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.

3,736 thoughts on “Common Design vs. Common Descent

  1. Mung: So DNA replication is an inevitable consequence of semiconservative replication of DNA. Just brilliant. Any more gems of wisdom?

    Your arguments, if one can even call them that at this stage, have regressed to the point of meaningless nonsense. Given that you have nothing left of sense to add I think we can conclude this discussion: Evolution predicts a nested hiearchy.

  2. Rumraket: Evolution predicts a nested hiearchy.

    If by “evolution” you mean “semiconservative replication of DNA.” But no one but you and dazz (and perhaps Allan) define evolution that way.

    Is it the atheism, the evolutionism, or the combination of the two that leads people here to cling to such obvious nonsense? Why not just admit that you were wrong?

    Evolution doesn’t predict semiconservative replication of DNA, and given semiconservative replication of DNA you will have a nested hierarchy. No evolution required.

  3. dazz:

    This is ridiculous

    Word lawyering. It’s all Mung has.

    After 15-odd years in the evolution debates.

  4. Allan,

    Even HGT events give rise to nested gene trees.

    For those particular genes, sure. But those trees will then clash with the trees produced by vertical inheritance, which is how we determine that HGT occurred in the first place.

    What we are concerned with in this thread is the objective nested hierarchy — the one that reflects the actual pattern of common descent. While the results of an HGT event can help establish that pattern in later generations, as those results are passed down via vertical inheritance, the HGT event itself creates a “false” signal that makes it harder to discern the prior pattern of common descent.

    Hence my earlier statement:

    Branching descent does indeed generate a nested hierarchy, as a simple matter of logic. That hierarchy may or may not be inferable, however. Whether it’s inferable depends on other things such as the amount of horizontal transfer and the rate and nature of the genetic changes.

  5. Mung: Is it the atheism, the evolutionism, or the combination of the two that leads people here to cling to such obvious nonsense?

    Nice to have yet another confirmation that the disagreement here is between those who see it in terms of observation, and those who see it in terms of religion. There are flat earthers, and geocentrists, and evolution rejectors, and cultural reactionaries, and when you scratch the surface of any of these, you find religion.

    I suspect that superstition comes more naturally to the human brain than science. Science is very much an acquired taste, while superstition is apparent even in the cradle.

  6. Mung,

    After being informed that you misinterpreted what I wrote why would you repeat this silly nonsense?

    In case you missed it:

    Mung: Except that I did not say that DNA replication has nothing to do with evolution.

    But nice try.

    Do try to keep up Allan.

    I’m prepared to accept that’s not what you meant, but it’s certainly what you said. If one says ‘semiconservative DNA replication predicts a nested hierarchy’, and you say ‘nothing to do with evolution then’, the reader only has a certain amount to go on.

  7. Mung,

    So DNA replication is an inevitable consequence of semiconservative replication of DNA. Just brilliant. Any more gems of wisdom?

    No, common descent is an inevitable consequence of semiconservative replication of DNA. I know you’re sore because you feel I’ve misinterpreted you, but you don’t have to go out of your way to do the same.

  8. keiths,

    No, the point is that gene trees are useful for reasons other than ‘proving the nested hierarchy’. One might wish to trace the history of – say – a retroviral insert; one does not simply start at the point it enters vertical descent; it has its own evolutionary history.

  9. Allan,

    For the purposes of this thread — “Common Design vs Common Descent” — the central issue is the existence of the objective nested hierarchy, and the conditions under which we can successfully infer it.

    HGT — particularly if it is rampant — can make the inference more difficult, or even impossible.

    And the fact that HGT could be rampant in a guided evolution scenario is one of the reasons that the ONH we see is fatal not only to the hypothesis of common design, but to guided evolution as well.

  10. keiths,

    The fact that the expectation of common descent applies to HGT’d genes as well as vertically inherited ones means that it is entirely within the scope of the thread. In all instances – whole-genome or segment – Common Descent and Common Design sit as opposing explanations for the pattern. CD would need to explain commonalities in viral sequences and transposons just as much as those in whole-organism comparisons.

  11. Allan Miller: I’m prepared to accept that’s not what you meant, but it’s certainly what you said.

    It’s certainly what I wrote. But “nothing to do with evolution then” didn’t have “semiconservative DNA replication” as it’s subject. The discussion was over whether evolution predicts the nested hierarchy.

    Here was the exchange:

    Allan: Even lower-level, it’s an inevitable consequence of semiconservative replication of DNA.

    The IT in your comment referred to the nested hierarchy.

    Mung: So it has nothing to do with evolution, and claiming it’s a prediction of evolution is utterly gratuitous.

    The IT in my sentence referred to the same thing as your IT. The nested hierarchy.

  12. Rumraket: You have now discovered that evolution happens because organisms imperfectly reproduce.

    Evolution is possible because organisms imperfectly reproduce. That doesn’t make evolution and imperfect reproduction the same thing.

  13. Mung, to Allan:

    The IT in my sentence referred to the same thing as your IT. The nested hierarchy.

    Which means your sentence was wrong:

    So it has nothing to do with evolution, and claiming it’s a prediction of evolution is utterly gratuitous.

    Christ, Mung.

  14. keiths:
    Allan,

    For the purposes of this thread — “Common Design vs Common Descent” — the central issue is the existence of the objective nested hierarchy, and the conditions under which we can successfully infer it.

    HGT — particularly if it is rampant — can make the inference more difficult, or even impossible.

    And the fact that HGT could be rampant in a guided evolution scenario is one of the reasons that the ONH we see is fatal not only to the hypothesis of common design, but to guided evolution as well.

    Yes, but even very fast evolution without HGT could also obscure any ONH signal as well. Many viruses seem to evolve too quickly to maintain the information of the relationships they may have with other viruses. Glycolysis also seems likely to be related in organisms, but there’s no meaningful signal of relatedness among many versions, apparently in part because it seems to be a very old means of releasing useful energy..

    As with any information, nothing ensures that meaning must survive.

    Glen Davidson

  15. Glen,

    Yes, but even very fast evolution without HGT could also obscure any ONH signal as well.

    Right, which is why I wrote:

    Branching descent does indeed generate a nested hierarchy, as a simple matter of logic. That hierarchy may or may not be inferable, however. Whether it’s inferable depends on other things such as the amount of horizontal transfer and the rate and nature of the genetic changes.

  16. Allan:

    CD [common design] would need to explain commonalities in viral sequences and transposons just as much as those in whole-organism comparisons.

    Yes, but unless the creationist denies HGT altogether, it would be easy for him or her to accept HGT events from one “kind” to another. What really blows common design out of the water is the appearance of the transferred DNA in multiple “kinds”, in a way that matches the predictions of common descent. Vertical inheritance, in other words.

  17. Take a look at the dimwitted objections Mung has been raising in this thread, such as claiming that John miscounted the numbered areas in Sal’s “flower”.

    He resembles his avatar more with each passing day.

  18. keiths: Take a look at the dimwitted objections Mung has been raising in this thread, such as claiming that John miscounted the numbered areas in Sal’s “flower”.

    Poor keiths. Can’t make an argument without misrepresenting the facts. I never claimed that John miscounted the numbered areas.

    #keithsEffect

  19. As I said:

    It doesn’t take a genius to figure out that John was talking about the numbered areas within Sal’s flower.

    But it’s well beyond you, apparently.

  20. keiths,

    Yes, but unless the creationist denies HGT altogether, it would be easy for him or her to accept HGT events from one “kind” to another.

    Sure, but phylogenetic methods apply to those sequences. Deny phylogenetic realities, one denies the relationships between (for example) different families of retrovirus, or transposon, as well as the detective work involved in epidemiology.

  21. Yes, Mung is word lawyering, but he is also correct to point out that the nested hierarchy does not follow from “evolution” as we usually define it.

    Evolution defined as “semiconservative replication of DNA” or “imperfect reproduction” or even “change in allele frequency” does not predict a nested hierarchy of species.
    The simple reason is that lineage branching does not automatically follow from those definitions. No branching, no phylogeny, no nested hierarchy.

    As soon as speciation is considered part of the evolutionary process (which it is in my book), the whole argument evaporates.

  22. Corneel,

    Just to mention that at no point have I defined evolution as ‘semiconservative replication of DNA’. My point was that Mung appeared to adopt a position whose corollary was that semiconservative replication of DNA was ‘nothing to do’ with evolution.

  23. Corneel,

    As soon as speciation is considered part of the evolutionary process (which it is in my book), the whole argument evaporates.

    I’m not particularly enamoured of the ‘change in allele frequency’ definition personally. I prefer good old-fashioned ‘descent with modification’.

    And, even without speciation (see, for example, asexual organisms), survivors are bound to exhibit common ancestry – coalescence from the many upon the few. It’s a simple, albeit non-obvious, consequence of the evolutionary sampling process.

  24. Allan Miller: And, even without speciation (see, for example, asexual organisms), survivors are bound to exhibit common ancestry – coalescence from the many upon the few. It’s a simple, albeit non-obvious, consequence of the evolutionary sampling process.

    For asexual organisms that works, but not so for sexual populations. Sexual reproduction and recombination keep populations homogeneous and prevent the divergence of subpopulations.You either need a physical barrier or powerful diversifying selection to prevent incipient species from intermingling again.

  25. Allan,

    I’m not particularly enamoured of the ‘change in allele frequency’ definition personally. I prefer good old-fashioned ‘descent with modification’.

    So you are old school huh? 🙂

  26. Corneel,

    For asexual organisms that works, but not so for sexual populations. Sexual reproduction and recombination keep populations homogeneous and prevent the divergence of subpopulations.You either need a physical barrier or powerful diversifying selection to prevent incipient species from intermingling again.

    I’m dubious that it needs a formal barrier in absolute terms. I think the viscosity of gene flow drives divergence, given a large enough population. And, divergence itself can be reinforcing. As discussed in the ‘evolution of sex’ threade, homogeneity is an assumption of the models, not necessarily ‘a thing’!

  27. Corneel,

    So you are old school huh?

    Heh. Somewhat wary of population genetics, truth to tell. Which is not to say it tells us nothing, but that its simplifications can be misleading. Descent with modification is less contingent – there is always a lineage, but there isn’t always a neat homogeneous population.

  28. Mung: If by “evolution” you mean “semiconservative replication of DNA.” But no one but you and dazz (and perhaps Allan) define evolution that way.

    Again, semiconservative replication of DNA is an instance of evolution. There are other forms of evolution, but that is one way that an evolutionary process can is manifest.

    Is it the atheism, the evolutionism, or the combination of the two that leads people here to cling to such obvious nonsense? Why not just admit that you were wrong?

    Actually it’s the not-being-wrong.

    Evolution doesn’t predict semiconservative replication of DNA

    Semiconservative replication of DNA is an instance of an evolutionary process.

    and given semiconservative replication of DNA you will have a nested hierarchy. No evolution required.

    Given semiconservative replication of DNA you will have an instance of evolution. You can’t have semiconservative replication of DNA without it being an instance of evolution. And that instance of an evolutionary process predicts nesting hiearchies.

    You keep just being flat out wrong. Unambigously. Why not just admit it and move on?

  29. I mentioned earlier the phospho proteome. It should not be surprising there is also the METHYL PROTEOME.

    https://www.ncbi.nlm.nih.gov/pubmed/22246820

    Since its discovery more than 50 years ago, post-translational modification (PTM) of proteins via methylation has grown in prominence, its involvement having been recognised in a number of central processes in the cell. Of these, the best characterised is its role in the epigenetic code. However, there is increasing evidence that its role extends far beyond this and we propose that it is a key regulator in interactome dynamics. In this review, we focus on the role of methylation in regulating protein-protein interactions and illustrate, by providing a broad-scale summary of our current knowledge of methylation and its impact on systems biology, how this can ultimately affect interactome dynamics. We describe the variety of analytical techniques available for the study of the methylproteome, comment on their advantages and limitations, and consider how these tools can help elucidate how methylation regulates the dynamics of the interactome. The insights gained from methyltransferase-substrate networks will be summarised and the ability of protein methylation to facilitate or block protein-protein interactions as well as their interplay with other post-translational modifications, in particular phosphorylation, is highlighted. Finally, the importance of methylation in pathology-associated protein interaction networks will be discussed using examples involving human diseases and the p53 protein.

    This shows that what applies to histone modificaitons extends to other proteins. For Eukaryotes anyway, this piles onto Doug Axe’s numbers for improbability of protein evolution. This is relevant because what John Harshman calls phylongenetic explanations are actual post-hoc rationalizatations and implicit invocation of miracles — it’s not a a mechanistic explanation.

    John did not follow the prescription I outlined for a mechanistic explanation that one would see such as in physics and chemsitry, as in:

    0. state 0
    1. state 1 caused event 1
    2. state 2 caused event 2

    N. state N, the final state caused by event N

    Just saying it POOFED (John uses the word added), isn’t a mechanistic explanation. It’s little different than a creationist saying it POOFed except creationists are up front about it and evolutionist only pretend there isn’t a probablistic challenge because they circularly reason the nested hierarchy proves evolution because evolution proves the nested hierarchy.

    Below one can see all the methylatable sites that are methylated in cell phase and cell-type specific manners. This requires binding site specificity (ala Behe) and coordinated orchestration of events as these are discrete memory markings on the proteins. Ergo, proteins from one species to another may not be as malleable as one supposes unless weakly selectable function (weak because it is likely redundant) just breaks.

  30. So for postranslation modifications I mentioned

    glyco conjugation
    phospho proteome
    mythly proteome

    Look again at the following diagram and the Acetylation marks.

    It should not be surprising then that there is the ACETYLOME!!!!!

    https://www.nature.com/articles/srep29897

    Lysine acetylation is a dynamic and highly conserved post-translational modification that plays an important regulatory role in almost every aspects of cell metabolism in both eukaryotes and prokaryotes. Phytophthora sojae is one of the most important plant pathogens due to its huge economic impact. However, to date, little is known about the functions of lysine acetylation in this Phytopthora. Here, we conducted a lysine acetylome in P. sojae. Overall, 2197 lysine acetylation sites in 1150 proteins were identified.

  31. stcordova: This is relevant because what John Harshman calls phylongenetic explanations are actual post-hoc rationalizatations and implicit invocation of miracles — it’s not a a mechanistic explanation.

    You are still misunderstanding what phylogeny (or even phylongeny) is supposed to explain, and you keep doing it no matter how often I tell you. This is what despair looks like. But once again, to no purpose whatsoever: Phylogeny explains the nested hierarchy. It doesn’t explain the origin of a feature.

    Now, what causes the origin of a gene certainly depends on the individual gene, and we can’t get any of that from your favorite Venn diagram. But we do know that many genes result from duplication followed by divergence. That’s why there are gene families. Is that mechanistic?

    Just saying it POOFED (John uses the word added), isn’t a mechanistic explanation. It’s little different than a creationist saying it POOFed except creationists are up front about it and evolutionist only pretend there isn’t a probablistic challenge because they circularly reason the nested hierarchy proves evolution because evolution proves the nested hierarchy.

    Word salad, and once again focused on irrelevancies.

    No, evolution doesn’t prove the nested hierarchy. Data “prove” the nested hierarchy. Common descent explains the nested hierarchy while nothing else does, and so the nested hierarchy is evidence for common descent.

    Can you explain why there are by far fewer genes whose pattern requires two changes than require one change? I can.

  32. stcordova,

    It should not be surprising there is also the METHYL PROTEOME.

    Just as wrong as the ‘phosophoproteome’ as a universal brake on evolution at every site in a protein.

  33. Sal’s proteins are so occupied being targets for X-ylation, there’s no room for anything else.

  34. keiths: It doesn’t take a genius to figure out that John was talking about the numbered areas within Sal’s flower.

    But it’s well beyond you, apparently.

    No, it was quite obvious that John was talking about the numbers. I was talking about the areas. It took you to try to conflate the two when areas and numbers are clearly distinct entities.

  35. “Ignore” has disappeared, and I have “1 unread announcement” that I have no idea how to find. What happened?

  36. Rumraket: And that instance of an evolutionary process predicts nesting hiearchies.

    But evolution does not predict semiconservative replication of DNA. So it doesn’t predict the process that produces a nested hierarchy. So it doesn’t predict a nested ed hierarchy.

  37. John Harshman: “Ignore” has disappeared, and I have “1 unread announcement” that I have no idea how to find. What happened?

    You should see an Announcement link at the top of the page. Click on it.

  38. Mung,

    No, it was quite obvious that John was talking about the numbers. I was talking about the areas.

    John was talking about areas, which is why he used the word “areas”. The context made it obvious that he was talking about the numbered areas. I’ll bet even you realize that.

    Your objection is just a useless made-up ‘gotcha’ from someone who is desperate to participate, but has nothing worthwhile to offer. Don’t sweat it. You should be used to failure by now.

  39. Sal,

    The elephant is still in the room. Will you ever get around to telling us why your Designer just happened to implement an objective nested hierarchy out of the trillions of possibilities available to him?

  40. John, to Sal:

    Can you explain why there are by far fewer genes whose pattern requires two changes than require one change? I can.

    Right. Sal’s own “flower” defeats him.

  41. keiths:
    Sal,

    The elephant is still in the room.Will you ever get around to telling us why your Designer just happened to implement an objective nested hierarchy out of the trillions of possibilities available to him?

    Have you ever encountered a creationist who wanted to explain anything, other than with “god did it”?

    And they haven’t done the slightest to make “god did it” more plausible than trillions of other made-up logical possibilities.

    Glen Davidson

  42. I don’t expect him to answer. I just want to remind him, and the readers, that he keeps dodging the question.

    It’s easy enough to figure out why.

  43. Corneel,

    Yes, Mung is word lawyering, but he is also correct to point out that the nested hierarchy does not follow from “evolution” as we usually define it.

    Evolution defined as “semiconservative replication of DNA” or “imperfect reproduction” or even “change in allele frequency” does not predict a nested hierarchy of species.
    The simple reason is that lineage branching does not automatically follow from those definitions. No branching, no phylogeny, no nested hierarchy.

    Actually, branching does automatically follow from semiconservative replication of DNA, and it will lead to a nested hierarchy. Speciation is not required.

    For instance, we can infer phylogenetic relationships among pathogen strains even when no speciation occurs.

    For there to be a nested hierarchy of species obviously requires speciation, but who ever doubted that?

  44. Allan,

    Sure, but phylogenetic methods apply to those [HGT] sequences. Deny phylogenetic realities, one denies the relationships between (for example) different families of retrovirus, or transposon, as well as the detective work involved in epidemiology.

    But again, what creates the strong phylogenetic signal is (imperfect) vertical inheritance. The HGT event creates a marker in the recipient, but it is the subsequent branching descent of that marker that reinforces the objective nested hierarchy.

    This makes sense. We’re talking about common descent, after all, so it’s no surprise that vertical inheritance establishes the pattern, and that horizontal transfers are noise.

  45. Mung: But evolution does not predict semiconservative replication of DNA.

    That’s like saying the theory of gravity doesn’t an instance of gravity in effect.

    So it doesn’t predict the process that produces a nested hierarchy.

    It is the process that produces a nested hiearchy.

    So it doesn’t predict a nesteded hierarchy.

    Yes it does, it still does. The process that produces nested hiearchies is an instance of evolution. Given that instance of evolution, you will get a nested hiearchy. That instance of evolution entails the formation of a nested hierarchy.

    No matter how many times you repeat those three sentences it’s not going to stop being false.

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