Behe’s polar bears


Michael Behe has a problem: he uses polar bears as an example of how “damaging” a gene can have an advantageous effect. As Nathan Lents explains:

Behe offers them as an example of how harming genes can help an organism and lead to adaptive evolution. Imagine an ancestor bear population that looked pretty much like brown bears. Then came some random mutations that reduced the production or deposition of pigment into the fur of the bears. This made the bears white and – voilà! – the bears acquired natural camouflage in snowy climates so as to better sneak up on their prey.

This seems like a pretty straightforward example and most people will simply take it at face value. Behe jumps from this example to his claim that this is all that unguided mutations can do. However, even in this apparently “pro-Darwinism” example, Behe exaggerates his claims and misrepresents what science has actually revealed. The evolution of polar bears was not only a matter of harmful mutations.

The first part is fine: there are all kinds of ways a genetic change can produce an adaptive phenotype, and downregulating a gene is one of them. It’s the second part that’s the problem. Behe leaps from a few examples to an assertion that this is a universal rule, which is not the case. Lents shows another example in polar bears.

Look at those polar bears, slurping down all those sugary soft drinks. It’s a little known fact that they’re using Coca-Cola to wash down their diet of fatty, blubbery seals, and they pretty much eat nothing but meat and fat, which, if any of us tried the Polar Bear Diet, we’d be dead of coronary disease in short order. It would be interesting to know how these animals cope with a diet high in cholesterol and fats, so Lents cites a paper that looked at the molecular sequence of apolipoprotein B (APOB), a protein that is important in the transport of fats in the blood, and compared it to that of brown bears. Surprise — the form found in polar bears is better at clearing fats from the bloodstream.

Substantial work has been done on the functional significance of APOB mutations in other mammals. In humans and mice, genetic APOB variants associated with increased levels of apoB are also associated with unusually high plasma concentrations of cholesterol and LDL, which in turn contribute to hypercholesterolemia and heart disease in humans (Benn, 2009; Hegele, 2009). In contrast with brown bear, which has no fixed APOB mutations compared to the giant panda genome, we find nine fixed missense mutations in the polar bear (Figure 5A). Five of the nine cluster within the N-terminal ba1 domain of the APOB gene, although the region comprises only 22% of the protein (binomial test p value = 0.029). This domain encodes the surface region and contains the majority of functional domains for lipid transport. We suggest that the shift to a diet consisting predominantly of fatty acids in polar bears induced adaptive changes in APOB, which enabled the species to cope with high fatty acid intake by contributing to the effective clearance of cholesterol from the blood.

Clearly, the authors do not expect the polar bear APOB to be “broken.” Rather, a bare majority of the amino acid changes are in the most important region for the clearing of cholesterol from the blood. In other words, these mutations likely enhance the function of apoB, at least when it comes to surviving on a diet high in saturated fats.

So APOB in polar bears isn’t broken at all. It does carry mutations relative to brown bears, but they haven’t resulted in reduced functionality at all — quite the opposite, actually.

Comments

  1. bachfiend says

    I’m not certain whether this is relevant, but there is a condition in horses:

    https://en.m.wikipedia.org/wiki/Lethal_white_syndrome

    due to a mutation which leads to a completely white colour in foals, who die a few days after birth. But if it weren’t uniformly lethal, it would result in horses perfectly camouflaged for the Arctic.

    It’s probably not relevant. I would have to read Behe’s argument, but I don’t want to do that. He has the rare talent to be able to mangle science in such a way that even I can see it.

  2. zetopan says

    Behe is merely a replay of what some other cranks have done before him. John Hagelin claimed that physics used to be extremely difficult until he fell (or more likely voluntarily jumped) into the TM (Transcendental Meditation) movement, then “physics” became very easy. Of course he lacked self awareness to such an extreme that he failed to even recognize that he was no longer doing physics, but rather religion. Behe is a virtual copy of Hagelin and quite likely wants to be just as “great” and “revered” as Hagelin.* Some people are simply eager for brain death; it removes all of those scary aspects about living on a large lump of rock and dirt circling a mediocre star in the boondocks of a mediocre galaxy located in an uncaring universe (all of which will die out in the distant future).

    *Look up Hagelin + TM and you will be greeted with tons of websites extoling the “science” of TM with Hagelin as their “scientific” authority.

  3. chrislawson says

    Shorter Behe: “See this example of evolution at work? Proves that evolution doesn’t work.”

  4. rrhain says

    I’m confused: How can the down-regulation of a gene be considered “harmful” when it results in a greater fitness for the environment in which the organism finds itself?

    Surely Behe isn’t so fatuous as to think that any change in the genome that results in the removal or lessening of a trait is “harmful,” is he?

    Well, of course he is. Creationism is full of this idiocy that evolution can’t be true because all mutations are ‘harmful” (or if they think they can get away with the techno-babble, “deleterious”) even though the overwhelming number of mutations are neutral. And even if we grant that mutations that aren’t neutral tend to result in less fitness, it’s like they are willfully ignorant of how yahtzee works: If your mutations aren’t beneficial for allowing you to survive and reproduce, they’ll tend to be selected against and you’re left only with the ones that increase fitness.

    Evolution doesn’t have a direction.

  5. lucifersbike says

    I may be wrong, but I thought polar bears had a short thick pelt next to their skins and an outer layer of guard hairs that are translucent and hollow. Surely this is the result of a more complex adaptive process than simple losing the expression of a gene for pigment?
    [Please do not hit me, I am a linguist who is interested in science, and it’s nearly 50 years since i was last in the school lab].

  6. iiandyiiii says

    Behe’s a colossal fool, but don’t some arctic populations subsist (or historically they used to subsist) on a diet that’s pretty close to a polar bear’s diet?

  7. says

    @rrhain:

    I’m confused: How can the down-regulation of a gene be considered “harmful” when it results in a greater fitness for the environment in which the organism finds itself?
    Surely Behe isn’t so fatuous as to think that any change in the genome that results in the removal or lessening of a trait is “harmful,” is he?

    No, that’s not it. He’s not saying all downregulation is harmful. He’s saying that up-regulation is impossible without divine intervention, and is (poorly) using adaptive downregulation to prove that the “natural” evolution we see is only ever the result of breaking god-given genes that were perfect for past environments but are maladaptive in a new environment.

    He’s saying that evolution via downregulation is the only possible evolution until some god decides to tinker with genomes again.

  8. lochaber says

    I thought polar bears had dark skin, and light/clear hairs to maximize solar warming?

    Is camouflage really important to them? I thought they mostly hunted by waiting near breathing holes, and catching seals when the surfaced.

  9. Callinectes says

    Behe will probably argue that the polar bear version of APOB would be a problem in brown bears on a brown bear diet, and that therefore the increase in functionality constitutes a harmful mutation for the bears.

  10. raven says

    Behe is completely wrong on simple facts.
    Or more accurately, he is just lying.
    Creationism is a lie from beginning to end.

    The claim here is that there are no adaptive positive gain of function mutations.
    The fact is that there are many known and they are common.
    There is a better cholesterol metabolizing gene variant known in humans as well.

    Wikipedia ApoA 1 Milano
    Apolipoprotein A-1 Milano (also ETC-216, now MDCO-216) is a naturally occurring mutated variant of the apolipoprotein A1 protein found in human HDL, the lipoprotein particle that carries cholesterol from tissues to the liver and is associated with protection against cardiovascular disease. ApoA1 Milano was first identified by Dr. Cesare Sirtori in Milan,
    who also demonstrated that its presence significantly reduced cardiovascular disease,
    even though it caused a reduction in HDL levels and an increase in triglyceride levels.[1]
    and
    In the 1990s, researchers at the Cedars-Sinai Medical Center showed that injection of a synthetic version of the mutant ApoA-1 into rabbits and mice could reverse vascular plaque buildup.[2]:164

  11. raven says

    Contrary to what Behe claims, adaptive gain of function mutations are common and easily found anywhere and everywhere.
    Below is a study that quantifies adaptive mutations in a model E. coli system.

    Adaptive Mutations in Bacteria: High Rate and Small Effects
    Lília Perfeito1, Lisete Fernandes1,2, Catarina Mota1, Isabel Gordo1,*

    Science 10 Aug 2007:
    Vol. 317, Issue 5839, pp. 813-815
    DOI: 10.1126/science.1142284

    Abstract
    Evolution by natural selection is driven by the continuous generation of adaptive mutations. We measured the genomic mutation rate that generates beneficial mutations and their effects on fitness in Escherichia coli under conditions in which the effect of competition between lineages carrying different beneficial mutations is minimized. We found a rate on the order of 10–5 per genome per generation, which is 1000 times as high as previous estimates, and a mean selective advantage of 1%. Such a high rate of adaptive evolution has implications for the evolution of antibiotic resistance and pathogenicity.

  12. numerobis says

    if any of us tried the Polar Bear Diet, we’d be dead of coronary disease in short order

    Short life but probably long enough to have grandkids. The Inuit have some adaptations that help with a fat-heavy diet, but they aren’t entirely necessary.

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