More on function and common descent

SF Matheson, on his fascinating Quintessence of Dust blog, provides some useful clarification regarding the significance of the genetic evidence for common descent (see previous post), in a passionate, take-no-prisoners post entitled “Talking trash about ‘junk DNA'”.

In particular, Matheson emphasises that arguments for common ancestry based on non-coding DNA do not depend on assumptions as to the functionality of non-coding DNA, either in general or as regards the specific elements used as evidence for common ancestry:

To be brief: biologists make neither of those suppositions when they use non-coding DNA elements to establish common ancestry and particular evolutionary relationships. Whether or not a certain DNA element is “functional” doesn’t make it any less an indication of common descent, nor have biologists ever assumed universal non-function of non-coding DNA in the first place.

Instead:

Pseudogenes and mobile elements constitute overwhelming evidence for common ancestry, not because of “presumptions” regarding their function, but because they exhibit patterns of inheritance and location (within the genome) that are best explained by common descent.

Indeed, in some cases these “mobile elements” (such as SINEs) acquire functionality, without this undermining their usefulness as indicators of common descent:

Even if a particular mobile genetic element has been put to work by the genome in which it is embedded, its conserved location in particular lineages (and not in others) presents an observation that is readily explained by common ancestry. In other words, even when it’s true that a particular piece of non-coding DNA has a biological function, it’s not true that this falsifies the basic explanation of common descent.

Hence I remain persuaded by the evidence for common descent of humans and other primates as set out in my previous post.

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3 Responses to More on function and common descent

  1. Rick Ritchie says:

    Notice, however, that this changes the basis of your argument. Yesterday you argued “The significance of this non-coding DNA is that natural selection does not operate upon it: it just sits there without alteration, other than the occasional harmless mutation.” If the non-coding DNA has a function, then natural selection DOES operate on it. For in less functional offspring, you can expect a higher death rate.

    Then there is Matheson’s argument, “its conserved location in particular lineages (and not in others) presents an observation that is readily explained by common ancestry.” Readily explained, perhaps. As I said from the start, I can see why this is plausible. But it is one thing to say that x is readily explained by y, and another thing to say that x can only be explained by y.

    I want to argue some of this by analogy with some breeding experiments with foxes. There were some Russian breeding experiments with foxes where selecting for their willingness to be handled by humans brought about a bunch of traits that we find with domestic dogs. Within half a human lifetime, the foxes went from being wild to having floppy ears (like puppies), being multicolored, and answering to their names. I would have to assume that when you get puppy-like characteristics that some genetic information would have to itself look more puppy-like. Unless you can produce identical traits with completely different genetic coding. (I’m sure this is possible. I’m not sure how likely.) If the eye has independently evolved several dozen times in the course of history, as it is claimed, does the DNA show no similarity in creatures of those lineages?

    I would also expect that if non-coding DNA ends up having a biological function that selection would tend to have an impact on placement. To call a location “conserved” sounds a bit like question-begging. In the case of the Russian foxes, certain traits tended to “bundle” with other traits. I would expect that if non-coding DNA were to have a function, then its ideal location would be similar in similar creatures. Do we at this point know that a creature of this general makeup could survive if that non-coding DNA were not where it was, or if it survived that it would be as robust?

  2. John H says:

    Rick: to the extent that my argument in my previous post depended on non-functionality then that was my error and not Carroll’s. But the key points were (a) the shared SINEs cannot have arisen by chance; and (b) there is no evidence that they have any functionality (indeed, as I understand it the vast majority of SINEs are known to be defective and non-functional). Those point still stand.

    As for Matheson’s “readily explained”, that is the proper caution and restraint of a true scientist. I am under no such constraint 😉 – and, indeed, Matheson casts off that restraint in the rest of his post. There is no question of his “readily explained” being intended to leave room for an alternative, “design” explanation. I expect it has to be read in the light of Occam’s razor – since an explanation is available without invoking design, there is no need to invoke design.

    Unless you can produce identical traits with completely different genetic coding. (I’m sure this is possible. I’m not sure how likely.)

    Reading Carroll’s book, there are two main ways in which similar traits can occur without direct descent. First, where the same mutation occurs in the same gene shared by two animals – but the gene itself is shared due to their common descent. Second, similar traits can arise with wholly different genetic coding – Carroll gives the example of toxins in various animals that operate in much the same way (blocking a certain potassium pathway) but have wholly different genetic coding.

    If the eye has independently evolved several dozen times in the course of history, as it is claimed, does the DNA show no similarity in creatures of those lineages?

    I really do recommend you read Carroll on this. He has a fascinating section concerning this very question. The current understanding seems to be that the eye has not evolved wholly independently on as many occasions as had been suggested. Rather, the vast majority (or even all?) of eyes involve the same genetic building blocks but put together in different ways.

  3. Bror Erickson says:

    John H,
    “(a) the shared SINEs cannot have arisen by chance;”
    I think then we are agreed on atleast one thing. It wasn’t by chance. But ruling out chance does not rule out creation. What concerns me is not what we have in common with Chimps, but what we don’t have in common. Though common ancestry may explain a lot, does it explain all, and is it the only explanation. Is it the better explanation, and why? Do we know enough to make that determination? I suppose this is why I need to read this book.
    I still need to read the book. Really would like to but I am reluctant to buy it and the local library sucks; unless you like romance novels, and LDS liturature. (There is much more of that than you would believe.)

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