Common Design vs. Common Descent

I promised John Harshman for several months that I would start a discussion about common design vs. common descent, and I’d like to keep my word to him as best as possible.

Strictly the speaking common design and common descent aren’t mutually exclusive, but if one invokes the possibility of recent special creation of all life, the two being mutually exclusive would be inevitable.

If one believes in a young fossil record (YFR) and thus likely believes life is young and therefore recently created, then one is a Young Life Creationist (YLC). YEC (young earth creationists) are automatically YLCs but there are a few YLCs who believe the Earth is old. So evidence in favor of YFR is evidence in favor of common design over common descent.

One can assume for the sake of argument the mainstream geological timelines of billions of years on planet Earth. If that is the case, special creation would have to happen likely in a progressive manner. I believe Stephen Meyer and many of the original ID proponents like Walter Bradley were progressive creationists.

Since I think there is promising evidence for YFR, I don’t think too much about common design vs. common descent. If the Earth is old, but the fossil record is young, as far as I’m concerned the nested hierarchical patterns of similarity are due to common design.

That said, for the sake of this discussion I will assume the fossil record is old. But even under that assumption, I don’t see how phylogenetics solves the problem of orphan features found distributed in the nested hierarchical patterns of similarity. I should point out, there is an important distinction between taxonomic nested hierarchies and phylogenetic nested hierarchies. The nested hierarchies I refer to are taxonomic, not phylogenetic. Phylogeneticsits insist the phylogenetic trees are good explanations for the taxonomic “trees”, but it doesn’t look that way to me at all. I find it revolting to think giraffes, apes, birds and turtles are under the Sarcopterygii clade (which looks more like a coelacanth).

Phylogeny is a nice superficial explanation for the pattern of taxonomic nested hierarchy in sets of proteins, DNA, whatever so long as a feature is actually shared among the creatures. That all breaks down however when we have orphan features that are not shared by sets of creatures.

The orphan features most evident to me are those associated with Eukaryotes. Phylogeny doesn’t do a good job of accounting for those. In fact, to assume common ancestry in that case, “poof” or some unknown mechanism is indicated. If the mechanism is unknown, then why claim universal common ancestry is a fact? Wouldn’t “we don’t know for sure, but we believe” be a more accurate statement of the state of affairs rather than saying “universal common ancestry is fact.”

So whenever orphan features sort of poof into existence, that suggests to me the patterns of nested hierarchy are explained better by common design. In fact there are lots of orphan features that define major groups of creatures. Off the top of my head, eukaryotes are divided into unicellular and multicellular creatures. There are vetebrates and a variety of invertebrates. Mammals have the orphan feature of mammary glands. The list could go on and on for orphan features and the groups they define. Now I use the phrase “orphan features” because I’m not comfortable using formal terms like autapomorphy or whatever. I actually don’t know what would be a good phrase.

So whenever I see an orphan feature that isn’t readily evolvable (like say a nervous system), I presume God did it, and therefore the similarities among creatures that have different orphan features is a the result of miraculous common design not ordinary common descent.

5,163 thoughts on “Common Design vs. Common Descent

  1. Robin,

    . So the ancestors of zebrafish might well have been ancestral to all mice and chickens and humans, but current zebrafish are not.

    Great. Chickens are birds and mice are mammals. Mice are closer to humans then chickens. Is there a common ancestor of mice and birds that is not a common ancestor of humans?

  2. Erik: First and foremost, it matters what those characters *are* and what they *do*.

    Allan Miller: Absolutely wrong. You don’t need any information at all about function to be able to draw a tree – particularly on molecular data, something you seem singularly uninterested in.

    The fact that not much is needed to draw the tree is exactly the problem. You can draw a tree on anything.

    In order to be able to justifiedly claim what the tree represents- e.g. that the tree is about species evolving from a few to many, even more, that the tree demonstrates such evolution – you absolutely must know the substance behind the data. The data by itself does not tell you that, for example, manuscripts don’t breed while species do. It’s necessary to know independently what manuscripts are and what they do, if anything, and what species are and what they do.

    It’s not enough to know the data. It’s essential to know what the data is about.

    Erik: Is someone born with one leg missing the same as acquiring a unique novel distinguishing character?

    Corneel: Absolutely! But not a character that is likely to be heritable and become fixed in humans, wouldn’t you agree?

    See, I was right that there’s more to it than just being a unique novel distinguishing character. It has to be also heritable and fixed. There’s a loadful of presuppositions you are not being open about.

    Corneel:
    Not even species radiation after the flood? Do you believe in special creation then? If so, how do you reconcile special creation with the nested hierarchy of life?

    Let’s say dogs are domesticated wolves. Is that radiation?

    Nested hierarchy is a given. There’s above and below, and that’s how the universe is ordered. What is there to reconcile?

    Rumraket: Well if that was really how a common descent was inferred then I’d be right there with you. But it isn’t how it is inferred. So when you say “Darwin with his…” as if you are actually referring to the method by which common descent is inferred, you are simply attacking a straw man.

    Look, I know that there is more to taxonomy. However, Darwin is quotable the way I quoted him. To refute the alleged strawman, quote what he *really* thinks about taxonomy. Take your time.

    Rumraket: “The tree” can’t be consilient. Different, independent trees can be consilient with each other. That is the crucial point.

    I know. It may look like a crucial point to you, but it’s insufficient. It merely describes the complexity of the data. It still does not tell anything about the causality in the described substance itself.

    If the same data were gathered from artful series of dashes on sheets of paper and the data could be arranged in nested hierarchies, it would NOT justify the conclusion that the dashes and the sheets of paper multiply or change by themselves, not by any stretch of the imagination. A direct knowledge of the substance itself is categorically required.

    Rumraket: No, what matters is that those characters are heritable traits. THAT is what matters.

    Yes, good. But immediate observations show that traits are inherited along species, not across species. It’s a separate matter to demonstrate that traits are inherited across species, and I don’t know how you will be able to demonstrate that everything in biosphere is inherited from a one/a few original species, as advertized by UCA. Drawing trees will not help here.

  3. Rumraket,

    Why?

    Can you identify a functional sequence (can function on its own) that can be experimentally validated to have originated without an intelligent cause?

  4. stcordova: Common descent doesn’t explain orphan systems does it?No one here has shown that Theobald’s research explains orphan systems.I’ve provided some examples of orphan systems, including Orphan Genes, Taxnomically Restricted Genes, but that’s just the tip of the iceberg.

    Of course common descent doesn’t explain orphan systems, but there’s no reason it should. Common descent explains what it is intended to explain, the hierarchical pattern in phylogenetic data. Many of what you think of as orphan systems, when mapped onto a tree, can be shown to have evolved gradually, so common descent can certainly be used to help explain them..

    Common design doesn’t have to be an explanation, it can be an OBSRVATION.The octopus eye vs human eye, the placental and mammalian convergences are common designs independent of common descent.

    That’s prejudicial and confusing language, which you should avoid for the sake of clarity if for no other reason. If all you mean by common design is similarity, you have said nothing.

    Common descent can explain some common designs, but not all of them.That is clearly the case in the issue of convergences.

    Please stop using that language. Please reserve “common design” for the postulated actions of god in creating similar taxa from nothing. So, can common design explain convergence? Can common design explain nested hierarchy?

    What do you mean it explains nothing.What if the explanation of how God did it is beyond human comprehension. If it happened by a miracle, then by definition you won’t get an explanation. If you won’t accept facts unless you can comprehend them by being fed and explanation, then there are lot of truths in the universe you probably shouldn’t be accepting, including the evolution of orphan systems. You’re not applying the same standards of evidence to common descent, yet you apparently accept it, even without an explanation beyond, “it happened.”

    No, we know how common descent happens: reproduction within populations, splitting of populations (largely by speciation) and divergence. One great thing about that is that it predicts the sort of data we ought to see. And we do. What does common design predict? Nothing? And so it explains nothing. “God moves in mysterious ways, his wonders to perform” isn’t an explanation; it’s a denial that explanation is possible. You are free to do that, but it removes you from any possibility of doing science.

    And we can explain phenomena by miracles if there is any way of knowing what miracles are and are not to be expected. Take “kinds”. Are there any expectations of how we might recognize created kinds, whether two populations belong to the same kind or whether they belong to different kinds? As far as I can see, there are not, just because nobody can say what god would or would not do. There’s the death of science again.

  5. colewd:
    Rumraket,
    Can you identify a functional sequence (can function on its own) that can be experimentally validated to have originated without an intelligent cause?

    You didn’t answer the question. You seldom answer questions. Please try again. The questions was “Why?”, meaning “Why does a functional sequence of more than a few characters require design”?

    Also, what do you mean by “can function on its own”?

  6. colewd:
    Robin,

    Great.Chickens are birds and mice aremammals.Mice are closer to humans then chickens.Is there a common ancestor of mice and birds that is not a common ancestor of humans?

    No. Why do you ask?

  7. Bill,

    Do you finally recognize, and acknowledge, that your claim about the “reappearance” of genes in humans is based on a complete misunderstanding?

  8. John Harshman,

    No, we know how common descent happens: reproduction within populations, splitting of populations (largely by speciation) and divergence. One great thing about that is that it predicts the sort of data we ought to see. And we do. What does common design predict? Nothing? And so it explains nothing. “God moves in mysterious ways, his wonders to perform” isn’t an explanation; it’s a denial that explanation is possible. You are free to do that, but it removes you from any possibility of doing science.

    I don’t think reproduction explains the data in Sal’s flower. Maybe you can connect the dots. The pattern is what I would expect from design based on the re use of specific components ( genes) independent of genetic relationship.

  9. John Harshman,

    You didn’t answer the question. You seldom answer questions. Please try again. The questions was “Why?”, meaning “Why does a functional sequence of more than a few characters require design”?

    Because all the evidence points to design as the cause of long functional sequences such as phone numbers, books, computer programs etc.

  10. Paul C: Anything can be explained by “common design”. That’s why it explains nothing.

    Any nested hierarchy can be explained by common descent. That’s why common descent doesn’t predict the actual nested hierarchy. It explains nothing.

    Why this nested hierarchy and not some other nested hierarchy? It just happened, that’s all.

  11. John Harshman:

    No, we know how common descent happens: reproduction within populations, splitting of populations (largely by speciation) and divergence.

    No we don’t. You’re extrapolating small sample sizes to domains they don’t apply.

  12. colewd:
    John Harshman,

    I don’t think reproduction explains the data in Sal’s flower.Maybe you can connect the dots.The pattern is what I would expect from design based on the re use of specific components ( genes) independent of genetic relationship.

    Again we’re back to why?

    First, why would you expect anything of your unspecified and unlimited designer? You don’t exactly demand anything of your “hypothesis,” but only demand answers of the only theory that does provide answers, just not all of them, a fact that you attempt to exploit while ignoring your obligation to provide evidence for your claims.

    Secondly, since evolution involves gene loss and gene gain, how would it be possible for two lineages to avoid losing some of the genes that another two would not lose?

    Your saying what you’d “expect of design” simply tells us nothing, because you have provided no reason for such “expectations.” Meanwhile, the “flower” is essentially what would be expected of evolution. Just because Sal says something doesn’t mean anything, which you should catch onto after his many many failures.

    Glen Davidson

  13. colewd:
    John Harshman,

    Because all the evidence points to design as the cause of long functional sequencessuch as phone numbers, books, computer programs etc.

    You mean, evidence points to “design” as the cause of human-made objects?

    I’d say “wow,” if I knew of anyone who thought otherwise.

    Glen Davidson

  14. keiths,

    . So the ancestors of zebrafish might well have been ancestral to all mice and chickens and humans, but current zebrafish are not.

    Looks like Robin may be in the re appear camp. Lets see how this plays out.

  15. John Harshman: Please stop using that language. Please reserve “common design” for the postulated actions of god in creating similar taxa from nothing.

    LoL!!!

    John is lost unless he’s arguing against Young Earth Creationism and Fixity of Species.

  16. GlenDavidson,

    You mean, evidence points to “design” as the cause of human-made objects?

    No, the evidence points to design as the cause of sequences a subset of human-made objects.

  17. colewd:
    GlenDavidson,

    No, the evidence points to design as the cause of sequences a subset of human-made objects.

    No, you just made that up.

    There’s nothing special about “sequences,” no matter how much you want it to be otherwise. We recognize the difference between designed objects and life’s remnants easily in the archaeological record.

    Glen Davidson

  18. colewd:

    Looks like Robin may be in the re appear camp. Lets see how this plays out.

    Bill,

    I see no evidence that Robin is making that mistake, and anyway, the question is about you:

    Do you finally recognize, and acknowledge, that your claim about the “reappearance” of genes in humans is based on a complete misunderstanding?

  19. GlenDavidson,

    There’s nothing special about “sequences,” no matter how much you want it to be otherwise.

    The number of ways to arrange an 90 plus character phone number is orders of magnitude larger then the number of atoms in our universe and you claim there is nothing special about it? I disagree here. I think it is one of the most incredible mathematical phenomena there is.

  20. keiths,

    I see no evidence that Robin is making that mistake, and anyway, the question is about you:

    Lets see how it plays out. Be patient.

  21. colewd:
    GlenDavidson,

    The number of ways to arrange an 90 plus character phone number is orders of magnitude larger then the number of atoms in our universe and you claim there is nothing special about it?I disagree here.I think it is one of the most incredible mathematical phenomena there is.

    How many ways are there to arrange oxygen atoms in a vortex? How many ways are there to arrange hydrocarbon molecules (usually with some oxygen atoms–in thinner) in mixing into paint in turbulent patterns?

    Huge numbers commonly end computation in the real world. The complexity of a flaked edge is enormous. I have no idea why sequences are supposed to be special (physically, they’re just more complex structures) over the other arrangements of atoms. Oh, except that IDists try to pretend that they’re special, and insist that they must be designed.

    Glen Davidson

  22. colewd,

    Lets see how it plays out. Be patient.

    See how what plays out? You made the mistake. We’ve corrected you.

    And so I ask: Do you finally recognize, and acknowledge, that your claim about the “reappearance” of genes in humans is based on a complete misunderstanding?

    If you don’t recognize your error then the discussion is unlikely to get very far.

  23. GlenDavidson,

    Huge numbers commonly end computation in the real world. The complexity of a flaked edge is enormous. I have no idea why sequences are supposed to be special (physically, they’re just more complex structures) over the other arrangements of atoms. Oh, except that IDists try to pretend that they’re special, and insist that they must be designed.

    Glen, I consider the fact that we can communicate across the globe as phenomenal. We are using sequences to do it. Layered sequences just like the translation/transcription mechanism in cells. English letters that get translated to binary ASKI characters transmitted then back to english letters all in real time. While this is now common place it is still phenomenal.

  24. keiths: If you don’t recognize your error then the discussion is unlikely to get very far.

    Or if he does.

    He’s already back to digging his heels with IDist soundbites respecting sequences. It’s about fighting the enemy for them, not learning about the world and life.

    Glen Davidson

  25. keiths,

    See how what plays out? You made the mistake. We’ve corrected you.

    No one has come up with a coherent explanation of how reproduction can create the pattern is Sal’s flower. Until then the re appear hypothesis remains alive.

  26. colewd,

    No one has come up with a coherent explanation of how reproduction can create the pattern is Sal’s flower. Until then the re appear hypothesis remains alive.

    Yes, they have, and no, it doesn’t. If you can’t understand even that much, then this entire discussion is going to be fruitless.

    Your mistakes are fundamental, Bill.

  27. Bill,

    Notice how I keep asking you to draw the tree, indicating where you think the gene losses and “reappearances” are occurring?

    Why not actually do that and attach a photo of your drawing to your next comment?

  28. keiths,

    Yes, they have, and no, it doesn’t. If you can’t understand even that much, then this entire discussion is going to be fruitless.

    Your mistakes are fundamental, Bill.

    Can you carry the argument or just make an assertion? Try to explain the patterns.

  29. Draw the tree, Bill.

    I even gave you instructions a few days ago:

    Damn, Bill. This isn’t difficult. If you can’t picture it mentally, then draw the relationships on a piece of paper.

    Humans are more closely related to mice than to chickens, which means they share a most recent common ancestor (MRCA) that is not shared with chickens. Draw that and label the ancestor AHM, for “ancestor of humans and mice.”

    AHM shares a most recent common ancestor with chickens. Draw that and label the ancestor AHMC, for “ancestor of humans, mice and chickens.”

    You should now have a tree with AHMC at the root. One branch leads from AHMC to chickens; the other leads from AHMC to AHM.

    There are two branches from AHM. One leads to humans and the other leads to mice.

    You are trying to explain why a particular gene G is present in humans and chickens but not in mice. The obvious answer is that G was present in AHMC and AHM. It got passed to chickens and humans, but somewhere on the path from AHM to mice it got lost.

    Just one event: a gene loss. No genes lost and regained.

    I sincerely hope that you can figure out how to extend the tree to include zebrafish and the additional common ancestor.

  30. colewd:
    Robin,

    Great.Chickens are birds and mice aremammals.Mice are closer to humans then chickens.Is there a common ancestor of mice and birds that is not a common ancestor of humans?

    No. That would not be possible.

    See attached for an example.

    To put this another way, since mice and humans are both mammals and humans evolved from a common ancestor of mice, any ancestor of mice will be an ancestor of humans.

  31. Can you carry the argument or just make an assertion? Try to explain the patterns.

    Most of the pattern is very simple. Closer relatives share more genes than distant ones. Every region of Sal’s flower marking a clade has more genes in it that the ones that don’t. Regions that require a single gain or loss (per gene) to explain have more genes in them than those that require multiple gains or losses. All that maps pretty well onto a tree. If you added lots more species it would map even better. If you looked at individual genes rather than totals it would map even better than that, and most of the gains could be seen to be duplications, and most of the losses could be seen to be only partial, with one species or another retaining a pseudogene. Again, with more species the picture would be clearer.

    Contrast your explanation of “re-use of parts”. Why should particular parts be re-used in that pattern rather than some other? Why should most of that re-use match the expections of phylogeny? Why should god have inserted pseudogenes? Why are all those re-used genes different from each other in ways that fit the tree? You can’t just toss off this explanation. You have to defend it against the data. And when you do that, you lose.

  32. keiths,

    Great.Chickens are birds and mice aremammals.Mice are closer to humans then chickens.Is there a common ancestor of mice and birds that is not a common ancestor of humans?

    No. Why do you ask?

    Here is John’s answer. Now you can draw the tree and explain the ancestral pattern without a group of genes re appearing or the same number of genes being lost independently in two lineages.

  33. colewd:
    John Harshman,

    Because all the evidence points to design as the cause of long functional sequencessuch as phone numbers, books, computer programs etc.

    I believe various papers showing function in random protein and DNA sequences have been cited to you before. Did you forget or do you have some way of dismissing all that research?

  34. colewd: Here is John’s answer. Now you can draw the tree and explain the ancestral pattern without a group of genes re appearing or the same number of genes being lost independently in two lineages.

    The solution is the last part: genes are fairly often lost independently in two lineages. You’ve been told that before. Did you forget again?

  35. Robin:

    No. That would not be possible.

    Agreed, but the diagram I provided shows genes that only humans and chickens share and then genes that only mice and chickens share!!!!!!!!!

    The solution by evolutionary biologists is to postulate the ancestor of all 3 had all these isolated genes (and then some), and then lost them in a way to create the pattern in the diagram.

    Sometimes the terms used to describe this process is Incomplete Lineage Sort (ILS). But that is beside the point. This essentially requires the ancestor of Mice, Humans, and Chickens get a bit of a poof of all these genes in the first place, and lose them.

    The requisite evolutionary pathway then goes something like: new Ancestor with a POOF of new genes, followed by gene loss of those genes in the descendants coupled with poofs of more orphan genes… rinse and repeat.

    The problem of orphan genes appearing for species and ancestors of species is so bad, evolutionists have gone into denial that orphan genes exist in humans! This is bad for science:

    The one week I was running the News desk for Denyse O’Leary, I pointed out:

    1,177 human orphan genes removed by evolutionists from databases

    1,177 human orphan genes removed by evolutionists from databases

    Here is a case of evolutionary bias causing misrecognition of orphan genes in humans. Orphan genes are presumed protein coding genes that exist in only one species and have such non-similarity to anything in any other species they are called orphans (a play on words of the ORF acroym for Open Reading Frame).

    This came up in the Nelson-Velasco debate where Velasco said there are 0 orphan genes, and Nelson pointed out the reason some say they are zero is because of their biases.

    Nelson has been vindicated as I pointed out in New Mechanism of Evouion — POOF

    Here’s is the proof of this cover up Distinguishing protein-coding and noncoding genes in the human genome:

    This whole thing about assuming the NIH ENCODE project is wrong, or assuming human orphan genes don’t exist, this is all premature hasty conclusions. That isn’t good science.

    There are numerous orphans in all sorts of species. This is a problem.

    In addition to that, as I pointed out, the wider the sampling of creatures the more genes are shown to be necessary in the common ancestor of a group. GlenDavidson said it figuratively well: “this means LUCA has 7 million genes.”

    Granted the oprhans have not be confirmed by transcriptome analyses, but this is also true of many genes that aren’t orphans. It is known that some genes are only expressed for a few hours and then never heard from again. For this reason, it is brutally difficult to prove they are active or not. But the orphans are there, nonetheless.

  36. keiths,

    You are trying to explain why a particular gene G is present in humans and chickens but not in mice. The obvious answer is that G was present in AHMC and AHM. It got passed to chickens and humans, but somewhere on the path from AHM to mice it got lost.

    No were not. Were trying to explain why 73 genes are existent in humans and Zebra fish but not chickens and mice.

  37. John Harshman,

    The solution is the last part: genes are fairly often lost independently in two lineages. You’ve been told that before. Did you forget again?

    So your claim is that the same number of genes are independently lost in two separate lineages independently by reproduction?

  38. colewd,

    No were not. Were trying to explain the existence of why 73 genes are existent in humans and Zebra fish but not chickens and mice.

    Good grief, colewd. The comment I quoted is from an earlier discussion in which you were arguing for the “reappearance” of genes.

    My point in quoting it was so that you could finally draw the frikkin’ tree, according to the instructions contained therein. Please do so and indicate where you think the gene losses and “reappearances” are occurring.

  39. Along the lines of the difficulty of determining active genes, Cornelius Hunter describes genes that get expressed in only 16 cells out of the hundreds of trillions in a human! These genes are silent for the other hundreds of trillions of cells.

    http://darwins-god.blogspot.com/2017/01/regulatory-genes-are-expressed-for-but.html

    Regulatory Genes Are Expressed For But a Few Hours

    “Grabbed by Evolution”
    How would you explain the evolution of a small set of genes that are expressed for but a few brief hours—when we consist of only 8-16 cells—in a finely-tuned choreography unique to placental mammals? The answer, of course, is to use teleological language because the evolutionary explanation is so transparently unrealistic. To wit, Ignacio Maeso explains:

    It was really shocking to find these genes are only read for a pulse of a few hours in our entire lifetime. … They are found on chromosome 19, known to be an unstable part of our genome. Think of it as a bubbling cauldron of DNA, with individual bits of DNA being added and taken away, occasionally forming whole new genes. At the dawn of placental mammals, 70 million years ago, these genes emerged and were grabbed by evolution to perform a new task, acting to control what cells do in the earliest stages of development.

    As usual, the infinitive form tells the tale.

  40. Robin,

    By “re appear camp”, Bill means “reappear camp”. He apparently thinks that you believe, as he does, that genes that were lost magically reappeared later.

  41. Mung: Any nested hierarchy can be explained by common descent. That’s why common descent doesn’t predict the actual nested hierarchy. It explains nothing.

    Any mountainrange can be explained by plate tectonics, that’s why plate tectonics doesn’t predict a particular mountainrange. It explains nothing.

    Why this nested hierarchy and not some other nested hierarchy? It just happened, that’s all.

    Why a mountain with the exact shape of the Mt Everest, instead of a mountain with another shape? Oh gee it must have been designed.

  42. stcordova: The solution by evolutionary biologists is to postulate the ancestor of all 3 had all these isolated genes (and then some), and then lost them in a way to create the pattern in the diagram.

    Sometimes the terms used to describe this process is Incomplete Lineage Sort (ILS). But that is beside the point.

    It’s not only beside the point, it’s wrong. You do not appear to know what “incomplete lineage sorting” means. It refers to ancestral polymorphisms maintained through two or more speciations, with different loss of some variants in descendants. That isn’t at all what is being proposed here.

    This essentially requires the ancestor of Mice, Humans, and Chickens get a bit of a poof of all these genes in the first place, and lose them.

    No, no big poof is necessary. All you need is that in the time since the sarcopterygian (human, mouse, chicken) clade split from the actinopterygian (zebrafish) clade, either various genes arose at various times over the course of hundreds of millions of years, or that the zebrafish lineage lost them, or, more likely, a little of both. Surveying more species would shed light on just what happened.

    The requisite evolutionary pathway then goes something like: new Ancestor with a POOF of new genes, followed by gene loss of those genes in the descendants coupled with poofs of more orphan genes… rinse and repeat.

    Well, sort of. Stripped of the silly language, all you’re saying is that from time to time new genes arise and that from time to time old genes are lost. What’s the problem with that? We know of several mechanisms by which both of these things can happen.

    The problem of orphan genes appearing for species and ancestors of species is so bad, evolutionists have gone into denial that orphan genes exist in humans!

    The actual problem is that you are switching between two different definitions of “orphan gene” without noticing. One definition would refer to a gene without homologous sequences in any other group. That applies mostly to bacteria. Another definition would refer to a gene that isn’t a gene in any other group, even if there are homologous sequences elsewhere. That definition applies to the orphan genes in humans, most of which have non-genic homologs in chimps and/or gorillas. Any argument is over whether the sequences actually function as genes in one or another species, which requires more than just finding an open reading frame, but which fortunately is irrelevant to our discussion here. Further, the diagram you reference isn’t even talking just about orphan genes by either definition, but includes new members of old gene families, for which gene duplication is the obvious explanation.

  43. keiths,

    Harshman already made the claim of why this happened.

    The solution is the last part: genes are fairly often lost independently in two lineages.

    The fact that this is observed is conclusive evidence that reproduction alone is not the cause of the diversity we are observing.

  44. colewd:
    John Harshman,

    So your claim is that the same number of genes are independently lost in two separate lineages independently by reproduction?

    Where do you get “the same number of genes” from? Lots of genes are lost in various lineages. The little Venn diagram only counts how many fall into each of the overlapping regions. Some genes were lost in mice. Some genes were lost in chickens. Some were lost in both, presumably just by chance. It’s just the intersection of two sets.

  45. colewd: Harshman already made the claim of why this happened.

    The solution is the last part: genes are fairly often lost independently in two lineages.

    The fact that this is observed is conclusive evidence that reproduction alone is not the cause of the diversity we are observing.

    You will have to explain why that’s evidence at all, let alone conclusive.

  46. Mung,

    Not so. Erik is quite clearly making an argument. If you don’t want to address it, or can’t, just say so. No need to blame Erik.

    Are you able to articulate ‘Erik’s argument’ in simple terms so I can understand it, then? So far, all I see is repeated denial of the validity of phylogenetic trees as representing phylogenies. Which is not really an argument.

  47. stcordova: How would you explain the evolution of a small set of genes that are expressed for but a few brief hours

    Like I would explain all forms of environmentally induced gene regulation. An interaction between the environment and the a regulatory element is beneficial and therefore retained by natural selection. The expression is active if and when the environmental signal is present.

    The evolution of regulated operons in the laboratory is an observed fact.

    Reconstructions of the evolutionary history of transcription factors have, for example, showed how hormone-controlled transcription factors have diversified over geological time and how novel DNA binding capacities have emerged by duplication and divergence of ancestral molecules:
    McKeown AN, Bridgham JT, Anderson DW, Murphy MN, Ortlund EA, Thornton JW.
    Evolution of DNA specificity in a transcription factor family produced a new gene regulatory module.
    Cell. 2014 Sep 25;159(1):58-68. doi: 10.1016/j.cell.2014.09.003

    Figure 1. Evolution of Novel Specificity Occurred via a Discrete Shift between AncSR1 and AncSR2.
    (A) Architecture of SR response elements. All SRs bind to an inverted palindrome of two half-sites (gray arrows) separated by variable bases (n). x indicates sites at which ERE and SREs differ.
    (B) SR phylogeny comprises two major clades, which have nonoverlapping specificity for ligands (stars) and REs (boxes). Preferred half-sites for each clade are shown; bases that differ are underlined. Ancestral and extant receptors are colored by RE specificity (purple, ERE; green, SREs; pink, extended monomeric ERE). The orange box indicates evolution of specificity for SREs; number of substitutions on this branch and the total number of DBD residues are indicated. Nodal support is marked by the approximate likelihood ratio statistic (aLRS): unlabeled, aLRS 1 to 10; one solid dot indicates aLRS 10 to 100; two solid dots indicate aLRS > 100. Scale bar is in substitutions per site.
    (C) AncSR1 specifically activates reporter gene expression driven by ERE (purple bar) with no activation from SRE1 (light green) or SRE2 (dark green); AncSR2’s specificity is distinct. Bar height indicates fold activation relative to vector-only control with SEM of three experimental replicates.
    (D) Ancestral binding affinities reflect distinct specificities for ERE versus SREs. Bars heights indicate the macroscopic affinity (KA,mac) of binding to palindromic DNA response elements, measured using fluorescence polarization; error bars show SEM of three experimental replicates. Colors as in (C).
    (E–G) The components of macroscopic binding affinity—affinity for a half-site (K1) and cooperativity of binding (u)—by AncSR1 and AncSR2 were estimated by easuring binding to a half-site and a full palindromic RE and then globally fitting the data to a model containing both parameters. Error bars show SEM of three experimental replicates. See Figure S1 and Tables S1, S2, and S3.

  48. colewd:
    keiths,

    No one has come up with a coherent explanation of how reproduction can create the pattern is Sal’s flower.Until then the re appear hypothesis remains alive.

    Bill, it’s really not that complex.

    Some point waaay back when there’s a Common Ancestor to the group of current organisms zebrafish, chickens, mice, and humans. That CA split at some point. This CA has 73 genes we see in both zebrafish and humans BEFORE THE SPLIT. The split creates a group of organism that ultimately lead to zebrafish with the 73 genes. The other group is the ancestor of chickens, mice, and humans. It continues along and then splits. One group eventually leads to Chickens. That group loses the 73 genes. The other group is the ancestor of all mammals and STILL HAS THE 73 genes. The group splits at some point, one group being the ancestor of mice and the other group being the ancestor of humans. The first group LOSES THE 73 genes. The second group still has the 73 genes.

    What’s the problem?

Leave a Reply