if two lineages are no longer using some gene, its independent loss is not that hard to happen. If one lineage contains one more, or one less, gene from some gene family in a module than another, not too much of a surprise either.

    There’s also the possibility that the “modules” or the “families” or the “genes” in a particular organism are not part of the database used to build the figure for several reasons, from lack of coverage in the annotation process, mistakes in the annotation process, missing information in the genome sequences (most eukaryotic genome sequences are fragmentary), poor annotation of the genomes in the first place (the genes could be there, but the software to find genes missed it), etc. I think John gave you a few reasons too.

    I would not jump to conclusions from “missing genes,” though I don’t know what conclusion you’re trying to jump into.

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  23. Entropy,

    I haven’t read that piece of crap, so I don’t know if the authors used a special language.

    It appears that there is a one to one correspondence between gene families and modules.

    Every gene family is introduced in a single module and inherited by all modules that depend on that module.

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  24. colewd:
    It appears that there is a one to one correspondence between gene families and modules.

    No Bill. That doesn’t make sense. each circle is a module, and its diameter corresponds, roughly, to the number of gene families in the module. Whatever those two words are supposed to mean, they don’t mean the same thing.

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  25. colewd:
    John Harshman,

    What does this mean to you?

    It means what it says. What I can’t figure out is why you think it’s some kind of argument against common descent.

    colewd:
    John Harshman,

    Gene loss does not look like a reasonable explanation for the pattern.

    Why?

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  26. colewd:
    Entropy,

    It appears that there is a one to one correspondence between gene families and modules.

    That’s your fourth successive misunderstanding of the same simple figure. Quit digging?

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  27. John Harshman,

    That’s your fourth successive misunderstanding of the same simple figure. Quit digging?

    Maybe I do misunderstand but you have failed to support your assertion that I don’t. I am ok to drop this for now as it is not that important.

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  28. John Harshman,

    Poor Bill.

    Maybe, but until you make a reasonable scenario that the gene loss of 100 of the same genes in mice and humans is reasonable I would say.
    Poor John 🙂

    Your claim that there may be measurement issues here is duly noted but unsubstantiated at this point.

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  29. colewd:
    John Harshman,

    Maybe, but until you make a reasonable scenario that the gene loss of 100 of the same genes in mice and humans is reasonable I would say.
    Poor John

    Your claim that there may be measurement issues here is duly noted but unsubstantiated at this point.

    It’s “Poor Bill” because you understand nothing of what you read, here and in the paper we’re discussing, and forge on anyway.

    Genes are gained and lost all the time. out of the thousands of lost genes, a few have been lost in lineages that include chimps and rats but humans and mice . Note that you don’t actually know when any of these genes were lost. Presumably in the chimp lineage after splitting from the human lineage, which is at least a fairly short period as lineages go, but mice and rats are separated by many nodes, and I suspect that a further investigation of rodent taxa will find that the various genes were lost on different branches. Nothing here is surprising. (I also remind you that this gross data set is not a very good way of deciding what species have or don’t have homologous sequences.) You should note that the “modules” corresponding to taxa have many more gene families than the ones that don’t. Why should that be? Note also that most of the non-taxon “modules” also correspond to single losses on the tree (that is, a gene family is best reconstructed as being lost once), which again fits the tree.

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  30. John Harshman,

    Why should that be? Note also that most of the non-taxon “modules” also correspond to single losses on the tree (that is, a gene family is best reconstructed as being lost once), which again fits the tree.

    It also fits the dependency chart without claiming gene loss.

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  31. John Harshman,

    Note that you don’t actually know when any of these genes were lost.

    Sure we don’t but can you come up with a reasonable scenario how this happened twice with the same 100 genes?

    Genes are gained and lost all the time.

    Only based on common descent as a working assumption.

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  32. colewd: Only based on common descent as a working assumption.

    No observationally so. You keep ignoring that this is an observed phenomenon. The pattern we see when we do comparative genetics does not require us to postulate a mechanism that has not been observed operating in extant populations of organisms.

    Duplications, insertions, deletions, substitutions, inversions, shufflings, transpositions. They have all been observed to take place.

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  33. colewd: Me: Note that you don’t actually know when any of these genes were lost.

    Bill: Sure we don’t but can you come up with a reasonable scenario how this happened twice with the same 100 genes?

    What do you mean “the same 100 genes”? Those genes were grouped together precisely because, out of all the thousands of genes lost at various times in various places, they had the same pattern. It’s like you flipping a coin a thousand times, grouping together 100 times that it came up heads, and asking me to justify all those heads being together.

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  34. Rumraket: Duplications, insertions, deletions, substitutions, inversions, shufflings, transpositions. They have all been observed to take place.

    Please link to the YouTube videos.

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  35. John Harshman,

    It’s like you flipping a coin a thousand times, grouping together 100 times that it came up heads, and asking me to justify all those heads being together.

    I will concede for the sake of argument that 1000 genes were lost in mice and humans and we are just looking at 10% of those genes that match. How would you argue that the coin has 2 sides and not 10000 or 20000?

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  36. Alan Fox: What doesn’t “Design” predict? Anything at all?

    I suppose junk DNA. Because ID fans seem always to be upset at the notion that such a thing exists. I would have thought a Designer who had a sense of humor could design junk DNA too, but that’s not the way fans of ID think.

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  37. Alan Fox,

    What doesn’t “Design” predict? Anything at all?

    It does not predict the outcome of rolling two dice 🙂

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  38. colewd:
    John Harshman,

    I will concede for the sake of argument that 1000 genes were lost in mice and humans and we are just looking at 10% of those genes that match.How would you argue that the coin has 2 sides and not 10000 or 20000?

    I’m afraid that was more word salad. Please try harder to make sense. I’m not sure that even you know what you meant by that.

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  39. Joe Felsenstein: I suppose junk DNA.Because ID fans seem always to be upset at the notion that such a thing exists.I would have thought a Designer who had a sense of humor could design junk DNA too, but that’s not the way fans of ID think.

    Maybe with the exception of the pufferfish that has virtually no so-called “junk DNA…just as evolution predicted… 😉

    The problem with 90% of human so called “junk DNA” is that the Designer interconnected it with the 90% of the human brain that is not being used by evolutionists… If the great majority of evolutionists’ brain is not functioning due to optimism bias, they can’t make the obvious inference that either there is something wrong with their evolutionary predictions, or with their brains….
    They choose to stick to the evolutionary formula instead:
    evolution is like a box of chocolates, you never know what you are going to get…

    In some cases though the “junk DNA” issue could very well be related to the sombrero being sewed to the 10% of the ‘functioning’ brain….

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  40. John Harshman,

    I am merely saying that the population size of genes in mammals is not 2 (flip of a coin) but 20000. I think your point is correct except for the population size.

    If you have 1000 genes deleted and 100 of those deletions show up in both mice and humans your problem is calculating the odds of 100 of the same genes missing in both humans and mice out of 20000 total genes and a deletion population of 1000 genes in each animal.

    The issue with this calculation is that not all 20000 genes can survive a deletion event. Certainly PRPF8 cannot. If the population of survivable deletions is too small then your hypothesis is DOA. If it is large it is statistically improbable.

    The tree requires the goldilocks scenario.

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  41. colewd:
    John Harshman,

    I am merely saying that the population size of genes in mammals is not 2 (flip of a coin) but 20000.I think your point is correct except for the population size.

    If you have 1000 genes deleted and 100 of those deletions show up in both mice and humans your problem is calculating the odds of 100 of the same genes missing in both humans and mice out of 20000 total genes and a deletion population of 1000 genes in each animal.

    The issue with this calculation is that not all 20000 genes can survive a deletion event.Certainly PRPF8 cannot.If the population of survivable deletions is too small then your hypothesis is DOA.If it is large it is statistically improbable.

    The tree requires the goldilocks scenario.

    It’s another evolutionary mystery just like this one:

    “A separate but related study published today in Genome Research reports yet another unexpected finding from a comparison of the three great ape genomes. A team led by Mikkel H. Schierup and Thomas Mailund of Aarhus University in Denmark (both co-authors of the Nature report) discovered that some regions of the human genome more closely resemble the orangutan than the chimpanzee. This reflects the fact that at the time humans split off from a common ancestor with chimps, both species had the same ancestral orangutan DNA. But humans and chimpanzees have evolved separately for millions of years. In the process, chimps for mysterious reasons lost some orangutan DNA that humans retained.

    Orangutan Genome Full of Surprises

    http://www.sciencemag.org/news/2011/01/orangutan-genome-full-surprises

    Or

    Orangutan seems more closely related to humans than chimp to humans…. Just like evolution, and Harshman, predicted…lol

    https://www.sciencedaily.com/releases/2009/06/090618084304.htm
    Who needs to go to comedy clubs?

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