tgamble

<a href="http://arn.org/docs/behe/mb_indefenseofbloodclottingcascade.htm" target="_blank">http://arn.org/docs/behe/mb_indefenseofbloodclottingcascade.htm</a>

I know Miller has responded but what about his accusations concerning Dolittle?

I'm also puzzled on this response

First, it's interesting to note that he apparently has no problem with Common descent.

Second, who gives a shit if NS was involved at all? The point is that gene duplication provides a NATURAL explanation for allegedly IC systems. Why NS wouldn't be involved (better systems would be selected for) is beyond me.

I'd like to get some feedback on some of the more technical claims made by Behe. Especially those concerning Dolittle.

Thanks.

[ December 17, 2002: Message edited by: tgamble ]</p>

simian

The Behe quote would seem to imply that Behe feels that common desent does not imply natural selection - which is consistent with his previous claims - NS is not doing it, the hand of god is. Although I will note that I would expect his claim be along the lines of the genetic changes being the hand of god, NS can do the rest.

Back to my armchair.

Simian

lpetrich

In fairness to Behe, that is a reasonable view.

And, in fact, a variety of non-Darwinian mechanisms have been proposed, as well as variations of Darwinism, like how much selection vs. how many frozen accidents and how much neutral drift.

tgamble

Well, yes. But it's Behe who claims either NS or ID. He doesn't give a third option.

I guess the point I'm making is that Behe claims that if NS can't do it, ID must. Then he wonders why his opponents use NS as an explanation instead of an unnamaed third option.

What the explanations show, even if NS is over emphesized, is not Id is not nesasary.

scigirl

I couldn't get that link to work, let's see if this one does the trick:

<a href="http://arn.org/docs/behe/mb_indefenseofbloodclottingcascade.htm" target="_blank">Click Here.</a>

scigirl

Albion

"I know Miller has responded but what about his accusations concerning Dolittle?"

Well, Doolittle responded in 1999 (I think) to the initial attack which Behe made in Darwin's Black Box; I can't see any evidence of a response to this article. On the other hand, is Behe saying anything that he didn't say before?

tgamble

II. Russell Doolittle's Criticism

a. Mice lacking clotting factors have severe health problems
In its issue of Feb/March 1997 Boston Review featured a symposium discussing Darwin's Black Box and Richard Dawkins' Climbing Mount Improbable. Among the dozen essays contributed by academics was one by University of California-San Diego biochemist Russell Doolittle (Doolittle 1997); (Prof. Doolittle's essay can be found at <a href="http://www.polisci.mit.edu/bostonreview/BR22.1/doolittle.html" target="_blank">http://www.polisci.mit.edu/bostonreview/BR22.1/doolittle.html</a>). I had devoted a chapter of Darwin's Black Box to the blood-clotting cascade, asserting that it is irreducibly complex and so does not fit well within a Darwinian framework. Doolittle, an expert on blood clotting, disagreed. Prefacing a discussion of globin homology, he remarked that "the genes for new proteins come from the genes for old ones by gene duplication," later adding "This same kind of scenario can be reconstructed for a host of other physiological processes, including blood clotting." Then, citing a paper by Bugge et al. (Bugge et al. 1996) entitled "Loss of fibrinogen rescues mice from the pleiotropic effects of plasminogen deficiency," he commented:

Recently the gene for plaminogen [sic] was knocked out of mice, and, predictably, those mice had thrombotic complications because fibrin clots could not be cleared away. Not long after that, the same workers knocked out the gene for fibrinogen in another line of mice. Again, predictably, these mice were ailing, although in this case hemorrhage was the problem. And what do you think happened when these two lines of mice were crossed? For all practical purposes, the mice lacking both genes were normal! Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. Music and harmony can arise from a smaller orchestra. (Doolittle 1997)

The implied argument appears to be that the cited work shows the clotting system is not irreducibly complex, so a simpler clotting cascade might be something like the one that lacked plasminogen and fibrinogen, which could be expanded into the modern clotting system by gene duplication. Perhaps there are other stable systems of lesser complexity, and the entire cascade could then be built up by small steps in what is thought to be the typical Darwinian pattern. However, that interpretation depends on a mistaken reading of Bugge et al. (1996).

Bugge et al. (1996) note that the lack of plasminogen in mice "results in high mortality, wasting, spontaneous gastrointestinal ulceration, rectal prolapse, and severe thrombosis. Furthermore, plasminogen-deficient mice display delayed wound healing following skin injury." On the other hand, if the gene for fibrinogen is knocked out, the result is failure to clot, frequent hemorrhage, and that "pregnancy uniformly results in fatal uterine bleeding around the tenth day of gestation." (Suh et al. 1995) The point of Bugge et al. (1996) was that if one crosses the two knockout strains, producing plasminogen-plus-fibrinogen deficiency in individual mice, the mice do not suffer the many problems that afflict mice lacking plasminogen alone. Since the title of the paper emphasized that mice are "rescued" from some ill-effects, one might be misled into thinking that the double-knockout mice were normal. They are not. As Bugge et al. (1996) state in their abstract, "Mice deficient in plasminogen and fibrinogen are phenotypically indistinguishable from fibrinogen-deficient mice." In other words, the double-knockouts have all the problems that mice lacking only fibrinogen have: they do not form clots, they hemorrhage, and the females die if they become pregnant. They are definitely not "[f]or all practical purposes . . . normal." (Doolittle 1997) (Table 1)

The probable explanation is straightforward. The pathological symptoms of only-plasminogen-deficient mice apparently are caused by uncleared clots. But fibrinogen-deficient mice cannot form clots in the first place. So problems due to uncleared clots don't arise either in fibrinogen-deficient mice or in mice that lack both plasminogen and fibrinogen. Nonetheless, the severe problems that attend lack of clotting in fibrinogen-deficient mice continue in the double knockouts. Pregnant females still perish.

An important lesson exemplified by Bugge et al. (1996) is that it can be worse for the health of an organism to have an active-but-unregulated pathway (the one lacking just plasminogen) than no pathway at all (the one lacking fibrinogen, which exhibited fewer overt problems). This emphasizes that model scenarios for the evolution of novel biochemical systems have to deal with the issue of regulation from the inception of the system. Most important for the issue of irreducible complexity, however, is that the double-knockout mice do not merely have a less sophisticated but still functional clotting system. They have no functional clotting system at all. They are not evidence for the Darwinian evolution of blood clotting. Therefore my argument, that the system is irreducibly complex, is unaffected by that example.

{edited to fix link - sci}

[ December 17, 2002: Message edited by: scigirl ]</p>

tgamble

If anyone's interested, Evokskeptic just posted a typically ignorant rant on creationtalk.

<img src="graemlins/boohoo.gif" border="0" alt="[Boo Hoo]" /> <img src="graemlins/boohoo.gif" border="0" alt="[Boo Hoo]" /> <img src="graemlins/banghead.gif" border="0" alt="[Bang Head]" /> <img src="graemlins/banghead.gif" border="0" alt="[Bang Head]" />

lpetrich

That seems to be the case; the ID guys are curiously reluctant to mention non-ID, non-NS mechanisms of evolution.

One non-NS mechanism completely consistent with Darwinism is random fixation, also known as the founder effect or genetic drift or frozen accidents. Selectively-neutral evolution, such as much molecular-level evolution, is known to proceed in that fashion; this is Motoo Kimura's theory of neutral selection.

However, on the less-random side, there are theories like

Inheritance of acquired characteristics
Direct induction by the environment
Orthogenesis (evolution by internal forces; includes vitalist theories)

Poor Lamarck got his name attached to IAC when actually he believed in a form of orthogenesis as the major mechanism of evolution.

Interestingly, molecular evolution produces a statistical form of orthogenesis, which sometimes yields a well-defined rate of divergence (the "molecular clock").

[ December 17, 2002: Message edited by: lpetrich ]</p>