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. J-Mac:

    Why would I believe in common descent and nested hierarchies if evidence points to more than one origins of life?

    Allan:

    It doesn’t. Venter Is Wrong.

    And even if he were right, it wouldn’t support goofy ideas like the separate creation of humans. Creationists are screwed either way.

  2. Allan Miller: J-Mac,

    So, would it or would it not the code mycoplasma use work in human cells?

    Yes or No?

    Probably not, no. There are many genes one could take from many organisms that would not work in many others.

    Since it is only 1 difference out of 64, why wouldn’t work?
    How do you think it evolved if only 1 difference out of 64 prevents that code to be functional?

    Can you explain that, since I know you can’t prove it experimentally… 😉
    Let’s listen to the excuses… lol

  3. stcordova,

    Sal, you are right that naive application of a simple formula in a complex situation can lead to error. Then again, naive rejection can also lead to error. Perhaps you could get specific and detailed about some particular case in need of explanation and I could try to come up with something to explain it.

    And once more: this is all irrelevant to common descent. I am merely indulging your off-topic obsessions.

  4. stcordova: I was a bit appalled he’d try to apply it to LARGE bacterial populations spread around the globe.

    I have my very own private population that I carry around with me.

  5. J-Mac,

    Since it is only 1 difference out of 64, why wouldn’t work?
    How do you think it evolved if only 1 difference out of 64 prevents that code to be functional?

    It prevents it being functional when moved between species that have been separated for over a billion years. This does not mean that the ancestral Mycoplasma code could never work in any common ancestor. Anyway, a Single Code To Rule Them All would seem to be more a prediction of what is laughably called ‘Design Theory’ than of Common Descent.

    Can you explain that, since I know you can’t prove it experimentally… 😉
    Let’s listen to the excuses… lol

    My, you’re a very open-minded fellow, aren’t you?

    I’m sure you won’t have any trouble explaining why Common Design is a better explanation than Common Descent, for two codes differing at only one position – at a STOP, as almost all variant codes do?

  6. Mung,

    Yes. Indicating a separate origin.

    Haha. You haven’t noticed the other 61, then? 61 identical, 3 different, so it’s a separate origin. Well, if you say so. I would beg to differ. No doubt you’d apply the same logic to a protein that differed in 3 positions out of every 64.

    Same question to you: what’s the Design reason for different codes, varying around STOP? There must be one, right, ‘cos it can’t possibly be evolution?

  7. Allan Miller: You haven’t noticed the other 61, then? 61 identical, 3 different, so it’s a separate origin. Well, if you say so. I would beg to differ.

    So the code differences didn’t figure at all into the symbiotic theory?

  8. Mung,

    So the code differences didn’t figure at all into the symbiotic theory?

    What does symbiotic theory have to do with separate OOL?

  9. Allan Miller:
    J-Mac,

    It prevents it being functional when moved between species that have been separated for over a billion years. This does not mean that the ancestral Mycoplasma code could never work in any common ancestor. Anyway, a Single Code To Rule Them All would seem to be more a prediction of what is laughably called ‘Design Theory’ than of Common Descent.

    My, you’re a very open-minded fellow, aren’t you?

    I’m sure you won’t have any trouble explaining why Common Design is a better explanation than Common Descent, for two codes differing at only one position – at a STOP, as almost all variant codes do?

    You are too much Allan! But why should I even be surprised?
    Let’s start from the foundation…
    What was Venter’s famous mumbo-jumbo that many called “the creation of the artificial life”? What did he actually do? Do you even know?

  10. Mung: So the code differences didn’t figure at all into the symbiotic theory?

    Lol
    The code configuration is the least of Darwinist’s problems with symbiotic theory…

    “It is far more likely that the host cell would have digested the invasive photosynthetic and energy producing bacteria rather than entering an endosymbiotic relationship since phagocytosis, which is the mechanism for feeding, is the same mechanism by which the endosymbionts are assumed to have entered the cell. Although some supporters of the theory state that the digestive enzymes had disappeared, the cell would not have survived without being able to digest engulfed food for nutrients if this was the case.

    Who can argue with that?

  11. keiths: What does symbiotic theory have to do with separate OOL?

    AFIAK nothing. Why?

    Better yet, answer the question I asked of Allan. What factored into the symbiotic theory if not differences in the genetic code?

  12. Allan Miller: Anyway, a Single Code To Rule Them All would seem to be more a prediction of what is laughably called ‘Design Theory’ than of Common Descent.

    O’RLY?

    What evolved first? The code or the species? Don’t forget at attach the evidence because I don’t think I can take more baseless speculations today… 😉

  13. J-Mac, to Allan:

    Don’t forget at attach the evidence because I don’t think I can take more baseless speculations today…

    You’ve given up creationism, then?

  14. keiths:

    What does symbiotic theory have to do with separate OOL?

    Mung:

    AFIAK [sic] nothing. Why?

    Because the discussion is about single vs separate origins of the genetic code(s), and you came down on the side of “separate”:

    Allan:

    Our nuclei even differ from our mitochondria at 3.

    Mung:

    Yes. Indicating a separate origin.

    But I’m also beginning to think that you had no idea what Allan and J-Mac were discussing, since you wrote this:

    What factored into the symbiotic theory if not differences in the genetic code?

    Are you confusing sequences with codes?

  15. Who can argue with that?

    I would say that anyone who knows anything at all about endosymbionts would have no problem demonstrating that your quote is false. Have your kids look up all the living examples of endosymbionts/symbionts and then you can all have a good discussion focused on the erroneous nature of the quote you pulled from somewhere without providing any citation.

  16. PeterP: I would say that anyone who knows anything at all about endosymbionts would have no problem demonstrating that your quote is false.

    Hmmm…A new kid on the block but a well known, same incoherence…
    What amazes me the most is that many commentators here have an unusual ability to contradict themselves in the same sentence… 😉

  17. J-Mac: What amazes me the most is that many commentators here have an unusual ability to contradict themselves in the same sentence

    It may be informative were you to actually point out the contradictions and incoherence. But of course you can’t do that, can you? And you’ve left now anyway so it does not really matter.

    But it’s a interesting tactic also used by the likes of Mung. Say that evolution is contradictory and incoherent without actually making the case for that.

    And in any case, to make that case you’d have to have a level of understanding that it’s obvious neither of them have. I guess it’s just a “gut feeling”.

  18. J-Mac: What evolved first? The code or the species? Don’t forget at attach the evidence because I don’t think I can take more baseless speculations today…

    In all your time here J-Mac you never said what you believed and then provided a basis for that belief. And yet you feel able to accuse others of what you yourself are guilty of.

    This may help: https://en.wikipedia.org/wiki/Psychological_projection

  19. keiths: Are you confusing sequences with codes?

    No.

    keiths: But I’m also beginning to think that you had no idea what Allan and J-Mac were discussing…

    keiths: Because the discussion is about single vs separate origins of the genetic code(s), and you came down on the side of “separate”:

    Let me know when the light comes on, however dim it may be.

    The question that is raised is what it takes to establish “separate origins.” Allan comes down on the side of “three is not enough” without telling us how much is enough. So I asked about the principle involved in making such a determination.

    I give, by way of example, endosymbiosis and asked whether or not this small difference in the codes had anything at all to do with making the case of the endosymbiotic theory. If not, so be it. But so far no one has addressed it. Aren’t mitochondria though to have a separate origin?

    And no one addressed my questions about making phylogenies of relatedness of human families. Do phylogenetic methods not work within species? Surely you and I have a common ancestor keiths. 🙂

  20. Histones are a beautiful illustration of some of the many posttranslational modifications that happen on proteins of complex eukaryotes.

    In fact, we are finding also sorts of chemical machines put specialized informational markers on proteins of which the histone modifications are small subset. For this to happen, something on the protein sequence must surely present itself as an address and docking site for marchines involved in reading, writing, and erasing post translational modifications.

    Because we’re finding so many post translational modifications on so many proteins, and because these modification surely entail sequence recognition which entails sequence specificity (like say a unique street address), I don’t think the protein sequence can be modified willy nilly. If 88% of the sequences of the same kind of protein differ between species, especially for complex eukaryotes, a good portion of it could easily be attributable to different road signs and parking lots for molecular machines servicing the post translational modifications on the protein.

    Think for a moment what it must entail to modify the tails of the following proteins such as these histones (diagram below).

    What is true for histones, we’re finding to be true of other proteins all over complex eukaryotic cells. How can individual residues be modified and read in an orchestrated manner unless there is some sequence specificity?

    One of the important post translational modifications is collectively called the Phospho Proteome.

    https://en.wikipedia.org/wiki/Phosphoproteomics

    Phosphoproteomics is a branch of proteomics that identifies, catalogs, and characterizes proteins containing a phosphate group as a post-translational modification. Phosphorylation is a key reversible modification that regulates protein function, subcellular localization, complex formation, degradation of proteins and therefore cell signalling networks. With all of these modification results, it is estimated that between 30% – 65% of all proteins may be phosphorylated, some multiple times.[1][2] Based on statistical estimates from many datasets, 230,000 156,000 and 40,000 phosphorylation sites should exist in human, mouse, and yeast, respectively.[2]

    Compared to expression analysis, phosphoproteomics provides two additional layers of information. First, it provides clues on what protein or pathway might be activated because a change in phosphorylation status almost always reflects a change in protein activity. Second, it indicates what proteins might be potential drug targets as exemplified by the kinase inhibitor Gleevec. While phosphoproteomics will greatly expand knowledge about the numbers and types of phosphoproteins, its greatest promise is the rapid analysis of entire phosphorylation based signalling networks.[3]

    Add to this the fact many proteins, about half in the human, are also conjugated with glycans!!!!

    How the heck will this work if there isn’t some specificity in sequence for the machines to find, read, write and erase these informational marks on the proteins. So proteins are more than what we assume, they also provide parking lots and road signs for molecular machines to dock just like DNA does.

    The fact that God could arrange these differences between species hierarchically as well as attaching function to these differences showcases God’s genius. Random walks don’t create such amazing labyrinths of complexity. This is where phylogenetic explanations fail to explain anything. Common design by miraculous special creation is more believable to me.

  21. Mung,

    The question that is raised is what it takes to establish “separate origins.” Allan comes down on the side of “three is not enough” without telling us how much is enough. So I asked about the principle involved in making such a determination.

    No, you stated that a three-codon difference in the code pointed to separate origins:

    Allan:

    Our nuclei even differ from our mitochondria at 3.

    Mung:

    Yes. Indicating a separate origin.

    That was a dumb mistake, so Allan corrected you:

    Haha. You haven’t noticed the other 61, then? 61 identical, 3 different, so it’s a separate origin. Well, if you say so. I would beg to differ. No doubt you’d apply the same logic to a protein that differed in 3 positions out of every 64.

  22. Mung,

    I give, by way of example, endosymbiosis and asked whether or not this small difference in the codes had anything at all to do with making the case of the endosymbiotic theory. If not, so be it.

    No, you actually argued that it did:

    What factored into the symbiotic theory if not differences in the genetic code?

    To anyone who understands biology, it’s obvious that one would look for sequence differences, not code differences, in investigating the endosymbiotic hypothesis.

  23. Sal:

    Common design by miraculous special creation is more believable to me.

    And the 10^38 pound elephant remains in the room:

    Sal,

    Are you ever going to get around to telling us why your God is so obsessed with unguided evolution and intent on mimicking it? Why the objective nested hierarchy, when trillions of other options are available to him?

  24. Mung,

    Aren’t mitochondria though to have a separate origin?

    No. They are thought to have shared a common ancestor with the organism that engulfed them. Which ought to be obvious, given that their genetic code differs by only 3 codons out of 64.

  25. stcordova: The fact that God could arrange these differences between species hierarchically as well as attaching function to these differences showcases God’s genius.

    Was that an attempt to explain the nested hierarchy? If so, would you care to expand and defend that attempt?

  26. keiths: They are thought to have shared a common ancestor with the organism that engulfed them. Which ought to be obvious, given that their genetic code differs by only 3 codons out of 64.

    How many differences more would there need to be, exactly, to support the hypothesis of an un-shared ancestry between the “host” and the symbiont?

    Objectively.

  27. Mung: Allan comes down on the side of “three is not enough” without telling us how much is enough.

    And keiths. I just love how evolutionary theory allows one to pick and choose.

  28. keiths: That was a dumb mistake, so Allan corrected you:

    If by “corrected” you mean “made an unsupported bald assertion for which I am supposed to take his word for it.”

  29. Mung,

    It was your assertion:

    Allan:

    Our nuclei even differ from our mitochondria at 3 [code positions].

    Mung:

    Yes. Indicating a separate origin.

    We’re laughing at your claim. Tell us why you think it indicates a separate origin, so we can laugh some more.

  30. And for extra laughs, tell us why you thought that code differences were more important than sequence differences for the endosymbiotic hypothesis:

    Mung:

    What factored into the symbiotic theory if not differences in the genetic code?

    keiths:

    Are you confusing sequences with codes?

    Mung:

    No.

  31. J-Mac,

    Who cares about Venter? I asked a simple question. The thread title is ‘Common Design vs Common Descent’. So, what is the Common Design explanation for variant codes – the overwhelming commonality, and the reason for variation?

  32. Mung,

    What factored into the symbiotic theory if not differences in the genetic code?

    You are, I am sure, familiar with the evidence for endosymbiotic theory. You seem to be suggesting above that it is solely based upon the differences in genetic code. I’m puzzled by that, because I know you know that isn’t the case.

    Genetic code variants aren’t a particularly reliable phylogenetic marker (which is not to say that they aren’t such a marker at all – it’s just that the same variant code can easily be arrived at independently). Whether mitochondrial and nuclear codes differed at 0, 1, 2 or (as is the case) 3, doesn’t tell us they had common origin. What tells us they probably had a common origin is the 64, 63, 62 or (as is the case) 61 positions that are the same.

  33. Mung,

    Allan comes down on the side of “three is not enough” without telling us how much is enough.

    And keiths. I just love how evolutionary theory allows one to pick and choose.

    You are, I presume, a grown man, and can evaluate propositions for yourself. If you don’t think 61 invariant assignments is enough to suggest common origin of the code, then that is what you think. It’s not for ‘evolutionary theory’, or me, to tell you what you should think to be a reasonable threshold.

  34. stcordova,

    Random walks don’t create such amazing labyrinths of complexity.

    Yes they do (one good assertion deserves another).

  35. stcordova: The fact that God could arrange these differences between species hierarchically as well as attaching function to these differences showcases God’s genius.

    The fact that God could also decide NOT to arrange these differences between species hiearchically means you can’t just assume that he did.

    On the other hand, evolution absolutely requires this pattern to be manifest. So it can only be evidence for evolution, it can’t be evidence for God because he could have done it another way.

    Random walks don’t create such amazing labyrinths of complexity.

    When all else fails, just assert what you are trying to prove. Let me try this for a second: Random walks do create such amazing labyrinths of complexity.

    Hold on, I need a fancy diagram to go with my post too. And some fancy-sounding quotation from a paper. Here goes:
    From
    Geeta N. Eick, Jennifer K. Colucci, Michael J. Harms, Eric A. Ortlund, Joseph W. Thornton.: Evolution of Minimal Specificity and Promiscuity in Steroid Hormone Receptors Published: November 15, 2012 https://doi.org/10.1371/journal.pgen.1003072

    Steroid hormone receptors (SRs) are an excellent model for the evolution of specificity. SRs are hormone-activated nuclear transcription factors with distinct specificities for endogenous steroid hormones and exogenous substances. In all SRs, the activating hormone binds in an internal cavity within a well-conserved ligand binding domain (LBD), causing the LBD to change conformation, attract coactivator proteins, and increase transcription of target genes [17]. The SR family diversified through a series of gene duplications that took place during early chordate and vertebrate evolution [18].
    (…)
    Here we characterize in detail the evolutionary trajectory of changes in ligand specificity/promiscuity in the SR protein family, as well as the underlying structural mechanisms for promiscuous responses to non-target ligands. For this purpose, we use ancestral protein resurrection (APR), which uses computational phylogenetic techniques to infer ancestral protein sequences from an alignment of their present-day descendants, followed by gene synthesis, molecular functional assays, and experimental studies of protein structure to directly characterize them. APR represents a powerful strategy for experimentally testing hypotheses about the structure and function of ancient proteins [21], [22]. By dissecting the structure-activity criteria by which ancient receptors distinguished among ligands – and tracing how those criteria changed over time – we sought to gain insight into the evolution of specificity versus promiscuity in the SR family. We also sought to determine whether an understanding of a protein family’s history can reveal explanatory principles for understanding and predicting the ligands to which its members will respond.

    (…)

    An evolutionary explanation for SR-mediated endocrine disruption

    Predicting ligands that interact with intended and secondary protein targets is an important goal in pharmacology and toxicology, but understanding from first principles which targets will respond more or less promiscuously has proven difficult [5], [16]. The concept of minimal specificity predicts that ER’s capacity to be disrupted by exogenous phenolics is inherited from AncSR1. To test this possibility, we characterized the ability of several xenoestrogens to activate AncSR1. As predicted, we found that AncSR1 is activated by the strong nonsteroidal ER agonists diethylstilbestrol and genistein and is competitively inhibited by the ER antagonists 4-hydroxytamoxifen and ICI182780 (Figure 3B).

    Our observations provide an historical explanation for the greater susceptibility of ERs than naSRs to activation by pollutants, pharmaceuticals, and dietary compounds. Extant ERs inherited AncSR1’s simple ligand-recognition criterion requiring little more than an aromatized A-ring with a 3-hydroxyl (Figure S8). Although this rule provided sufficient specificity throughout virtually all of vertebrate evolution, ERs are now exposed to – and fortuitously activated by – a wide range of aromatized pharmaceutical, industrial, and agricultural substances of the appropriate size and shape that have come into large-scale production only in the last century [19].

    In contrast, the more restrictive specificity of AR, PR, GR, and MR – which reflects the greater variety of endogenous potential activators to which they were exposed during evolution – makes them susceptible to activation by fewer synthetic substances than ERs, although they can still be disrupted by some novel substances, such as nonaromatized 19-norsteroids used as synthetic androgens. As predicted, we found that AncSR2, like its descendants, is insensitive to the aromatized xenoestrogens (Figure S9).

    Taken together, our findings suggest that analysis of a protein’s history and the chemical milieu in which it evolved can provide useful information for predicting the endogenous and exogenous ligands that can interact with it.

    So exploring the evolution of homonal transcription factors gave important and meaningful insights relevant to understanding the mechanisms of potential drugs and pharmacological compounds.

    And now for figure 3:

    Figure 3. Evolution of minimal specificity.
    A, Evolution of ligand-recognition criteria on the SR phylogeny. For each ancient and extant receptor, the criteria that distinguish activating ligands from other endogenous steroids are shown in brackets. Rules labeled “not” indicate significantly strongly reduced sensitivity when the specified moiety is present; other rules indicate strongly increased sensitivity when the moiety is present. The structures of representative endogenous hormones – estrogens (E), androgens (A), progestagens (P) and corticosteroids (C) – that were synthesized at each point in time are shown. Green portions of each hormone show moieties that satisfy the receptor’s rules; red portions violate rules. Each receptor’s rules are sufficient to allow activation by only a single class of hormones (gray boxes). The evolution of corticosteroid synthesis is indicated; AncSR2’s criteria would not have been sufficient to distinguish corticosteroids from progestagens. Inset: common steroid structure with A-ring and key carbons labeled. Dose-response curves for extant receptors are shown in Figure S7. B, AncSR1 is activated/antagonized by xenoestrogens in a luciferase reporter assay. IC50, concentration at which half-maximal inhibition was achieved in the presence of estradiol (EC80 = 200 nM). Each point shows the mean and SEM of three replicates.

  36. stcordova: The fact that God did not arrange these differences between species hierarchically as well as not attaching function to these differences showcases God’s genius.

    Spot the difference.

    stcordova: The fact that God could arrange these differences between species hierarchically as well as attaching function to these differences showcases God’s genius.

  37. Wrt the genetic code’s implications for possible separate origins, It can’t just be about the number of changes to the code that is important, but also the nature of those changes combined with other phylogenetic and comparative molecular evidence.

    It would seem absolutely fantastic that an organism should share common descent with another, if it had extreme genetic code rearrangements (such as if the arginine(among the largest, basic amino acids) codon was switched to glycine(smallest, non-polar amino acid), and glutamic acid(large, acidic) switched to alanine(small, non-polar), the start and stop codons were reversed, and phylogenetic analysis of any suspected orthologous genes consistently put them at some extremely long branches.

    You can’t really just look at the number of codon differences alone, you have to look at what those differences are and put them in a larger biochemical context. Which other things are different about the cell and it’s biochemistry and genetics, and in what way and how much? I think you also have to factor in the fraction of the species diversity out there that has been sampled. Could you plausibly potentially bridge some of the differences you observe with greater taxon sampling?

    I’m no systematist, but even from what little I know it seems way too simplistic to me to just count the number of genetic code-differences by itself as a measure of common vs independent origin. This is why, even when genetic code-differences are observed, they confirm the pattern rather than contradict it, as they are the types of differences you’d expect to result from blind tinkering through random sampling with mutations. They are mostly the least-used amino acids, or codons used near the ends of proteins (stop codons). And even then, some times these code-differences are restricted to only a small subset of proteins, or are stochastic effects from low side-activity of certain enzymes.

  38. Rumraket,

    Wrt the genetic code’s implications for possible separate origins, I can’t just be the number of changes to the code that is important, but also the nature of those changes combined with other phylogenetic and comparative molecular evidence.

    It’s not really the changes, it’s the things that are the same. 61/64 is pretty strong evidence on its own, IMO.

    But yeah, even if there were no identical assignments in two species, the fact that they had ribosomal protein synthesis with tRNA charging would be reasonable evidence of common origin.

  39. stcordova: The fact that God could arrange these differences between species hierarchically as well as attaching function to these differences showcases God’s genius. Random walks don’t create such amazing labyrinths of complexity. This is where phylogenetic explanations fail to explain anything. Common design by miraculous special creation is more believable to me.

    Not only was life created, it even miraculously contains the evidence that strongly correlates with it having evolved. That God could include such an amazingly superfluous signal when designing life simply shows how truly magnificent God’s design work is.

    It’s like the flood, not only did it have to be supernatural to happen as told in Genesis at all, it miraculously left behind all of the evidence you’d expect of an ancient earth and of the progression of life that would have to exist had life evolved over deep time.

    Design just gets more and more amazing the closer we look at it, since God spared no expense to include entirely useless signals that would indicate something else entirely to those naive enough not to believe in design.

    Glen Davidson

  40. CharlieM: I believe that in living systems the parts reflect the whole and I have no problem believing in common design (of sorts) and common descent…

    Corneel: Mmmmmmmno doesn’t cut it, I think. If you explain species change and divergence as a process analogous to cell differentiation in individual development, you are simply describing the phylogenetic process. Even though the derived characters are arising from design (of sorts), the vertical inheritance along lineages still make it 100% common descent.

    Nothing you have said here contradicts what I have written.

    Perhaps I am missing something. Where does common design come in?

    In the case of the individual all the cells have one common (unconscious) aim, to develop and maintain the unity of the organism which enables it to develop into a self-conscious rational being. Regarding the evolution of earthly life, it is difficut to take a detached view and see the overall picture because we are in the middle of it. But I believe that life is a unity in the same way that an individual organism is a unity. Life is a progressive development where rational self-consciousness becomes concentrated in individual organisms. Human self-consciousness does not just appear from nowhere it grows out of the life of the earth in the same way that the flowers of a rose grows out of the maturing plant.

  41. GlenDavidson,

    Not only was life created, it even miraculously contains the evidence that strongly correlates with it having evolved.

    The nested hierarchy is proof of God’s greatness. There is no nested hierarchy. Both positions essayed by Sal at various times.

  42. Allan Miller:
    GlenDavidson,

    The nested hierarchy is proof of God’s greatness. There is no nested hierarchy. Both positions essayed by Sal at various times.

    Sal’s the Baghdad Bob of Young Earth Creationism.

  43. Allan Miller,

    What tells us they probably had a common origin is the 64, 63, 62 or (as is the case) 61 positions that are the same.

    I have just twigged that Mung may be simply talking of the fact that the components of the endosymbiotic pairing came from different places. I, however, was talking of their common ancestry.

  44. John Harshman:

    Was that an attempt to explain the nested hierarchy? If so, would you care to expand and defend that attempt?

    Yes, because it explains what wouldn’t be a good explanation, namely, common descent without miracles.

    I was pointing out the even though proteins shared among species may have 88% differences in the same protein, it doesn’t mean the protein in one species can necessarily change to be a protein in another species without breaking something in the process.

    The sequence constraints appear in at least 3 levels for a gene:

    DNA Genome
    RNA Transcriptome
    Amino Acid Proteome

    I showed just one challenge of changing sequences at the proteomic level constrained by post-translational modifications. No one is even attempting a counter of the technical points.

    I believe God did it miracles, you believe evolution did it without miracles. I showed just for complex proteomes, evolution without miracles would be a miracle! You want to believe it that’s fine, but a mechanistic explanation would settle the argument, none of which anyone has provided in sufficient detail.

  45. stcordova,

    […] in sufficient detail.

    How much detail is ‘sufficient’ – given that you have zip for your own pet explanation?

  46. stcordova: Yes, because it explains what wouldn’t be a good explanation, namely, common descent without miracles.

    You say “yes”, and then you go on as if the answer were “no”, completely abandoning any attempt to expand on what you had said. I had hopes, but you still don’t understand the difference between common descent and the origin of innovation. Until you can grasp this simplest of distinctions, nothing you say will be on point.

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