monkenstick

not really, but a poster at the EVC forum called peter borger seems to think so

he ranks right up there with randman for irritation factor.

Check it out, I just don't think this guy can be argued with;

<a href="http://www.evcforum.net/cgi-bin/forumdisplay.cgi?action=topics&forum=Evolution&num ber=5&DaysPrune=20&LastLogin=" target="_blank">http://www.evcforum.net/cgi-bin/forumdisplay.cgi?action=topics&forum=Evolution&num ber=5&DaysPrune=20&LastLogin=</a>

Quetzal

Monk: I've been following the threads. He's getting beaten up pretty badly, IMO. Although much more sophisticated in the way he expresses himself, he's as hermitically sealed as Philip - just more coherent. The one to watch over there is Tranquility Base.

theyeti

Not too long ago, I ran across an argument from this Borger fellow about genetic redundancy in calmodulins. Since I take an interest in calmodulins, I decided to look up the paper he referrenced. It turned out that the paper said almost the exact opposite of what Borger was saying. He claimed that a knock-out mouse with a disfunctional calmodulin was normal. In fact, no knock-out had been performed. He claimed that the three calmodulin genes were identical. In fact, each one is different. The paper he referrenced showed how each of the genes is regulated and expressed differently, and then went on to explain that this is why three copies are maintained with little variation via natural selection. As is depressingly common, Borger is either displaying extremely sloppy scholarship, or is being deliberately dishonest. I wouldn't take anything he says seriously. However, I bet that you could refute most of his arguments just by looking up the papers he cites!

BTW, I got a good laugh out of this one:

Do you think he noticed the phrase, "even in the presence of severe physiological defects"? What a fucking idiot.

theyeti

Quetzal

theyeti: He's still arguing about mouse knockouts. I thought he was talking about the plasminogin and fibrinogin experiments. Something about how redundancy proves design. I always thought it was the other way around... (i.e., it's not irreducibly complex if you can knock out something in a cascade and have a functional organism...)

theyeti

The plasminogen and fibrinogin knock-outs were not viable -- only the double knockout. And I'm pretty sure that it wasn't as healthy as the wild-type (mother's didn't survive child-birth very well due to bleeding or something). That's all you need to put paid to his argument right there. The significance of these studies was initially directed at Behe who claimed that the blood clotting cascade was IC. The removal of two components resulting in a functioning system would seem to pose problems for that, but Behe pointed out that the system only works again when both proteins are added. I think he's got a point there, but nonetheless, good scenarios for the evolution of <a href="http://www.antievolution.org/cgi-bin/ikonboard/ikonboard.cgi?s=3d53f020b29bffff;act=ST;f=9;t=3" target="_blank">blood clotting</a> (and other systems that Behe brought up in DBB, like the <a href="http://www.talkdesign.org/faqs/Evolving_Immunity.html" target="_blank">immune system</a>) have been proposed. IMO, all that it takes to falsify the IC argument is to show a plausible evolutionary pathway for any IC system. Once this is done, IC can no longer be considered a barrier to evolution. You might still have reasons to think that a particular IC system can't evolve, but it won't be merely due to its being IC. Therefore, the IC argument has been refuted. But anyway, you're right that Borger is using a contadictory line of reasoning with his redundancy BS.

About mouse knock-outs: No one who knows what they're talking about is so naive as to think that knock-outs are a definitive screen for gene function. Rather, they are simply a starting point to see if the gene in question has any dramatic physiological effects. More subtle effects that would be selectable in the wild won't be noticed in the lab. The reason is obvious. Knock-out organisms are maintained in conditions which are ideal for their growth and survival. They're kept at a constant temperature, given a nutrient rich diet and plenty of water, kept safe from predators and the whims of the environment, etc. They don't have to compete with each other for resources or mates, nor are they subject to disease. Any genes which would help an organism cope in the wild with these problems would not have their effects noticed in the lab. Subtle differences in behavior or nutritional chemistry are likely to be highly selectable in the wild, but unless the researcher is expecting them in advance, there is no way to test for them in the lab, since the conditions must be controlled. Again, Borger is a fucking idiot for not knowing this.

theyeti