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 Replies to “Common Design vs. Common Descent”

  1. Allan Miller
    Ignored
    says:

    Mung,

    I honestly don’t know why that should be the case. Especially considering that eukaryotes are just a conglomeration of bacteria inside an archaeon.

    Do you think no-one noticed a gaping flaw in the logic till Denton came along? And no-one has noticed it since either? Try “why are there more differences between mammals and fish than within mammals or within fish, especially since mammals are just supposed to be hairy fish?” to see if your logic holds up.

  2. Neil Rickert
    Ignored
    says:

    Mung: You want a car to go faster, you remove stuff.

    I think I’ll just remove the engine, so it will go faster.

  3. keiths keiths
    Ignored
    says:

    Neil:

    I think I’ll just remove the engine, so it will go faster.

    Um, Neil?

  4. colewd
    Ignored
    says:

    keiths,

    To defend common design in the face of a number as huge as 10^38 is idiocy of the highest order. Creationism is flat-earth stupid.

    How does it match the tree? A selected primate is 14 AA away from the human sequence and a reptile is 13 AA. This high level claim appears to be false.

    Have you seen Sal’s diagram where 153 genes are shared by chickens and humans but not mice.

    I don’t know what you are smoking but please share 🙂

  5. John Harshman John Harshman
    Ignored
    says:

    Allan Miller: The difference between bacteria and eukaryotes should be greater than that between any 2 eukaryotes, incidentally. That’s what I’d expect. Isn’t it?

    I don’t think so, necessarily. Remember that cytochrome c is a nuclear gene that has been transferred from the mitochondrial genome. Now, once that gene got into the nucleus, it would evolve at the nuclear rate, which for most eukaryotes is much slower than the typical bacterial rate. Then again, the mitochondrial rate is probably faster than the bacterial rate, so more evolution in the eukaryote lineage until that transfer to the nucleus happened. It’s a complicated scenario, and I’m not quite sure how the expectation comes out.

  6. John Harshman John Harshman
    Ignored
    says:

    keiths:
    John, to colewd:

    You’re confusing colewd with Sal, John.

    Oops.

  7. colewd
    Ignored
    says:

    Allan Miller,

    The fact remains – my existence is due to a long succession of ‘lucky accidents’, as well as some more regular processes. That’s where I came in. You haven’t dealt with that by insisting on focussing your microscope on the fresh Allan-zygote, and calling the process beyond that ‘deterministic’.

    We agree here on the wording.

    From a scientific view point I am trying to find the cause of Allan. The objective is not to determine the probability of Allan prior to the event, that is irrelevant. In the case of making a human being I can collect lots of data on the process.

    In the case of evolution how would I collect data to understand the process?

  8. John Harshman John Harshman
    Ignored
    says:

    colewd: How does it match the tree? A selected primate is 14 AA away from the human sequence and a reptile is 13 AA. This high level claim appears to be false.

    I’ve explained this once, and you appear to have missed it. We don’t build trees based on number of differences, since that requires an absolutely perfect molecular clock, with zero standard deviation of rates. What we do instead is build trees based on least-squares fit of distances to a tree, or, better, by fit of individual changes to a tree. I guarantee that by either of those methods the “selected primate” is going to come out on the tree near the human, and much nearer than the “reptile”.

    Have you seen Sal’s diagram where 153 genes are shared by chickens and humans but not mice.

    Yes. Whatever do you imagine it means? I think it means that mice have lost 153 genes found in the amniote ancestor and retained in humans and chickens. Is that a shock to you? We could of course pinpoint the losses more accurately with a bigger sample of species. Bet they all happened at different times.

  9. colewd
    Ignored
    says:

    John Harshman,

    Bill: Are you aware that cytochrome c in multicellular organisms preforms more functions than electron transport?

    John: No, I’m not. Is it true? And so what it it does?

    It has additional functions such as binding Apaf-1 for initiating apoptosis. Here is an interesting paper that shows the functional differences between human and mouse Apaf-1 and cytochrome c

    Interspecies Variation in the Functional Consequences of Mutation of Cytochrome c
    Tracy M. Josephs, Moira E. Hibbs, Lily Ong, Ian M. Morison, Elizabeth C. Ledgerwood Published: June 18, 2015 https://doi.org/10.1371/journal.pone.0130292
    Abstract
    The naturally occurring human cytochrome c variant (G41S) is associated with a mild autosomal dominant thrombocytopenia (Thrombocytopenia Cargeeg) caused by dysregulation of platelet production. The molecular basis of the platelet production defect is unknown. Despite high conservation of cytochrome c between human and mouse (91.4% identity), introducing the G41S mutation into mouse cytochrome c in a knockin mouse (CycsG41S/G41S) did not recapitulate the low platelet phenotype of Thrombocytopenia Cargeeg. While investigating the cause of this disparity we found a lack of conservation of the functional impact of cytochrome c mutations on caspase activation across species. Mutation of cytochrome c at residue 41 has distinct effects on the ability of cytochrome c to activate caspases depending on the species of both the cytochrome c and its binding partner Apaf-1. In contrast to our previous results showing the G41S mutation increases the ability of human cytochrome c to activate caspases, here we find this activity is decreased in mouse G41S cytochrome c. Additionally unlike wildtype human cytochrome c, G41S cytochrome c is unable to activate caspases in Xenopus embryo extracts. Taken together these results demonstrate a previously unreported species-specific component to the interaction of cytochrome c with Apaf-1. This suggests that the electrostatic interaction between cytochrome c and Apaf-1 is not the sole determinant of binding, with additional factors controlling binding specificity and affinity. These results have important implications for studies of the effects of cytochrome c mutations on the intrinsic apoptosis pathway.

  10. colewd
    Ignored
    says:

    John Harshman,

    I’ve explained this once, and you appear to have missed it. We don’t build trees based on number of differences, since that requires an absolutely perfect molecular clock, with zero standard deviation of rates. What we do instead is build trees based on least-squares fit of distances to a tree, or, better, by fit of individual changes to a tree. I guarantee that by either of those methods the “selected primate” is going to come out on the tree near the human, and much nearer than the “reptile”

    I understand this but Keith’s claim is for a single gene and claiming perfect tree alignment. The primate in question is clearly an outlier and shuts down his claim of a perfect fit to the tree. If you say there is an exception because of possible differences in the molecular clock, then his claim is meaningless. Just change the clock rate any all data fits.
    John Harshman,

    Yes. Whatever do you imagine it means? I think it means that mice have lost 153 genes found in the amniote ancestor and retained in humans and chickens. Is that a shock to you? We could of course pinpoint the losses more accurately with a bigger sample of species. Bet they all happened at different times.

    It means that common design is a better explanation of the data.

  11. John Harshman John Harshman
    Ignored
    says:

    colewd:
    John Harshman,

    I understand this but Keith’s claim is for a single gene and claiming perfect tree alignment.The primate in question is clearly an outlier and shuts down his claim of a perfect fit to the tree.If you say there is an exception because of possible differences in the molecular clock, then his claim is meaningless.Just change the clock rate any all data fits.

    I’m afraid you understood nothing of what I said. Let me try again: fit to a tree has nothing to do with the gross number of similarities. There is no exception. Phylogenetic analysis does not depend on a molecular clock at all. Clock rate is irrelevant. Rather than assuming differences in clock rate to enable a tree inference, we actually read the differences in clock rate by looking at the tree.

    It means that common design is a better explanation of the data.

    You will have to explain why common design explains the data. I see that Sal hasn’t attempted an explanation either. But common descent explains the data quite well, provided you look at the individual genes and at enough species. Once more, you can tell where the genes are lost, and gene losses are just another example of characteristics that fit and reinforce the tree.

  12. colewd
    Ignored
    says:

    John Harshman,

    You will have to explain why common design explains the data. I see that Sal hasn’t attempted an explanation either. But common descent explains the data quite well, provided you look at the individual genes and at enough species. Once more, you can tell where the genes are lost, and gene losses are just another example of characteristics that fit and reinforce the tree.

    John, as far as I am concerned this data falsifies orthodox common descent.

    153 lost genes as an explanation is ridiculous.

    Common design pops to the surface because only design explains the radical changes in DNA across lineages. I have been extremely skeptical of the orphan gene story and this seals it.

  13. GlenDavidson
    Ignored
    says:

    colewd: Common design pops to the surface because only design explains the radical changes in DNA across lineages. I have been extremely skeptical of the orphan gene story and this seals it.

    Or in other words, you’re not interested in explaining anything in context, merely in denying the meaning of the evidence that exists.

    You don’t want to make sense of biology, you think that not making sense serves your purpose better. The trouble, of course, is that you do not make any sense of biology, and many people do want to do so and have followed the evidence both for the sake of understanding for understanding’s sake, and for practical reasons.

    That this sort of fact-driven interest is anathema to you is really just fine, the only problem is that you want your denial to be recognized as something other than the lack of desire for understanding that it is. But it cannot be recognized as anything but apologetics and pseudoscience by those who would rather understand the world and to further knowledge.

    Glen Davidson

  14. keiths keiths
    Ignored
    says:

    colewd,

    10^38.

    You’re in denial.

  15. colewd
    Ignored
    says:

    GlenDavidson,

    That this sort of fact-driven interest is anathema to you is really just fine, the only problem is that you want your denial to be recognized as something other than the lack of desire for understanding that it is. But it cannot be recognized as anything but apologetics and pseudoscience by those who would rather understand the world and to further knowledge.

    Dude, have you taken a serious look at the data Sal posted. Genes starting with Zebra fish disappearing and returning to the human lineage absent from chicken and mice. This destroys any concept of the tree of life from the view of orthodox common descent. The only possibility is Sal’s data is wrong.

  16. GlenDavidson
    Ignored
    says:

    A person interested in getting to the truth of the matter wouldn’t have had much trouble finding this video on Youtube. It’s a video version of this paper.

    The point is made that cytochrome c apparently has had variable rates of evolution, with accelerated evolution in primates a few tens of millions of years back. By contrast, crocodylians have generally had much lower rates of evolution–“In their 2014 study using whole genome-alignments, Richard Green and colleagues found that alligators and crocodiles have “exceptionally low rates of evolution relative to mammals” (Green et al. 2014, 1254449-3).” So the creationists compare cytochrome c changes between slowly evolving organisms and the bushbaby, which belongs to a group where cytochrome c changes have been relatively rapid, especially soon after bushbaby and ape lineages separated.

    Once again, creationists treat data like a bludgeon to destroy the offending knowledge, while actual scientists research the differences that superficially may be surprising. And then whine when we won’t agree to teach their anti-knowledge stance to schoolkids.

    Glen Davidson

  17. GlenDavidson
    Ignored
    says:

    colewd:
    GlenDavidson,

    Dude, have you taken a serious look at the data Sal posted.Genes starting with Zebra fish disappearing and returning to the human lineage absent from chicken and mice.

    Why did you make that up? I don’t see the slightest thing about genes disappearing and returning to the human lineage, not in the article linked to his diagram. The article does mention that “70 per cent of protein-coding human genes are related to genes found in the zebrafish.” Not what Sal mentioned, as he can explain it no more than you can [well, I notice later that he did, but didn’t deal with it, preferring to rubbish evolution than to deal with facts].

    This destroys any concept of the tree of life from the view of orthodox common descent.The only possibility is Sal’s data is wrong.

    The only thing I can see is that you didn’t understand the article.

    Glen Davidson

  18. colewd
    Ignored
    says:

    GlenDavidson,

    The only thing I can see is that you didn’t understand the article.

    Look at the diagram that shows shares genes between groups. You will see genes unique to humans and zebra fish 73 of them. You will see genes that are shared with chickens and humans but not mice 153 of them. This goes on and on. Glen, show your responsive to conflicting data or lets stop discussing this.

  19. keiths keiths
    Ignored
    says:

    colewd,

    John already explained it to you:

    Whatever do you imagine it means? I think it means that mice have lost 153 genes found in the amniote ancestor and retained in humans and chickens. Is that a shock to you? We could of course pinpoint the losses more accurately with a bigger sample of species. Bet they all happened at different times.

    Why is that so difficult for you to understand?

  20. GlenDavidson
    Ignored
    says:

    colewd:
    GlenDavidson,

    Look at the diagram that shows shares genes between groups.You will see genes unique to humans and zebra fish 73 of them.You will see genes that are shared with chickens and humans but not mice 153 of them.This goes on and on.Glen, show your responsive to conflicting data or lets stop discussing this.

    So what? You can’t bullshit that genes were lost and then reappeared just because we share 153 with chickens but not mice. Are genes ever lost? Why would chickens and humans lose the very same ones that mice do?

    It’s outrageous that you assume your one evolution-denying interpretation to be true, when it’s known that genes are lost, and it would be absurd to think that all lineages would lose exactly the same ones. You’re not discussing at all, you’re cherry-picking and ignoring context and mechanism, all in order to agree with some of the most egregious pseudoscientists on the planet (and, I guess you think, your god).

    Glen Davidson

  21. John Harshman John Harshman
    Ignored
    says:

    colewd:
    John Harshman,

    John, as far as I am concerned this data falsifies orthodox common descent.

    153 lost genes as an explanation is ridiculous.

    Common design pops to the surface because only design explains the radical changes in DNA across lineages.I have been extremely skeptical of the orphan gene story and this seals it.

    I have no idea why you say any of those things. Please try to present some kind of argument or explanation for your opinions, rather than just the opinions.

  22. GlenDavidson
    Ignored
    says:

    colewd:
    GlenDavidson,

    Look at the diagram that shows shares genes between groups.You will see genes unique to humans and zebra fish 73 of them.You will see genes that are shared with chickens and humans but not mice 153 of them.This goes on and on.Glen, show your responsive to conflicting data or lets stop discussing this.

    Or to put it another way, all of the well-sequenced genomes mentioned in that article happened to retain various genes that others did not. If you ever considered this in context it would (should, at least) make eminent sense, it’s pretty much what you’d expect to happen over the course of evolution. None of the overlaps with humans and only one other organism is especially outsized compared with the others, except for the mice who are much more closely related to us, rather, humans and zebrafish share 73 that the others don’t, while chickens and humans share 48 that the others don’t.

    Chance alone would seem adequate to explain it, although I doubt that only it is responsible for lost genes.

    The truth is that I have the suspicion that you’re somehow assuming that humans evolved from mice and chickens (modern ones, even), hence the crack, “Genes starting with Zebra fish disappearing and returning to the human lineage absent from chicken and mice.” You seem to be thinking that if mice and chickens don’t have them they had to come from miracles or something like that, since we couldn’t have gotten them from mice or chickens. But that’s nonsense, because we didn’t evolve from either mice or chickens (or zebrafish, for that matter).

    Maybe that’s not what you’re assuming, but, if not, I can’t make any sense of your objection.

    As it happens, we do share with mice far more genes (1,602) that don’t exist in chickens or in zebrafish*, just as you’d expect from our much more recent divergence from mice than from the other two. Again, what you’d suppose from evolutionary mechanisms.

    Glen Davidson

    *Than the 48 we share with chickens alone, or the 73 we share with zebrafish alone, of course.

  23. Allan Miller
    Ignored
    says:

    John Harshman,

    Granted – more properly, mine was the naive expectation, the baseline pattern from constant rate.

  24. Allan Miller
    Ignored
    says:

    colewd,

    153 lost genes as an explanation is ridiculous.

    How many lost genes would be acceptable?

  25. keiths keiths
    Ignored
    says:

    colewd:

    153 lost genes as an explanation is ridiculous.

    Allan:

    How many lost genes would be acceptable?

    And why?

  26. Allan Miller
    Ignored
    says:

    colewd,

    If it is correct what we are observing in nature like atoms, molecules, and living organisms were created outside space time. Science struggles outside space time.

    This is just descent into gobbledegook. Design is very much a within-time process. ‘Outside spacetime’ has the same woo-quality as invoking ‘dark energy’, ‘quantum entanglement’, etc to explain organic change. It adds nothing, explains nothing, and has no reason to be there other than a placeholder for ‘ummmmmmm … ‘.

  27. Allan Miller
    Ignored
    says:

    I wonder if anyone can provide a design explanation for the differences in cytochrome c in different organisms, and the remarkably ‘tree-like’ pattern of those differences?

    Cytochrome c is involved in electron transport. Electrons are pretty much the same the universe over. And transport – take it from here, shove it there; how hard can that be?

    Why would this need to be different in different organisms? One might expect some variation correlated with respiratory demands – for example, I might expect whales to at least potentially have a different requirement to hippos, say, or frogs to fish, due to a different profile of oxygen demand. But the pattern that emerges correlates not with respiration at all, but with apparent genetic distance established by other, independent means.

  28. Rumraket Rumraket
    Ignored
    says:

    colewd: 153 lost genes as an explanation is ridiculous.

    Good, you have now utterly falsified all special creationism.

    They say the original created kinds contained all the total genetic variation of their respective, arbitrarily defined clades, and that all the diversity of life we see today evolved through “genetic entropy” by massive loss of genes in all those independent lineages.

    So the ancestor of all rodents, for example, contained all genes found in all rodents ever, but all the individual species of rodents evolved from that universal rodent ancestor by the different lineages losing huge amounts of genes that were present in that ancestor.

    And the same for beetles. And ants. And bovines (or whevever the hell it is they define the “kind” taxonomic rank). All these species have ORFan genes and indeed, some times entire ORFan systems, which would all have to have been present in their common ancestors, and was gradually lost in different proportions in different lineages as the diversity of today evolved.

  29. stcordova
    Ignored
    says:

    colewd:

    153 lost genes as an explanation is ridiculous.

    Its actually a little more than that, and more subtle. 🙂

    The chicken has to lose:

    57 genes shared by the mouse and zebra fish
    2059 genes shared by the mouse human and zebra fish
    73 genes shared by the human and zebrafish

    73 + 2059 + 57 = 2189 genes lost by the chicken line as it evolved from the common ancestor of all the creatures in the diagram

    conversely the human had to lose

    57 genes shared by the zebra fish and mouse
    89 genes shared by the chicken mouse and zebrafish
    43 genes shared by chicken and mouse
    129 genes shared by the chicken and the zebra fish

    57 + 89 + 43 + 129 = 318 genes lost by the human line during evolution

    and the mouse has to lose:

    73 genes shared by the human and zebrafish
    105 genes shared by the human chicken and zebra fish
    48 genes shared by the human and chicken
    129 genes shared by the chicken and zebra fish

    73 + 105 + 48 + 129 = 355 genes lost by the mouse line during evolution

    The ancestral core shared genes was
    129 genes shared by chicken and zebra fish
    89 genes shared by chicken mouse and zebra fish
    10,660 shared by all
    105 shared by humans and zebra fish and chickens
    73 shared by humans and zebra fish
    2059 shared by mouse human and zebra fish
    57 shared by mouse and zebra fish

    129 + 89 + 10,660 + 105 + 73 + 2059 + 57
    = 13,173

    So the chicken line started with 13,173 of the original set and then lost 2059 of them.

    The problem is that the common ancestor as we go back farther in time ends up needing more and more common genes to support the reductive evolution. One can’t reduce from something one doesn’t have!

    That is the picture of the reductive evolution needed. It’s not just reductive evolution but more like reductio ad absurbdum.

  30. OMagain
    Ignored
    says:

    stcordova: It’s not just reductive evolution but more like reductio ad absurbdum.

    What is the less absurd explanation? If you don’t have one, can you accept you just have to accept the absurd one until you can provide a better one?

  31. GlenDavidson
    Ignored
    says:

    stcordova: Its actually a little more than that, and more subtle.

    The chicken has to lose:

    57 genes shared by the mouse and zebra fish
    2059 genes shared by the mouse human and zebra fish
    73 genes shared by the human and zebrafish

    73 + 2059 + 57 = 2189 genes lost by the chicken line as it evolved from the common ancestor of all the creatures in the diagram

    conversely the human had to lose

    57 genes shared by the zebra fish and mouse
    89 genes shared by the chicken mouse and zebrafish
    43 genes shared by chicken and mouse
    129 genes shared by the chicken and the zebra fish

    57 + 89 + 43 + 129 = 318genes lost by the human line during evolution

    and the mouse has to lose:

    73 genes shared by the human andzebrafish
    105 genes shared by the human chicken and zebra fish
    48 genes shared by the human and chicken
    129 genes shared by the chicken and zebra fish

    73 + 105 + 48 + 129 = 355 genes lost by the mouse line during evolution

    That is the picture of the reductive evolution needed.It’s not just reductive evolution but more like reductio ad absurbdum.

    That’s absurd on the face of it, since many genes counted would be genes that appeared after tetrapods diverged from their fish ancestors. Don’t you know anything about evolution? Well, not much, of course.

    Then just a quick use of Google shows a fairly recent source estimating around 10,000 pseudogenes in the human genome. Gee, I wonder where they could have come from.

    So Sal’s doing the usual bang-up job of dealing with evolutionary issues, glib, and without the minimum of understanding of what’s involved in order to discuss it properly.

    Glen Davidson

  32. stcordova
    Ignored
    says:

    Note the problematic pattern for reductive evolution to happen as John Harshman suggested.

    The common ancestor of human and zebra fish needs a minimum of 73 genes.

    The common ancestor of zebra fish, humans and mice needs:
    2059 genes.

    The common ancestor of zebra fish, mice, men, and chickens needs 10,660 genes.

    Note the progression as the sampling size is increased, the more creatures sampled that share genes, the bigger the number of the genes necessary in the supposed ancestor!

    Rather than suggesting the common ancestor was simple and had few genes, the requirement to generate this pattern is that the ancestor was complex and had many genes. At this rate one then postulates the ancestor of all creatures had many many genes, maybe even more than any of its descendants!

    Reductive evolution indeed, reductio ad absurbdum.

    ERRATA: see the correction here, I understated the problem. It’s worse than what I just stated:

    http://theskepticalzone.com/wp/common-design-vs-common-descent/comment-page-12/#comment-193062

  33. OMagain
    Ignored
    says:

    stcordova: Note the progression as the sampling size is increased, the more creatures sampled that share genes, the bigger the number of the genes necessary in the supposed ancestor!

    Supposed ancestor? Then what is the true explanation? Nothing is related, and everything was created independently? Then why are any genes shared at all?

  34. GlenDavidson
    Ignored
    says:

    stcordova:
    Note the problematic pattern for reductive evolution to happen as John Harshman suggested.

    The common ancestor of human and zebra fish needs a minimum of 73 genes.

    The common ancestor of zebra fish, humans and mice needs:
    2059 genes.

    The common ancestor of zebra fish, mice, men, and chickens needs 10,660 genes.

    Note the progression as the sampling size is increased, the more creatures sampled that share genes, the bigger the number of the genes necessary in the supposed ancestor!

    Rather than suggesting the common ancestor was simple and had few genes, the requirement to generate this pattern is that the ancestor was complex and had many genes.At this rate one then postulates the ancestor of all creatures had many many genes, maybe even more than any of its descendants!

    Reductive evolution indeed, reductio ad absurbdum.

    I guess that means that LUCA must have had something like 7 million genes.

    It’s so obvious now.

    Glen Davidson

  35. OMagain
    Ignored
    says:

    Here’s my misunderstanding, look at my misunderstanding it’s absurd! Therefore I’ve proven common descent is false based on my misunderstanding of it!

    Where will you be publishing this valuable insight Sal?

  36. OMagain
    Ignored
    says:

    GlenDavidson: I guess that means that LUCA must have had something like 7 million genes.

    It’s makes much more sense that a time traveller who was his own son and father did it.

  37. stcordova
    Ignored
    says:

    Glen:

    I guess that means that LUCA must have had something like 7 million genes.

    Finally, glen see the problem with the assumption of common descent. If not LUCA, some ancestor needs lots of genes, and if so, it requires a POOF!

    Like I said, evolutionists need miracles to rescue their theory but never will admit it.

  38. stcordova
    Ignored
    says:

    Actually I mis-stated the problem:

    The common ancestor of all those in the diagram need:

    129 + 89 + 10,660 + 105 + 73 + 2059 + 57 = 13172

    My mistake was understating the difficulty of LUCA. The wider the sample space, the bigger the proximal-LUCA gets.

    Reductio ad absurbdum.

  39. GlenDavidson
    Ignored
    says:

    stcordova: Like I said, evolutionists need miracles to rescue their theory but never will admit it.

    Well, that, or evolution, with real mechanisms like gene duplication and subsequent modification.

    Glen Davidson

  40. Allan Miller
    Ignored
    says:

    There are 10,660 genes held in common by all groups on that Venn diagram. I wonder why? I wonder how their differences map, treewise? Is there a Fruit Bat way to dehydrogenate lactate, then a Haddock way, then a Crocodile way? Or to charge a particular tRNA, or ligate a nick in DNA …

    Puts me in mind of a Spike Milligan cartoon: a hand grasping a carrot, captioned: “The World Record way to hold a carrot”

  41. Allan Miller
    Ignored
    says:

    stcordova,

    Reductio ad absurbdum.

    You’re right, your analysis is absurbd.

  42. Allan Miller
    Ignored
    says:

    So, I’ve got two bacteria that have 4000 genes in common and five in each not found in the other. Does that mean their common ancestor must have had 4010 genes?

  43. stcordova
    Ignored
    says:

    There are 10,660 genes held in common by all groups on that Venn diagram

    Because that’s all that’s left after the 2,512 of 13,172 were stripped off. You do realize what will happen if the sample size is increased and the trend of increasing number of genes in some sort of LUCA continues, don’t you? Glen seemed to see the light, has the bulb come on for you yet?

  44. OMagain
    Ignored
    says:

    If only there was some magic where new genes could arise…

  45. OMagain
    Ignored
    says:

    stcordova: Like I said, evolutionists need miracles to rescue their theory but never will admit it.

    It seems to me the theory is in no need of rescuing. It’s productive, it continues to generate new knowledge. It’s taught in all the good universities, unlike ID/YEC.

    That it has not explained the origin of life to your satisfaction matters not.

  46. OMagain
    Ignored
    says:

    heh

  47. Mung Mung
    Ignored
    says:

    GlenDavidson: Why would chickens and humans lose the very same ones that mice do?

    Common design.

  48. Mung Mung
    Ignored
    says:

    Allan Miller: I wonder if anyone can provide a design explanation for the differences in cytochrome c in different organisms, and the remarkably ‘tree-like’ pattern of those differences?

    Sure. That’s the way the designers wanted it.

  49. Mung Mung
    Ignored
    says:

    GlenDavidson: I guess that means that LUCA must have had something like 7 million genes.

    Give or take a few orders of magnitude. But yes.

    Looks like the evolutionists here are finally beginning to grasp just how silly their theories really are!

  50. colewd
    Ignored
    says:

    Allan Miller,

    Allan Miller,

    I wonder if anyone can provide a design explanation for the differences in cytochrome c in different organisms, and the remarkably ‘tree-like’ pattern of those differences?

    Cytochrome c is involved in electron transport. Electrons are pretty much the same the universe over. And transport – take it from here, shove it there; how hard can that be?

    Why would this need to be different in different organisms? One might expect some variation correlated with respiratory demands – for example, I might expect whales to at least potentially have a different requirement to hippos, say, or frogs to fish, due to a different profile of oxygen demand. But the pattern that emerges correlates not with respiration at all, but with apparent genetic distance established by other, independent means.

    Cytochrome c has additional uses in multicellular species such as binding to Apaf-1 to initiate apoptosis.

    Interspecies Variation in the Functional Consequences of Mutation of Cytochrome c
    Tracy M. Josephs, Moira E. Hibbs, Lily Ong, Ian M. Morison, Elizabeth C. Ledgerwood Published: June 18, 2015 https://doi.org/10.1371/journal.pone.0130292
    Abstract
    The naturally occurring human cytochrome c variant (G41S) is associated with a mild autosomal dominant thrombocytopenia (Thrombocytopenia Cargeeg) caused by dysregulation of platelet production. The molecular basis of the platelet production defect is unknown. Despite high conservation of cytochrome c between human and mouse (91.4% identity), introducing the G41S mutation into mouse cytochrome c in a knockin mouse (CycsG41S/G41S) did not recapitulate the low platelet phenotype of Thrombocytopenia Cargeeg. While investigating the cause of this disparity we found a lack of conservation of the functional impact of cytochrome c mutations on caspase activation across species. Mutation of cytochrome c at residue 41 has distinct effects on the ability of cytochrome c to activate caspases depending on the species of both the cytochrome c and its binding partner Apaf-1. In contrast to our previous results showing the G41S mutation increases the ability of human cytochrome c to activate caspases, here we find this activity is decreased in mouse G41S cytochrome c. Additionally unlike wildtype human cytochrome c, G41S cytochrome c is unable to activate caspases in Xenopus embryo extracts. Taken together these results demonstrate a previously unreported species-specific component to the interaction of cytochrome c with Apaf-1. This suggests that the electrostatic interaction between cytochrome c and Apaf-1 is not the sole determinant of binding, with additional factors controlling binding specificity and affinity. These results have important implications for studies of the effects of cytochrome c mutations on the intrinsic apoptosis pathway.

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.