Intelligent Design

GR Has Returned (Not General Relativity, But Glucocorticoid Receptors)

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In collaboration with Joe Thorton and his group, Eric Ortlund has come out with a new paper on GR. I’ve just very quickly looked at the news summary. We’ll want to wait until Michael Behe gives us an analysis of what these latest findings mean, but until such time, we can enjoy this quote:

“What this highlights is how proteins that end up evolving new functions had those capacities, because of their flexibility, at the beginning of their evolutionary history,” says lead author Eric Ortlund, PhD, associate professor of biochemistry at Emory University School of Medicine.

Although almost tautological, this, however, nicely links Aristotle’s ‘efficient’ and ‘final’ causes—as it should be in things teleological.

5 Replies to “GR Has Returned (Not General Relativity, But Glucocorticoid Receptors)

  1. 1
    Mung says:

    Life is flexible. Therefore, ID is false.

  2. 2
    REW says:

    We’ll want to wait until Michael Behe gives us an analysis of what these latest findings mean

    He’ll say that this demonstrates loss of function- the loss of the inhibitory conformation, which evolution is fully capable of. But creating the GC receptor in the first place required ID

  3. 3
    Virgil Cain says:

    Well REW, do you have any evidence or any way to test the claim that natural selection, drift or neutral constructive did it? Until you do there is no need to whine about Behe or ID

  4. 4
    PaV says:

    REW:

    Behe has addressed stuff that’s come out of Thornton’s lab before. He gives you his scientific take on it.

    This GR is now being revisited. From what I can see, the situation is worse now than it was years before when they did similar experiments. It looks like they’re willing to admit they have no idea how the “evolution” of GR happened, but that it did:
    “What this highlights is how proteins that end up evolving new functions had those capacities, because of their flexibility, at the beginning of their evolutionary history, . . . ”

    When this came out, I analyzed Thornton’s paper, and reached a much more critical assessment of their results than Behe did. I shared this with him in private correspondence. Behe is much more gracious than I would have been. But it looks like I may have been right. It looks like they’re stumped. But, again, I will ceded the ground to the molecular biologist, of which I haven’t the expertise.

    BTW, as I’m recalling the original paper on GR, the “loss of function” is something that is part of Thornton’s analysis. It was ‘viable’, i.e., ‘functional,’ pathways they were searching for. The cunundrum was something like this: one had to have two ‘sets’ of mutations in place; and, IIRC, if you had the one ‘set’ in place, then the mere presence of one of the other ‘set’ of mutations would completely destroy function. IOW, they would die. And you couldn’t bounce from a mutation from one set, and then another from the other set. Hence, there was no ‘functional’ pathway from, let us say, A (‘ancient protein’) to B (‘present day protein’).

    Try to have an open mind.

    [P.S. I went back to the correspondence, and apparently there are four groups of mutations: X,Y,Z and W.]

  5. 5
    PaV says:

    This little tidbit from the article:

    How could a single mutation have conferred such a dramatically new function? Anderson et al. found that the ancient scaffolding protein uses the same part of its surface to bind to the spindle-orienting molecular marker as the ancient enzyme used to bind to its target substrate molecule, and the two partner molecules happen to share certain key chemical properties. This fortuitous resemblance between two unrelated molecules thus set the stage for the simple evolution of a function that is now essential to the complexity of multicellular animals

    You just can’t beat raw luck.

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