You’re welcome for the link- infact, it does ‘go on’ and the points brought up by the poster you quoted are refuted once again in hte very next post- so let’s keep going here (And by hte way- nothign that was posted claiming Behe ‘quote miend’ was relevent- what was left out did nothign to udermine what Behe was stating- but let’s do pretend that it did, shall we?
“David Marshall says:
Your claim to objectivity, Mr. / Mrs Allen, is hard to believe, reading some of your other postings. But all right, let’s take your arguments at face value. Here, it seems to me, you’re missing the ball. You may even be swinging for the wrong fence.
Behe is not primarily making an apriori argument in this book. He is arguing from the actual history of evolution among pathogens. The point about chloroquine resistence is that in fact it has not arisen that often. Resistence to atovaquone, by contrast, appears to arise very quickly; every third person, he says. (59) He ascribes the difference to the fact that the former requires two mutations, the latter, just one.
If you want to refute Behe on this point, what you need to prove is that (1) CQ resistance actually demands more than two mutations. (To show that potentially profitable mutations arise more frequently than Behe claims), or (2) CQ resistance actually appears far more often — exponentially more often — than Behe claims.
If you can do one of these two things, then it seems to me that you will have made his position in this book less comfortable. Until then, you’re just batting theory around. In fact, some of your arguments seem to actually make his point stronger.”
Irreducible Complexity is nothing more then a god of the gaps argument. So far every system that Behe has identified and claimed was irreducible has been shown to be reducible. His claims about the flagellum were proven wrong(cut it down by 40 components and you have the type III secretory system) nearly a decade ago. His claims that the blood clotting cascade were irreducibly complex were shown to be false when it was pointed out that the dolphin's immune system worked just fine without a component that Behe said was required. His latest claim of an irreducible system is contained within this book where he argues that cilia HAVE to have the IFT to form. This is again shown to not be the case by the published literature.
As you can see irreducible complexity is nothing but a god of the gaps explanation. When one system that was proclaimed to be IC is explained or demonstrated to NOT be IC, then Behe simply picks another system and says, “What about that one?”.
David,
I'm not sure whether you simply haven't understood any of the critiques of Behe’s probability estimates or if you are being willfully ignorant. I THINK you are just jumping in without any idea of what you are talking about in an attempt to defend Behe. For starters you say:“If you want to refute Behe on this point, what you need to prove is that (1) CQ resistance actually demands more than two mutations.”
Which leads me to think you don't understand what everybody is talking about in regards to CQ resistance. Behe’s false assertion is that CQ resistance requires two SIMULTANEOUS mutations to occur. The reality is that the published literature clearly shows that the mutations for CQ resistance occur gradually, one mutation at a time. No one has said anything about CQ resistance needing more then 2 mutations. For one thing, that would be HELPING Behe’s claim, not refuting it. As such, your claim that in order to “refute Behe” I would have to show that CQ resistance requires more then 2 mutations makes no sense. The whole point of this little exercise is to point out that Behe’s false assertion greatly exaggerates the difficulty in CQ resistance by claiming that both mutations have to happen simultaneously. This one simple distortion allows Behe to radically alter the probability of CQ resistance arising via evolution(exponentially so actually). You seem to have totally missed the argument here. BOTH sides of the argument actually. Your entire comment is based around your faulty understanding of this issue.
Two other points: first you don't have to take my points at face value. I provided links to the original review that Behe was responding to as well as links to the published scientific literature that disproves Behe’s claims about CQ resistance. If you don't believe me, read them yourself. Second, it's Mr. Allen. ;-)
Mr. Behe,
how does your probability calculation deal with the documented fact that a chloroquine-resistant species of malaria without one of the mutations you discuss (at position 220)? Isn't this an example of sequential evolution?Secondly, are you serious when you claim that specific protein-protein interactions evolve only with difficulty? If so, you are making a good case for revocation of your biochemistry diploma.
Pretty much every protein will interact with any other protein, depending on conditions and concentrations (as anyone who has performed pulldown or shift assays can tell you; but you should know that yourself by now). If a weak interaction provides a selective advantage, further mutations ANYWHERE in the interaction region that strengthen this interaction IN ANY WAY will be highly selected for. This does not require specific point changes at specific positions, but any kind of change at any position where initial weak binding contact occurs; and this counts for interaction surfaces of BOTH proteins (i.e. both can change).
Given the scope of freedom most proteins have to change sequence without impairing function, I find your “argument” so removed from reality that I can't believe anyone who has taken a junior biochemistry class would buy it.
This, incidentally, has nothing to do with the reality of evolution. Even if theory of evolution was incorrect, and there really is a Designer, it makes no difference. Based on hard, published data about known behavior of proteins and known incidence and effect of mutations, your arguments are completely incorrect.
“I know you've challenged Behe’s assumption that the two mutations need to occur at the same time.”
No, I didn't challenge his claim, the peer reviewed and published science did. I posted a link to the relevant research which clearly shows Behe is wrong.
“But Behe’s argument is not primarily based on theoretical calculations about how difficult mutations might be”
Actually, yes it is. It's the core argument in his book which is clearly evident by the number of times he references his bogus probability of 1x10^20. Attempting to define false “limits” to evolution was the entire purpose of his book. Behe’s false probability argument was the best he could come up with for this.
I not even sure what you are trying to say when you are talking about “given a certain number of bugs per patient” etc.
“If, as I think you claim, the first mutation confers a slightly positive effect, and is therefore selected for, it would be even more puzzling why the appearance of both mutations together is so rare.”
You are correct. I don't think you intended to do it, but you just saw through Behe’s argument. The simple fact is it's no where near as hard as Behe leads his readers to believe for sequential mutations to both occur and combine. It seems you are starting to understand. :-)
“My point about whether two or more mutations would be needed was not to question the fact that it does take two mutations, but simply to point out a logically possible response to Behe, whether it is empirically viable or not.”
David, I don't think you understood what was being discussed. Otherwise you wouldn't have said that in order to “disprove” Behe I would have to show that it takes more then 2 mutations for CQ resistance to arise. Again if you don't want to believe me, go back and use the link I provided and read it for yourself. The cited article lays it out in black and white.
Mr. Fischer,
you are misinformed on several levels.
First, we do know quite a bit about malaria (I stated that I personally don't know the exact epidemiological information, but that does not mean such information does not exist).
Second, we know pretty much exactly how DNA changes, and how mutations are inherited. Some exotic cases are still matters of research, but the process that underlies the vast majority of evolution is well understood.
Third, we do NOT see an obstacle to formation of complex systems. This is a fact that follows from both theory and experiment: interactions and new activities arise constantly, and the more we research, more weak interactions or weak side activities we are finding.
The protein I'm working on, for example, has one clear catalytic activity. But then it was discovered that it also binds DNA and serves as a transcriptional activator. Then several weak/rare interactions with other proteins were discovered. Then it was found that three different modification (acetylation, phosphorylaton, nitrosation) at different places alter its DNA-binding specificity, changing which genes it activates and which it supresses. And similar stories keep jumping up all over the place, once sufficient research has been done.
So we do know a great deal about the “underlying DNA”, and how it exactly changes. In laboratory and nature, we have observed all required processes: evolution of new protein interactions, evolution of new signalling pathways, evolution of new catalytic activities.
I don't know how I can be more clear about this: we have not found anything in nature that cannot be explained by these processes. Every step is known and seen - all that needs to happen is for these steps to occur one after another, and change is inevitable.
Perhaps there is something in nature, some biochemical or physiological system, which cannot be explained with current models of natural selection. But if there are such things, we haven't found them yet.
This is the second point that should be very clear. There is no known process that counters mutation/selection under changing pressures.
In other words, according to everything we know about DNA and genetics, unless an organism lives in a pretty much absolutely unchanging environment, it WILL change over time. These changes will involve creation of novel biochemical systems of the kind Behe simply states cannot be created; the truth is the direct opposite, it seems that it is impossible for such systems NOT to be created, if the laws of genetics are what they seem they are.
Behe’s entire argument used to rest on picking poorly understood biochemical systems, and stating that they are irreducibly complex. This obviously didn't work - over the years, the systems he used were slowly examined, described, and it was found that there is nothing irreducibly complex about them. So his new approach is to simply fudge the numbers, and directly obfuscate well known facts of biology; a wise choice, given that this approach has served generations of old-style creationists very well.
Even Behe would not agree that every case of evolution results in a loss of genetic information.
Besides thousands of examples in biology (simplest of which are many forms of antibiotic resistance in bacteria, often stemming from evolution of a novel gene without any other change or loss of functionality), Behe himself cites the example of malarial evolution - in which, however you turn it, new functionality (specific resistance to chloroquine) has evolved without any “loss of genetic information”.
You also repeat the old creationist canard, this time in truly ludicrous formulation of “fruit flies never became dogs”. Of course, they can't - they can only evolve slowly, with small stepwise changes. Even under significant pressure, they will “still look like fruit flies” to laypeople for a long time - no matter how profound the genetic changes.
You seem to have a very strange idea of what evolution is and what it entails.
And finally, I just ran into a truly nice example that shows evolution of things that Behe flatly says are impossible - evolution of an integral membrane ion channel protein complex (involving three subunits, that associate through protein-protein interactions), from completely random sequence. The protein did not evolve from other proteins, but arose through recombination of a RNA-coding gene, a stretch of noncoding DNA, and some inserted random nucleotides.
The details can be seen here:
http://www.pandasthumb.org/archives/2007/05/on_the_evolutio_1.html#more