Clotted rot for rotten clots

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As noted in my previous post, on 16 February Dr. Vincent Cassone debated Intelligent Design advocate Dr. Michael Behe. The debate was sponsored by the TAMU Veritas Forum.

One of the items in this outline of the debate is a recurring theme for Behe.

“Behe … Brings up the clotting cascade, and points out an error made by Russ Doolittle in a Boston Review article in 1997. Doolittle mischaracterized a 1996 paper on double knockout mice lacking two proteins in the clotting cascade. Behe introduces a theme for the evening: if Russ Doolittle, the world’s expert, makes mistakes about the clotting cascade, then there is no evidence that it arose by DEM.”

Behe has brought up Doolittles alleged “mistake” several times. Would it surprise you that Behe is being less than forthright?

Well, aside from Behe’s flawed logic in that quote (assuming Behe was correctly reported), here is what Russ actually said in the Boston Review article. This is near the end of a longish article.

” Let me conclude by mentioning that support for the Yin and Yang scenario is now coming from another quarter. Thus, it has become possible during the last decade to “knock out” genes in experimental organisms. “Knockout mice” are now a common (but expensive) tool in the armamentarium of those scientists anxious to cure the world’s ills. Recently the gene for plaminogen 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!6 Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. Music and harmony can arise from a smaller orchestra. No one doubts that mice deprived of these two genes would be compromised in the wild, but the mere fact that they appear normal in the laboratory setting is a striking example of the point and counterpoint, step-by-step scenario in reverse!”(emphasis added by IFM)

6 is Bugge et al., “Loss of Fibrinogen Rescues Mice from the Pleiotropic Effects of Plasminogen Deficiency.” Cell 87 (1996): 709-19. [1]

Now, let’s be clear what Doolittle is stating here. 1) The example shows the interaction between regulatory proteins in the cascade. The modern clotting system is a balance between pro-coagulation factors and anti-coagulation factors (the Yin and Yang as he calls it)

The main point was to demonstrate that the delicate balance of forward and reverse reactions that regulate blood clotting came about in a step-by-step fashion. I summarized events with the metaphor of Yin and Yang, and emphasized that other similar point-and-counterpoint comparisons could be made.

2) The example shows that simpler systems than the full system can work in laboratory situations. 3) The mice in the example wouldn’t survive in the wild

Note that Doolittle is clearly relating the recovery in the double knockout mice to the excessive coagulation defects in the plasminogen knockout mice, not the overall life history of the mice (see below for some of the amazing results from the actual paper).

Behe has responded to Doolittle in several fora, saying he made a mistake. In this article Behe, quotes part of the paragraph. Behe carries on as if Doolittle thought these mice were excatly the same as wild-type mice in all respects. However, Behe omits the last section of Doolittle’s paragraph, with its qualifications and statement that these mice are by no means identical to ordinary mice and wouldn’t survive in the wild. At the most Doolittle is guilty of using jargon (compromised rather than die; however, researchers still tend to write that animals were sacrificed, rather than animals were killed, when describing experiments). It is Behe who is doing the mischaracterising, not Doolittle.

Now, I’ve read Bugge et al, and I think Behe’s statement not only mischaracterises Doolittle, but also mischaracterises the Bugge et al., paper.

Clotting occurs by a cascade of reactions initiated by either tissue damage (the extrinsic pathway) or contact with surfaces such as the basement membranes of blood vessels (the intrinsic or contact pathway). The ultimate effect of this cascade is to convert the soluble protein fibrinogen to the insoluble protein fibrin, which forms the basis of the clot that stops bleeding.

Note that this is the critical final step in clotting. Now, what happens when we knockout the gene for fibrinogen, making the mice unable to form fibrin (and hence clots)? Nothing much really. In the laboratory the fibrinogen knockout mice (Fib-/-) live normal lives with minor defects. They can’t carry a pregnancy beyond mid-term, but they should be dead from massive bleeding a day or two after birth, not living well into breeding age. The reason is that the clotting system not only stops bleeding from cuts and wounds, it also maintains the integrity of the blood vessels. Without a low level of clotting activity, the blood vessels (mostly the small ones) leak [note1].

Not only do the Fib (-/-) mice fail to die catastrophically after birth, but they fail to bleed to death from full skin thickness incisions. Remember, that fibrin is the ultimate product of the clotting pathway, yet these mice are coping well in the laboratory (in the wild they would probably be dead rapidly, researchers with scalpels are kinder than cats, pointy sticks and other natural hazards). Why is this so? Almost certainly because platelets are plugging the blood vessels and slowing the bleeding until ordinary serum proteins glob up [2]. This is of interest because this is basically the mechanism that primitive chordates such as tunicates use.

These animals have a low-pressure blood circulation system and use circulating haemocytes (a bit like white blood cells) to plug up any wounds. I’d like to emphasise that the vertebrate clotting system did not evolve in modern mammals with high-pressure circulatory systems, but developed between the tunicates (which have no readily identifiable components of the modern coagulation system) and cartilaginous-jawed fish (which have most of the pathways)[3]. It can be readily seen that a generalized “globbing system”, well short of the modern coagulation system would be an advantage over the tunicate hemolymph system, without requiring the specificity of the modern vertebrate coagulation system [note2].

So far I have just talked about establishing a clot by forming fibrin. However, when the blood vessel is repaired the fibrin has to be cleared away. This is performed largely by the enzyme plasmin, generated from its inactive precursor, plasminogen. This is part of the balanced “Yin/Yang” system that Doolittle talks about. Plasminogen knockout mice (Plg-/-) have no plasminogen. The Plg(-/-) mice are very sick. They fail to gain weight, have very poor wound healing, have numerous pathological changes and all die within 300 days [1].

So what happens when we knock out both plasminogen and fibrinogen? With both of these essential components gone the mice should be even sicker, right? Wrong! Plasminogen/Fibrinogen double knockouts gain weight almost at the rate normal mice do, have wound healing almost indistinguishable from normal mice and live for virtually the same time as normal animals. They do have a few pathological changes, but as Doolittle says, “for all practical purposes” these animal are normal (see the following figures, they are pretty amazing).

Plasminogen deficient mice (Plg-/-) vs double knockout mice, note the severe growth retardation corrected by fibrinogen knockout.

Wound healing, the plasminogen knockout mice (triangles) heal very slowly, while the Plg(-/-),Fib(-/-) mice (diamonds) not only fail to bleed to death immediately, but heal almost as fast as normal mice (squares).

Now, let me emphasise again that these animals fail to bleed to death catastrophically or do any of the horrible things that one would expect from Behe’s “irreducibly complex” scenario. As Doolittle says, this shows the Yin/Yan aspect of coagulation, with checks and balances that can be built up step by step.

Now, fibrinogen knockout mice cannot carry a pregnancy beyond day 10, neither can the double knockout mice. This is not particularly significant when by Behe’s ideas these mice should be dead shortly after birth, but conspicuously aren’t. In the wild, they wouldn’t be able to breed, but in the wild they would be dead long before breeding age. The way Doolittle frames his brief discussion, given the limitations of a newspaper article (“No one doubts that mice deprived of these two genes would be compromised in the wild”) is perfectly compatible with the facts of the Bugge et al., paper.

Behe says:

They [the double knockout mice] are decidedly not promising evolutionary intermediates.

Doolittle never claimed they were (“No one doubts that mice deprived of these two genes would be compromised in the wild”); after all, clotting evolved in protovertberates with low-pressure blood systems, not modern vertebrates (3,4). What Doolittle was pointing to was how the systems interact with each other, and how systems could be built up piecemeal. Behe seizes on a minor point, only made possible by not quoting the full text of Doolittle’s paragraph, and ignores the fact that fibrinogen deficient mice don’t bleed to death immediately after birth, as his scheme would predict.

This is not the only thing Behe has ignored. Miller has pointed out to Behe that whales and dolphins lack the contact pathway (Factor XII or Hageman Factor) (5). Furthermore, puffer fish don’t have the pathway either (3). So two groups of vertebrates can live happily without a major arm of the clotting cascade. Behe has not addressed this. This is a larger omission than Doolittle’s.

In summary, Behe misrepresents Doolittle. Basic courtesy would at least require Behe to include the full Doolittle paragraph in his articles, let alone ceasing to claim Doolittle made a mistake [note 3].

[1] Bugge et al., “Loss of Fibrinogen Rescues Mice from the Pleiotropic Effects of Plasminogen Deficiency.” Cell 87 (1996): 709-19.

[2] Camerer E, Duong DN, Hamilton JR, Coughlin SR. Combined deficiency of protease-activated receptor-4 and fibrinogen recapitulates the hemostatic defect but not the embryonic lethality of prothrombin deficiency. Blood. 2004 Jan 1;103(1):152-4.

[3] Jiang Y, Doolittle RF. The evolution of vertebrate blood coagulation as viewed from a comparison of puffer fish and sea squirt genomes. Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7527-32.

[4] Davidson CJ, Tuddenham EG, McVey JH. 450 million years of hemostasis. J Thromb Haemost. 2003 Jul;1(7):1487-94.

[5] Semba U, Shibuya Y, Okabe H, Yamamoto T. (1998). Whale Hageman Factor (Factor XII); Prevented Production Due to Pseudogene Conversion. Thrombosis Research 90(1):31-37

[note1] Thrombin knockout mice are embryonic lethal. However, it turns out that thrombin leads a double life as an embryonic tissue remodelling enzyme [2]. It is entirely possible that thrombin was co-opted from development remodelling enzymes. There is a lot of evidence that the that the complement system originated by co-opting tissue remodelling enzymes.

[note2] While its is easy to imagine a trysin-like enzyme chopping bits off a previously soluble protein to make it insoluble, making a protoclot, one issue that has been raised is how do you stop this primitive trypsin-like enzyme from clotting the entire blood, rather than where it is needed. A clue comes from the primitive chordate Amphioxus. It has trypsin circulating in its haemolymph (it doesn’t have blood like vertebrates), when the animal is injured, trypsin cleaves a bit off an enzyme activating the enzyme, which in turn produces a polymeric melanin which acts as a kind of glue to immobilize bacteria. Why isn’t trypsin activating this enzyme all the time? Trypsin is only activated in the presence of caclium released by tissue damage. This is a primitve, one step version of the calcium-activated clotting cascade. Pang Q, Zhang S, Wang C, Shi X, Sun Y. Presence of prophenoloxidase in the humoral fluid of amphioxus Branchiostoma belcheri tsingtauense. Fish Shellfish Immunol. 2004 Nov;17(5):477-87.

[note 3] At least one other webpage has Behe partly quoting Doolittle’s statement and omitting the qualifier, as well as proceeding as if the qualifier wasn’t there. Behe also repeats it often in lectures and talks.

Worse, the tale has grown in the telling.

Writing in a church magazine, http://www.floridabaptistwitness.com/3746.article Charles Colson had this to say…

Soon after the book was published, its thesis was challenged by the leading expert in America on cell structure, Dr. Russell Doolittle at the University of California. He cited a scientific study supposedly disproving irreducible complexity. Behe immediately researched it and found it proved just the opposite: It confirmed him. So Behe went back to Dolittle. In a phone conversation, Doolittle admitted he was wrong, but he has never made a public retraction.

Is this story true? Far from it. Mark Perakh emailed Dr. Doolittle, who generously allowed his reply to be quoted.

Doolttle Wrote:

Thanks for sending me the latest on the desperate tactics that these people avail themselves of. Others have written me in the past about my alleged “concession.” What happened is that Behe emailed me after my article appeared and challenged my tail-end assertion about the Bugge et al paper. I went back and read it more carefully, and indeed, I had overstated one aspect. It was inadvertant, and I apologized. Ah, rue the day with minds like theirs!

In my paper I raised the point of how mice without plasminogen were severely ill. Mice without fibrinogen are also unwell, although not as badly off as the plasminogen-lackers. However, the big point was that mice lacking both genes were considerably better off than the ones that only lacked plasminogen. I had said these mice were “..for all practical purposes..normal,” although I went on to qualify the statement about how the mice would doubtless be compromised in the wild. In fact, the paper makes it clear that the mice are not “normal” in that they don’t breed well, even though the individuals are not unwell. My original point, lost in all the persiflage, was that there is a “point and counterpoint” in the evolution of these two genes, as there is in the evolution of many interacting systems.

It’s truely annoying that the creationists (“Intelligent Designers”) get so much much mileage out these side-issues and refuse to confront the main message. Regards, Russell Doolittle

Who should make the retraction? Not Doolittle.

Web resources on the evolution of clotting. http://www.talkorigins.org/origins/[…]h/feb97.html

Miller on the evolution of clotting

Generalized review of Behe and irreducible complexity .

[IFM is not an active researcher in the coagulation field, but my first ever research project was studying the effects of snake venom on coagulation, I still have the platelet electron micrographs taken nearly 20 years ago.]

3 TrackBacks

Happy Birthday, Panda's Thumb from Dispatches from the Culture Wars on March 23, 2005 12:43 PM

Today is the one year anniversary of the Panda's Thumb, the group science blog that I and a few friends started to address the evolution/creationism/intelligent design controversy. They grow up so fast, don't they? And you really should check out... Read More

Behe's talk at the MacLaurin Institute ("Bringing God into the marketplace of ideas by communicating the Christian worldview with its transforming potential") last night exceeded my expectations of suckiness. It was an evening of phony r... Read More

Recent research has thrown an interesting spanner into one of the key, but slightly obscure claims Behe makes about Irreducible Complex (IC) systems. In Behe’s discussion of the mammalian clotting system (Darwin’s Black Box [DBB], 1996, pa... Read More

34 Comments

Behe has brought up Doolittles alleged “mistake” several times. Would it surprise you that Behe is being less than forthright?

What would surprise me even MORE, of course, would be for Behe to give us HIS scientific theory as to how the blood clotting cascade was intelligently designed. What does he think the designer did, specifically, to produce the blood clotting cascade? What mechanisms does he think the designer used to do whatever the heck it is he thinks it did? Where can we see these mechanisms in action today designing something else?

Or just like the rest of ID, uh, “theory”, does Behe’s “explanation” consist solely of “an unknown thing did an unknown thing at an unknown time using unknown methods” . … .

Brilliant analysis.

As ever, the basic problem is that creationists cannot be honest and defend their creationism with the facts at the same time. They must pick one or the other. It’s hard to remain outraged after a while. Yes, of course these people know exactly what they’re doing. But the alternative would be to admit error.

I’d like to point out that the knowledge that dolphins lack Hagemann factor goes back to the late 60s…

A.J. Robinson et al. 1969. Hagemann Factor (Factor XII) Deficiency in Marine Mammals. Science 166:1420-1422.

Ken Miller, Genie Scott, and Carl Zimmer were all on a panel at the 2001 convention of the NSTA. I was fortunate to have dinner with the group, and Diane Blackwood and Mark Todd came along as well. Mark is a marine mammal trainer I worked with when I was in San Diego. Mark, Ken, and I were seated at one end of the table, and we were discussing the ID arguments. Ken brought up Behe’s argument concerning the blood-clotting system, at which point Mark said, “You know that dolphins are missing a chunk of that system, right?” Well, no, but Mark consulted with Dr. Sam Ridgway and provided the reference to the Science article noted above. Miller was able to catch Behe flat-footed at the AMNH debate early in 2002 with that bit of information. Here’s to social chitchat as a force for science education…

Miller was able to catch Behe flat-footed at the AMNH debate early in 2002 with that bit of information.

At which point Behe admitted that both the blood clotting system and the rattrap are not irreducibly complex.

http://www.ncseweb.org/resources/ar[…]_31_2002.asp

Question:

If Michael Behe admitted back in 2002 that the blood-clotting mechanism is not IC, why is he still bringing it up in debates?

It seems to me that Behe is just posing as a research scientist and ID expert.

Go look at his web page at lehigh.edu, and compare it with the other members of the Department of Biological Sciences. His web page is notably lacking in the hard science publications that are so abundant in many of the other faculty members’ pages. And the research he does describe apparently has little or nothing to do with ID. A Google search turned up lots of references to ID but no references to anything like professional work except the peripheral Protein Science article.

Can Behe’s supporters point me to his solid professional work, ID or otherwise (no review articles, no responses to critics, no philosophy books, no debates)?

Air Bear,

You might try a PubMed search using “Behe MJ” as the query.

Assuming he’s the only MJ Behe, 36 publications since 1978 is hardly impressive for a biochemist. He’s only published one paper since 2000, and that one made some pretty bad assumptions about penetrations of a neutral mutation into a population as a model for evolution, IIRC.

Wasn’t it Euripides who first said, whom the gods destroy, they first make mad?

Creationism/ID is like that. As other threads here have noted, when it infects scientists, their work slows or stops.

Assuming he’s the only MJ Behe, 36 publications since 1978 is hardly impressive for a biochemist.

I rather suspect that the percentage of life sciences grad students who end up in an academic setting with a record of steady publication over 15-20 years is pretty low. Behe’s record doesn’t stand him at the top of any class, but it’s nothing to sneeze at, either.

There are plenty of reasons why Behe’s publication productivity has declined in the past several years. “Infection with ID” is one possible explanation, but it must compete with others, such as opting for a greater role in teaching and mentoring (students and younger faculty colleagues), or happening to work in a field that has moved on (and thus closed funding and research opportunities). Or even, perhaps, being too far ahead of his time (not with ID, but maybe with respect to some his work that studied the links between DNA methylation and conformation).

There is plenty about Behe and his pro-ID work to criticize. Attacking his record at Lehigh and CUNY only serves as a distraction.

There is plenty about Behe and his pro-ID work to criticize. Attacking his record at Lehigh and CUNY only serves as a distraction.

I agree, but the point is to drag this out when they try to hold him up as some great researcher. His track record is not impressive like they occasionally make it out to be.

What does Behe hold up as an “irreducibly complex system” nowadays?

Re: comment 21599 by Art. The practical absence of recent publications by Behe in his professional field (only one article since 2000 and even this article being of a doubtful quality, looking more like an attempt to tangentially bolster ID than to do a good professional research) may indeed, as Art says, have a number of various reasons. As such, it may not be a sufficient indicator of Behe’s declining scientific status. However, we cannot fail to notice that in the same almost five years Behe has published a substantial body of pro-ID stuff, quite vigorously defending his silly mousetrap, IC, etc., so it seems a good surmise that he abandoned his professional work because his enthusiasm is now directed mainly to ID justification.

Excellent job, Ian.

Re: comment 21604 by Katarina. Behe and Dembski continue to stubbornly insist that a mousetrap is an IC system.

This is one of those posts that people need to bookmark and link to whenever they hear the “Doolittle error” claim. Invariably in any conversation with an IDist where Doolittle’s name comes up (usually in blood-clotting discussions), the IDist will resort to that claim, ignoring the rest of Doolittle’s contributions to the evolution of this supposedly IC system.

Prince Vegita Wrote:

I agree, but the point is to drag this out when they try to hold him up as some great researcher. His track record is not impressive like they occasionally make it out to be.

Don’t confuse quantity with quality. Behe’s papers (excluding Behe & Snoke) are generally fine, and his papers on B-Z DNA transitions are well regarded. As others have said, attacking his publication record is a distraction.

Nelson Alonso’s comments on PT seem particularly ironic now

It wasn’t a false accusation. I’m pretty sure that Doolittle, unless he’s a stubborn imbecile, no longer believes that the mice were “for all practical purposes … normal” as he originally claimed. That makes Behe’s statement:

“But when the results turned out to be the opposite of what he had originally thought, Professor Doolittle did not abandon Darwinism. “

correct.

Comment 13258 I asked him to support his assertions

Wedgie World

Have you contacted Doolittle yet to establish the veracity of the quote? Perakh did for his article.

Nelson Alonso: No I have not contacted Doolittle and wouldn’t insult his intelligence by doing so. I sincerely believe that he no longer thinks that the double-knockout mice were “for all practical purposes normal” unless he is simply holding on to that false view disingenuously. People make mistakes with interpeting papers. It’s ok, it’s human, no one is perfect. I’m not saying he abandoned Darwinism, but neither did Behe.

See also This link

ID proponents have gotten enough mileage out of this one. What is telling though is that the arguments of ID have not much evolved in the last decade or so. Scientifically vacuous indeed.

Thanks, Wedgie World, for the time and effort you invested (mostly on ARN) in showing the unseemly attack of Nelson Alonso on my writing for what it was. He had the gall to accuse me of lying. Before doing so he better had to look at a mirror. Thanks to your effort he was forced finaly to half-heartedly concede that he was “too hasty.” The quotes given in this Ian Musgrave’s post show once more that the statements in my articles (and in my book) regarding Behe’s mischaracterization of Doolittle’s position were correct while Alonso’s rebuttals of my statements were false. Moreover, Musgrave’s excellent post should put an end to Behe and Co’s incessant claims about Doolittle’s alleged “mistake” and his alleged admission of such. Doolittle’s intepretation of Bugge et al’s data was certainly much better substantiated than Behe’s, Dembski’s, Colson’s and their ilk’s assertions to the contrary. But they defend the Glory of God after all (proper quotes can be furnished on request) so all means are apparently good for such a goal, and mere facts cannot be allowed to stand in their way.

I want to know which facts stand in the way of “the Glory of God.” I know of none and I don’t think anyone else does either. It is just one more mindless assumption just like the natural selection of allelic mutations. My own feeling is that God is no longer around any more and like Grasse feel:

“Let us not invoke God in matters in which He no longer has to intervene.” page 166.

John A. Davison, unfair of course, unbalanced by the testimony of several right here at Panda’s Thumb, EvC and elsewhere, and still unafraid to confront and expose the forces of Darwimpian ignorance, bigotry and mysticism wherever they may be found.

While my general rule is to ignore Davison comments, I couldn’t help notice this obvious attempt at hijacking the thread: Mark Perakh wrote

they defend the Glory of God after all … so all means are apparently good for such a goal, and mere facts cannot be allowed to stand in their way.

This has been documented countless times and is extremely relevant to the discussion here. Now Davison jumps in with

I want to know which facts stand in the way of “the Glory of God.”

… a meaningless distraction that would still be irrelevant even if it had meaning.

Mr. Davison, you should address your question to Dembski who frankly admitted (in his lecture in the Fellowship Baptist Church in Waco, TX, on March 7, 2004) that the real motivation behind his pro-ID activity, in particular behind his effort to destroy “naturalistic science,” is his desire to stand up for “the Glory of God.” Furthermore, in an essay [1] he wrote that ID advocates will “never capitulate” regardless of what the arguments of their opponents can be. To my mind, the combination of these two utterances fully justifies my statement which you seem to dislike. Now, I understand that you are a professor of biology at some university in Vermont. Don’t you think that using personal insults for arguments can only make those you ceaselessly assault, shrugg off your posts? Or you don’t give a rap for whether or not you can convince others but only are interested in venting your puerile anger? I’d not like to resort to such extreme measures as disemvoweling your posts when they become, as is often the case, beyond the limits of a calm exchange of views, so, once again, I am appealing to you to show more restraint and not to deviate from the thread’s topics. [1] Dembski’s statement about “no capitulation” can be seen at www.arn.org/cgi-bin/ubb/ultimatebb.cgi?ubb=get_topic;f=13;t=000483 (unless it has been removed; last accessed in March 2002).

Davison, you can’t offend Perakh or anybody else - the only possible reaction to your ramblings is to shrug off. Have you considered consulting a psychiatrist? Mania of greatness is a disease. I wonder why the management of this blog is so tolerant of your escapades? They are off-topic, rude, and mostly meaningless. Other trolls were banned for less.

Thread moderators note:

Off topic posts get dumped unceremoniously to the Bathroom Wall. Dr. Davidson’s post has just been so dumped. Consider youself on notice Dr. Davidson, more offtopic hijacking of treads will get you banned.

I don’t regard Ian’s post as “excellent” and “brillian”. It is a substitution of arguments: Michael argued that clotting system is IC while Ian proves that organism will not die in the absense of clotting system.

Instead of discussing this discrepancy the people talk about the prominency of Behe in bioscience. I believe a theory (reductionist (neo)darwinism in our case) should be able to answer a question of anybody - be it a professor or a farmer.

A man may survive without olfactory system, being deaf, numb or infertile. This obvious fact does not mean that the systems enabling the smelling, hearing, and reproduction are simple or complex, IC or not IC. They can be either. A modern car has many accessories, but the lack of one of them wouldn’t necessarily block the car’s function or explode it. This does not prove anything about the structure of these accessories.

The question of FXII is another story and I’m ready to discuss it, but it is clear that if the people are laughing off the IC problem they turn deaf ear to a problem of any complex system at all. Any system is IC in a way - the whole/emergent property/function of a system cannot be broken down (perhaps not the best verb) to its element - by definition. The function of “contact phase” elements, including FXII is not yet clear but the clotting system has many subsystems that have IC inside. The fibrinogen is first in queue.

The hierarchy of subsystems is not my “trick” this is usual analysis that is done by each of you every day.

I don’t regard Ian’s post as “excellent” and “brilliant”. It is a substitution of arguments: Michael argued that clotting system is IC while Ian proves that organism will not die in the absense of clotting system.

Instead of discussing this discrepancy the people talk about the prominency of Behe in bioscience. I believe a theory (reductionist (neo)darwinism in our case) should be able to answer a question of anybody - be it a professor or a farmer.

A man may survive without olfactory system, being deaf, numb or infertile. This obvious fact does not mean that the systems enabling the smelling, hearing, and reproduction are simple or complex, IC or not IC. They can be either. A modern car has many accessories, but the lack of one of them wouldn’t necessarily block the car’s function or explode it. This does not prove anything about the structure of these accessories.

The question of FXII is another story and I’m ready to discuss it, but it is clear that if the people are laughing off the IC problem they turn deaf ear to a problem of any complex system at all. Any system is IC in a way - the whole/emergent property/function of a system cannot be broken down (perhaps not the best verb) to its element - by definition. The function of “contact phase” elements, including FXII is not yet clear but the clotting system has many subsystems that have IC inside. The fibrinogen is first in queue.

The hierarchy of subsystems is not my “trick” this is usual analysis that is done by each of you every day.

Sorry for duplicate.

Wiolowan Wrote:

Michael argued that clotting system is IC while Ian proves that organism will not die in the absense of clotting system.

If the clotting system is IC, then removal of any part will cause that system to fail. This is Michael Behe’s definition. If the clotting system is IC, then removal of fibrinogen must cause the clotting system to fail catastrophically, and the animals should bleed to death shortly after birth, let alone survive surgical wounds.

They don’t, and I don’t show that organisms won’t die in the absence of a clotting system. Mice most certainly will die in the absence of a clotting system, but in the absence of fibrinogen, the pivotal last step in forming a clot, mice can call on other things to substitute (albeit poorly) for the missing fibrinogen. Given the whole point of the clotting system is to form clots and prevent bleeding, and that fibrinogen deficient mice can form clots of a sort using standard serum proteins and platelets, then according to Behe’s own definition, the clotting system is not IC.

But that wasn’t my point; the point was that Behe misrepresented Doolittle’s arguments. By accident or design he omitted crucial portions of Doolittle’s text that obviated Behe’s argument.

At the same time as misrepresenting Doolittle, Behe ignored a significant challenge to his theory. Regardless of whether you consider the clotting system is IC or not, the knockout mice give important clues as to how the clotting system evolved, which fits in with data from comparative anatomy, molecular phylogeny and studies of invertebrate clotting systems.

Ian writes:

“Given the whole point of the clotting system is to form clots and prevent bleeding, and that fibrinogen deficient mice can form clots of a sort using standard serum proteins and platelets, then according to Behe’s own definition, the clotting system is not IC.”

Could you provide me with a reference to this effect?

Guts Wrote:

Could you provide me with a reference to this effect?

Bugge et al., “Loss of Fibrinogen Rescues Mice from the Pleiotropic Effects of Plasminogen Deficiency.” Cell 87 (1996): 709-19.

Cheers! Ian

The question of FXII is another story and I’m ready to discuss it, but it is clear that if the people are laughing off the IC problem they turn deaf ear to a problem of any complex system at all. Any system is IC in a way - the whole/emergent property/function of a system cannot be broken down (perhaps not the best verb) to its element - by definition. The function of “contact phase” elements, including FXII is not yet clear but the clotting system has many subsystems that have IC inside.

Yikes. Where to begin?

Nowhere. i’ll let someone else argue with this person. For now, I’ll just amuse myself with the idea of people walking around with little Intel-like badges which say “IC Inside”.

What Wiolowan writes makes sense to me, although I suspect English is not his native language and there might be a miscommunication as a result.

Setting aside the notion that “genuine” IC implies the system could not have evolved (which I think is an absurdly false claim, and IC might be considered a normal result of evolution), I think it’s fair to say that EVERY complex adaptive system is necessarily IC. The function of any identifiable “part” (at whatever level of abstraction chosen) can’t be described without reference to its relationship with other parts. What each “part” does isn’t entirely internal, but largely a function of what all the other parts are doing.

And in this sense, we might consider that Ian Musgrave’s argument doesn’t work if we change the level of abstraction. By removing fibrinogen, Musgrave has produced a different system. We meddle with economic systems all the time. Each time we do so, we get a somewhat different economy. I think most of us dismiss this level because it’s trivially obvious: at this level, EVERY system is IC, and making any change at all simply creates a different system, but equally IC.

Yet biologists are often obligated to go there: One of the answers to Behe’s claims of non-evolvability is that Behe assumes no change of function, yet if all but the base is removed, Behe’s mousetrap becomes an effective paperweight. In other words, change or remove any part, and you change the system. If it can now function as something else, it really is an “irreducibly complex something else.”

Still, it should be clear that people aren’t “laughing off the IC problem” because there is no problem to be found, nor are they turning a deaf ear to how changes alter the nature of complex systems. In fact, such changes are what evolution IS.

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This page contains a single entry by Ian Musgrave published on March 22, 2005 7:37 PM.

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