Behe's Test, Take 2
by Bilbo(Yeah, yeah, I'm on vacation, and I was staying away from the library. Who knew I would stumble upon another computer linked to the internet and read what was going on at Behe's Test? So here I am trying to repair the damage. Who knew leaders of the ID movement could shoot themselves in the foot so many times? Oh yeah, we did.)
A very hearty, big "THANK YOU!!!" to our own, obsessive, compulsive Thought Provoker for finding and providing a link to Barry Hall's paper! I assumed that I would have to go to a college library and hope they carried the journal that Hall's paper was published in. It didn't occur to me that it would be online and for free. I suggest that anyone interested in pursuing this topic further, first read the paper. It's short, and despite the technical jargon, not that difficult to understand. But read it. Don't just scan it.
First, it turns out that Hall knew that there was already resistance to imipenem. He was trying to answer the question, if we continue using imipenem, will resistance increase?
These results predict, with >99.9% confidence, that blaIMP-1 will not evolve to confer increased resistance to imipenem.
Behe quotes this passage correctly, but then mis-paraphrases it as "achieve resistance." Why? Probably to try to keep things simple for his lay audience. Instead, his mis-paraphrase has caused a misunderstanding of what Hall was trying to do, making it look like Hall was wrong, and that Behe was wrong.
But Behe gets the interpretation of Hall basically right. From Hall's paper:
It is important to consider the effects of only one or two independent amino acid substitution mutations, because in nature mutations almost always arise one at a time, and each mutation must be fixed into microbial populations by selection….These results predict, with >99.9% confidence, that blaIMP-1 will not evolve to confer increased resistance to imipenem….
It is clear from this study that the risks associated with the presence of blaIMP-1 do not include the risk of evolving increased activity against imipenem.
Hall echoes Behe's point: If selection requires more than two unselected mutations, then it probably won't happen. And if Behe is right, then a double CCC (whatever he means by that) will never happen.
One additional note on Hall's paper: The only reason Hall thinks his prediction might be wrong is that his technique might not be sensitive enough to pick up resistance from one or two mutations:
That prediction depends on the sensitivity with which we can detect increased resistance in the laboratory. I cannot eliminate the possibility that increased resistance, below the level of laboratory detection, could be selected in nature.
Not from the possibility that three mutations occurred.
So did Behe interpret Hall correctly? Yes, even though he mis-paraphrased him.
Next question: Is Hall right? Thanks to Pez, we know that at least our own ID critic at large, Zachriel, agrees with Hall:
Many resistance genes evolve by single mutations. If it takes more than a couple of mutations (simultaneous, or each of which are not separately beneficial), then it is very unlikely nature will stumble on the solution. This isn't anything new.
Are there critics out there who disagree with Hall, Zachriel and Behe on this point? If not, then hasn't Behe established an edge to evolution (which it seems was already well-known, if we take Hall and Zachriel's word for it)?
All that's left to consider is Behe's second point, that more than two-binding sites require too many unselected mutations to be considered realistic.
(Now back to vacation. See ya' next week.)
August 21st, 2008 at 10:34 am
As I mentioned on the other thread, none of this is controversial. No one claims that multiple specific simultaneous point mutations is a typical evolutionary pathway. So Behe has shown that something no one ever thought happens is unlikely to happen. Next he will move on to prove that elephants can't fly.
If multiple specific simultaneous point mutations were a common occurrence I might be tempted to suspect ideas like Front-Loading or Joy's time-travelling thought waves had some merit. Instead we see much simpler evolutionary pathways that are better explained by MET.
Comment by Todd Berkebile — August 21, 2008 @ 10:34 am
August 21st, 2008 at 10:39 am
Hi Bilbo,
You are welcome.
I will copy the paper providing the analysis of the IMP-1 MBL when I get the time.
Comment by Thought Provoker — August 21, 2008 @ 10:39 am
August 21st, 2008 at 10:44 am
Wrong. Wrong. Wrong. As already pointed out on the other thread.
Showing the limitation of a single gene doesn't answer to what 'Darwinian evolution' can do in nature where many genes and organisms are interacting in a very complex manner. For instance, resistance to a different antibiotic might lead to fixation of an otherwise neutral mutation, then followed by a second selectable mutation for the trait at issue. Or the trait may evolve from a different gene and then be transferred between organisms. Or any of a number of possibilities that Behe just doesn't consider.
No. The equivocation on "edge" is highly misleading. You can't walk through a tree in the woods. You may not even be able to see the other side of the woods. But you can still walk through the woods. Behe is erecting a strawman, which you have reiterated.
What this really shows is that evolution is smarter than Behe.Comment by Zachriel — August 21, 2008 @ 10:44 am
August 22nd, 2008 at 12:04 am
Hi Bilbo,
I have read and reread Hall's paper.
I still have problems reconciling Behe's statement…
"In other words, more than two evolutionary steps would have to be skipped to achieve [imipenem] resistance, effectively ruling out Darwinian evolution."
…with what Hall said or meant.
You brought up the part about the distinction between achieved resistance and INCREASED resistance. Yes, that was technically a misinterpretation Behe made, but I suggest there were more fundamental differences between Behe's version and Hall's.
Hall's logic was specifically dependent on NOT skipping evolutionary steps. Hall specifically explained what it would mean if IMP-1 increased resistance in nature. It would mean his instruments weren't sensitive enough, not that steps would have been skipped.
I find it difficult to think Hall would consider "…effectively ruling out Darwinian evolution”. He built a model dependent on it. Unexpected answers would cause Hall to fix the model, not throw out the theoretical foundation it was built on.
Skipping the "In other words,…" for a moment. I offer that Behe's declaration that "…more than two evolutionary steps would have to be skipped to achieve [imipenem] resistance, effectively ruling out Darwinian evolution", was BEHE'S CONCLUSION not Hall's.
However, Behe did use the preamble, "In other words,…" which implies an interpretation of Hall's ideas. Unfortunately, this phrase has been overused to spin and frame arguments so much that its use can no longer be trusted.
When Bill O'Reilly or Rush Limbaugh start a sentence with "In other words,…" it is a given that what follows is the speaker's opinion and not an honest restatement of an opponent's ideas.
I suggest the content and situation surrounding Behe's statement on the impossibility of achieving imipenem resistance shows it was clearly Behe's opinion and conclusion, not Hall's.
Note, I am giving Behe the benefit of the doubt that he used the phrase "In other words,…" in a way that has become common when rendering a personal opinion.
The alternative is to conclude Behe misstated Hall's position, maybe intentionally.
To your original questions…
Q1. Is Behe's interpretation of Hall correct?
A1. It depends. When Behe stated…
“ In other words, more than two evolutionary steps would have to be skipped to achieve resistance, effectively ruling out Darwinian evolution.”
Was this Behe misinterpreting Hall or stating his own conclusion based on Hall’s work?
Other than this, Behe gave a reasonable fair and accurate summary of Hall’s paper and conclusions.
Q2. If so, is Hall right?
A2. Hall was not wrong. He correctly indicated what the study’s result suggested. I think the results suggested an incorrect conclusion, but that is a side point.
Q3. Does that make Behe right?
A1. Right about what? Is Behe right that “…more than two evolutionary steps would have to be skipped to achieve [imipenem] resistance”? I suggest not.
Is Behe right about common descent? Maybe, but Hall’s study doesn’t MAKE Behe right about that.
Comment by Thought Provoker — August 22, 2008 @ 12:04 am
August 22nd, 2008 at 1:02 pm
Gosh, computers keep popping up everywhere! The right-hand clicker thingy doesn't work on this one, so I'm not able to copy stuff. But I'll try:
TP, Hall tested for one and two amino acid changes, since this is all that (Darwinian) evolution can normally accomplish. Not finding any increase in resistance, Hall predicted that the bacteria would not evolve additional resistance? Why? Because (Darwinian) evolution normally can only make one or two unselected steps. In effect, Hall's prediction was confirming what Behe had been saying in his book. I'm not sure how to make that clearer to you.
Zachriel, you agree with Hall and Behe that evolution normally doesn't take more than one or two unselected step. Where you disagree with both Behe and Hall (I stress that for a reason), is that this allows us to rule out Darwinian evolution. You suggest that the bacteria may develop resistance to a different antibiotic, which could get it one step closer to developing additional resistance to imipenem. Or it could develop additional resistance by insertion from another bacteria that had developed additonal resistance. As to this second possibility, Hall acknowledges it at the end of his paper, saying that the other families in that type of bacteria would need to be tested also, before he could confidently predict no additional resistance. As to the first possibility, Hall doesn't address it. My guess is that he wouldn't consider it a likely route for evolution.
Why I stess Hall's name: Because you ignored it. You think this is only about Behe, and it isn't. You see, we have a wrestling match taking place between Behe and the critics in Madison Square Garden. Meanwhile, up the street, oblivious to the wrestling match, professional biologists like Hall are working away in their labs at medical research. Most likely, Hall doesn't give two figs about the wrestling match. He's just trying to find a way to determine if anti-biotics will work. And he's come up with one that seems to work for him: Find out if one or two evolutionary steps confer resistance. If not, then he's confident the will work without bacteria developing resistance. Why is that, Zach? Is it that Hall is just ignorant of all these other ways bacteria can evolve? Or is it that these other ways are so implausible that he doesn't take them seriously? Since he's staking his professional reputation in the medical community when he makes predictions like these, I'm guessing that he thinks your alternative evolutionary pathways are implausible enough that they don't have to be taken seriously.
So again, we have ideologues like you and Behe duking it out. Then we have researchers who have to deal with the real world. Researchers like Hall seem to be confirming the view of the world that Behe says is the real one.
Todd, since you agree with Behe that more than two simultaneous unselected mutational steps are as unlikely as elephants flying, then all Behe needs to show you is that most of evolution has required more than two simultaneous unselected mutational steps, and you'll accept ID, right?
Comment by Bilbo — August 22, 2008 @ 1:02 pm
August 22nd, 2008 at 5:24 pm
Hi Bilbo,
You wrote…
I hear you, but I suspect you are not hearing me. Even though the above summary is slanted it is still closer to correctly interpreting Hall's position than Behe's…
"In other words, more than two evolutionary steps would have to be skipped to achieve [imipenem] resistance, effectively ruling out Darwinian evolution."
Behe is stating that if imipenem resistance was achieved (as it was) that would mean"…two evolutionary steps would HAVE TO [have been] skipped". All possible Darwinian explanations are effectively ruled out.
Is Behe offering Hall's conclusions or his own?
It is my position ("can you hear me now?") that Hall's conclusions were clearly different than Behe's.
From Hall's paper…
"That prediction depends on the sensitivity with which we can detect increased resistance in the laboratory. I cannot eliminate the possibility that increased resistance, below the level of laboratory detection, could be selected in nature.
…
This study, alone, is not sufficient to justify reconsideration of policies concerning the use of imipenem. In order to understand the risks posed by metallo-β-lactamases, it will be necessary to conduct similar studies on representative members of each of the three metallo-β-lactamase subfamilies and to include all clinically relevant carbapenems in those studies."
Now that increased imipenem resistance in metallo-β-lactamase has been observed, what would Hall conclude? Do you think Hall would suggest a Darwinian explanation has been effectively ruled out? Would he suggest it was a designed, terrorist plot?
A more reasonable position is that Behe was stating his own conclusions, not Hall's. This doesn't mean Behe did anything wrong. Behe is entitled to his opinions.
If you want to point out that Hall said "in nature mutations almost always arise one at a time" as an opinion he and Behe have in common, be my guest. Zachriel agree's with this. Even, I agree with this.
I also generally agree with common descent. Does that mean Behe is right about the truth of common descent?
Not really.
There is a difference between agreeing the vast bulk of mutations happen in nature one at a time and trying to suggest a clear, definable "edge" between possible and impossible evolution.
It is more like Mike Gene's continuum between ducks and rabbits.
I have given you my answer to your three questions. What is yours?
Q1. Is Behe's interpretation of Hall correct?
(Is "In other words,…" Behe's interpretation of Hall's position?)
Q2. If so, is Hall right?
Q3. Does that make Behe right?
Comment by Thought Provoker — August 22, 2008 @ 5:24 pm
August 23rd, 2008 at 10:36 am
I discussed Hall in my first comment in the previous thread. Hall makes a very narrow claim. Behe takes this narrow claim and misapplies it to the general case.
* Behe ignores other evolutionary mechanisms. This is a simple and obvious syllogistic fallacy. (Let
A= evolution by point mutation of a single gene in a clonal, in vitro population, a subset ofB= all evolutionary mechanisms.Not Adoes not implyNot B.)* As to Behe's claimed "edge"—pointing out that certain adaptations may be out of reach of evolutionary mechanisms doesn't mean that organisms cannot continue to adapt in other directions. Another syllogistic fallacy. (Let
A= a particular evolutionary adapation, a subset ofB= all possible evolutionary adaptations.Not Adoes not implyNot B.)Comment by Zachriel — August 23, 2008 @ 10:36 am
August 25th, 2008 at 12:17 am
Bilbo, if your point is that simultaneous triple mutants are stupendously rare, then you are (as noted by several others), merely stating the obvious. Everyone already knows that.
Hall's data suggest that the next 1 or 2 mutational steps away from the resistance-conferring version of IMP-1 do not confer additional resistance to imipenem. His conclusion is that additional resistance to imipenem is not likely to arise due to mutations in IMP-1. In other words, he is proposing an "edge" for the function of one particular enzyme when it acts on one particular substrate. More specifically, it seems that he is proposing that the fitness landscape surrounding the current enzyme is not amenable to evolution toward increased resistance. It could be that the enzyme is simply not capable of doing more, or it could be that the mutational trajectory needed to acquire additional function is prohibitively long and/or complex.
Point being that Hall's work was not delimiting an "edge" to "darwinism" – that edge is already assumed to be what Behe says it is for a single step – but was specifically trying to determine whether selectable steps exist (nearby) for IMP-1 to more effectively detoxify imipenem. I think other commenters have said similar things so I won't further discuss Hall's work other than to reiterate that it was about IMP-1 and its limits, not about "darwinism" and its limits.
Now, where Behe is laughably wrong is not where he asserts that multiple simultaneous mutations are improbable, but where he assumes that multiple simultaneous mutations are required to achieve certain adaptations or outcomes. By playing bait-and-switch with readers like you, he has misled you into believing that evolutionary biologists have somehow proposed that something as complex as a "double CCC" arose in a single generation. That's a falsehood, and it looks suspiciously like outright dishonesty.
So when I look at your analysis of Behe, Hall, and the "question," I'm concerned about this claim more than anything:
Leaving aside the plain fact that "unselected" mutations regularly persist due to drift, epistasis, "hitchhiking" with selected mutations, etc., let's edit your sentence to make it accurate: "If Behe is right, then a double CCC will never happen ALL AT ONCE." And that, my friend, is a pitiful strawman.
Comment by SteveMatheson — August 25, 2008 @ 12:17 am
August 25th, 2008 at 7:08 am
Hi everyone,
as far as I understand Halls paper, there is no question as to wether a single amino-acid change can improve resistance to some carbapenems
Hall:Yano et al. (12) recently reported that IMP-6, which differs from IMP-1 by a single amino acid substitution, increases the MIC of meropenem 128-fold but does not increase the resistance to imipenem.
Here is Yanos paper:
http://www.pubmedcentral.nih.g...
So the mechanismen is already documented for meropenem. Hall investigates wether a different single amino-acid substitution would have a similar effect when testing for imipenem-resistance, which would have clinical implications for the use of imipenem. From his results, he concludes, that this particular mechanism is unlikely to be responsible for an increased imipenem resistance. Being prudent, he does not rule it out completely nor does he rule out other mechanisms
It is impossible to conclude from Halls paper:
a.) that a single amino-acid substitution cannot increase resistance to antibiotics - it can, as shown for meropenem and it can therefore be a selectable trait.
b.) that Hall makes any statement about how the initial resistance was achieved.
Therefore, no matter how you interpret Behes motives to use his particular wording, it is totally unconnected to the content of Halls paper.
all the best
Karla
(sorry, my english is a bit rusty)
Comment by Karla — August 25, 2008 @ 7:08 am
August 25th, 2008 at 2:23 pm
Has increased resistance to imipenem been observed? Evidence, please. If so, then Hall would conclude that either his techniques were too insensitive to pick up the one or two mutations it took to increase resistance, or that there was an insertion from a related bacterium.
I disagree. Hall refuses to assume that Darwinian evolution is all-powerful and will bestow increased resistance to imipenem, and that his lab results allow him to predict that increased resistance to imipenem will not occur, pending further tests on related bacteria. All Behe is saying is that such a position reflects what he has been saying: Darwinian evolution has a narrow range. Is Behe claiming that Hall's work proves his case? No.
Yeah, perhaps it's my fault for making this look like Behe was using Hall as a proof of his thesis. (Behe tries to prove his thesis in his chapter on the two-binding site rule. Whether or not he succeeded is a different question.) That wasn't my intent. My intent was that if Behe's thesis is correct, then researchers such as Hall are justified in looking for an edge to evolution when looking for new antibiotics or wondering how long the present antibiotics will remain effective. And if Hall's work is borne out by future results, I think you will see more and more researchers adopting his methods. And if their results are also borne out, I think we will see a healthy skepticism of Darwinian evolution develop. So that when we are told that all the multiple-protein complexes that the cell requires were the result of Darwinian processes, we'll view such claims with a raised eyebrow and demand to know how.
Hall tested for one or two mutations, Karla. Not finding increased resistance, he predicted that increased resistance would not evolve. This doesn't prove Behe's thesis, but it is consistent with it, and if enough researchers had similar results and predictions, would — it seems to me — certainly lend credence to Behe's thesis.
Comment by Bilbo — August 25, 2008 @ 2:23 pm
August 25th, 2008 at 5:04 pm
Bilbo, I'll give this one more try. Hall did not look for an "edge to evolution." He didn't even look at the ability of bacteria to become resistant to an antibiotic. He looked at the ability of one particular enzyme to confer additional resistance to one particular antibiotic. He concluded that this enzyme has no further capacity to increase its resistance-conferring activity, at least not through "darwinian" mechanisms. Your response to TP and to Karla suggest that you are missing – or ignoring – this very basic distinction. You say that Hall "predicted that increased resistance would not evolve." That's wrong. He predicted that increased resistance would not evolve from IMP-1, a particular gene carried on a particular plasmid. Ominously, it is one of three distinct but related genes on related plasmids, one of which already showed that it could give rise to 100+-fold increased resistance in a single mutational step.
(Side note: using the kind of embarrassingly bad logic that Behe has roped you into, this observation alone proves that Darwinism operates with such blinding speed and efficiency that only the regular intervention by the Intelligent Designer keeps the bacteria from obliterating all multicellular life within a few decades.)
Now, if Hall had postulated that evolution cannot give rise to further resistance to imipenem, he would have had to do a far more ambitious experiment, in which he used his mutagenization protocol on every plasmid on earth, and on every bacterial genome on earth, not to mention any genome that could serve as a source of genetic material for lateral transfer by plasmids and bacteriophage. At the end of this effort, he would be able to say that darwinian mechanisms are or aren't likely to yield further resistance to a single antibiotic.
I'm trying to get you to see that a single failure of selection to yield a particular result tells us precisely nothing about the "darwinian" process itself. It simply reveals a characteristic of the components under study. If someone studied the ability of, say, the human microcephalin gene to generate resistance to penicillin in S. aureus, and found that it never did even when extensively mutagenized, only a fool would conclude that this means that S. aureus is incapable of developing resistance to penicillin. Your reasoning here, and Behe's as well, is similarly bogus.
Finally, if that didn't help, let me try one more way of convincing you that this line of argument is damaging to your credibility as a design thinker. One of the most absurd aspects of Behe's argument in EoE is his propensity for pointing at things that haven't happened and concluding that they cannot happen. In any area of inquiry, this would be ridiculous. But in evolution, it's doubly irresponsible, because we often have a record of what did happen. Genomic analysis, using freely-available tools, can facilitate the identification of mutational trajectories that led to specific evolutionary changes, in biological function and in genomic structure. Instead of the duplicitously distracting focus on what has not occurred, let's see some serious thinking about what did occur.
Until I see that, I will consider further emphasis on this crude bait-and-switch to be a form of intellectual dishonesty.
Comment by SteveMatheson — August 25, 2008 @ 5:04 pm
August 25th, 2008 at 5:18 pm
From the guy who thinks that Behe's conduct as a scientist is unacceptable.
Or wait…. are you not a scientist?
"Intellectually dishonest", "laughable", "bait and switch"….
Steve's Guide to Bully Debating Tactics.
Gotta read the great chapter on how to not only convince others, but yourself too, that it's actually those with the opposing view who conduct themselves in an unacceptable manner.
Bait and switch, indeed, Steve.
Comment by Doug — August 25, 2008 @ 5:18 pm
August 25th, 2008 at 6:22 pm
Hi Bilbo,
You asked…
In Hall's study the level of imipenem resistance was 2ug/ml. From Hall's paper…
"In the presence of 100 μM IPTG, pIMP1 conferred an imipenem MIC of 2 μg/ml on the host strain DH5αE …the same level of resistance that has previously been reported for IMP-1 in E. coli."
The paper I link to earlier included this…
"In the present study, we describe a new blaIMP-1-carrying integron that contains a new aminoglycoside resistance gene and its dissemination among genetically unrelated clinical isolates recovered from a Brazilian hospital.
…
Strains showing combined resistance to ceftazidime (MIC, >16 µg/ml), imipenem (MIC, >16 µg/ml), and meropenem (MIC, >16 µg/ml) were routinely screened for MβL genes by standards PCRs (2, 9, 11)."
Generally, a resistance level of >16 µg/ml is an increase when compared to 2 µg/ml.
Assuming there is still interest in the thread, I won't be surprised to hear questions about whether or not the studies used the same standard and/or complaints about picky details.
I happen to have run across other studies that have put it in terms of INCREASED resistance, but that is beside the point. I am not trying to prove Hall was wrong. He wasn't wrong. He reported the study's results correctly and provided ample caveats just in case.
What Hall did was make statements about a very specific and very limited set of circumstanses. What Hall did not say, imply or conclude was "…more than two evolutionary steps would have to be skipped to achieve [imipenem] resistance, effectively ruling out Darwinian evolution."
Those were Behe's words. I suggest understanding the implication of Behe saying these words are the key to answering your three questions, Bilbo.
Are Behe's words an attempt at interpreting what Hall said and what Hall concluded, or are they Behe's own conclusions?
Bilbo, if you are still not ready to answer your own three questions, please at least answer this one…
Comment by Thought Provoker — August 25, 2008 @ 6:22 pm
August 25th, 2008 at 6:54 pm
Behe: snake oil for the rubes. If that isn't clear by now…
Hey Rock, thanks for the link to that paper (I don't remember in what thread it was).
Comment by Raevmo — August 25, 2008 @ 6:54 pm
August 25th, 2008 at 7:35 pm
Doug,
It seems you underestimate the reasoning capacity of the scientific community. Somehow, you imagine that we just don't like Behe's message, so we are willing twist his assertions and ignore some deep truth in his claims. It's not like that at all. It's just very easy for us to see the logical weaknesses in his assertions, to recognize his deceptive presentation by selective use of what's known, to deconstruct his strawman arguments, etc. There is no question in my mind that he is intellectually dishonest. These are not bullying tactics on the part of mainstream science, it is the stark realization that this snake oil salesman is very good at fooling those who wish to be fooled. That you cannot see it is unfortunate. But I can guarantee you that Behe will never gain any traction within the scientific community, not because scientists are closed-minded, or don't like the implications of his assertions, but because he hasn't got a worthwhile idea to sell. There is simply nothing scientifically defensible in his claims.
Comment by David E Levin — August 25, 2008 @ 7:35 pm
August 25th, 2008 at 8:13 pm
As no evolutionary biologists makes such an assumption, I'm not sure why you would say that. The Theory of Evolution is highly constrained on what we should expect to see.
You just emphasized the point. Hall makes a very narrow claim, and Behe then extends it fallaciously to "Darwinian evolution" generally.
Behe stretches his legs as far as he can, but no matter how hard he tries, no matter whose step he measures, a single step is limited by the length of one's legs. Behe then concludes that people can't walk farther than the length of a single step. Yes, a single step in evolution is limited by the available mechanisms of genetic diversity. But the path of evolution can proceed, just like a person who journeys on foot, one step at a time.
Comment by Zachriel — August 25, 2008 @ 8:13 pm
August 25th, 2008 at 8:27 pm
Zach and Raevmo (and anyone else),
I asked a question of our resident biologists.
http://telicthoughts.com/more-...
If either of you have a moment what would you have to say?
Comment by Pez — August 25, 2008 @ 8:27 pm
August 25th, 2008 at 8:54 pm
Pez,
Duplication of a single gene would not create a significant strain on metabolic demands. Therefore, there is no need to silence a duplicate. However, yeast (S. cerevisiae) provides an interesting example of what happens when an entire genome is duplicated. Most of the duplicates from an ancient genome duplication have been lost (through deletion). Those that were retained evolved specialized functions, mainly regulated expression in reponse to specific needs. Typically, if the genome has retained both duplicates, one is always expressed for its normal "housekeeping" function, but the other will be expressed only under certain conditions, as though its function is held in reserve to augment that of the main gene when the cell is under some sort of stress.
Comment by David E Levin — August 25, 2008 @ 8:54 pm
August 25th, 2008 at 8:55 pm
Hi Pez–
Short answer is no, a duplicated gene would not necessarily be selected against. In fact, I know of no mechanism that selects against extraneous genetic material. What does often happen to a duplicated gene is that one copy sustains an inactivating mutation and becomes a pseudogene; the fact that this mutation is not selected against is evidence that the two copies were completely functionally equivalent and had not diverged. I would point to the very large numbers of pseudogenes in eukaryotic genomes as clear evidence against your hypothesis.
I think you may be overestimating the economy of the cell. It's true that gene expression is regulated at various levels, but importantly it's also true that cells are robust to fairly significant changes in gene expression and copy number. Consider a person with only one good copy of the CFTR gene (that person is a carrier of cystic fibrosis), or a person with a duplication of a part of a chromosome, resulting in duplications of scores or hundreds of genes (very common, it turns out). These are systematic alterations in gene number that don't lead to obvious selection effects.
Comment by SteveMatheson — August 25, 2008 @ 8:55 pm
August 25th, 2008 at 9:02 pm
Steve,
But extra copy-related defects and haploinsufficiencies are also common. Trisomics (DSCR), for example. So, although your efficiency argument is well taken, it's not a given that there would be no selection pressure against an extra copy of a gene or a chromosomal region. This would be related to the specific gene function, not to metabolic inefficiency.
Comment by David E Levin — August 25, 2008 @ 9:02 pm
August 25th, 2008 at 9:06 pm
Thanks David,
I take it that you are saying that this is an observed effect in which the second gene is alternately expressed and repressed. Do you know what accounts for this selective regulation and the necessary feedback involved in stressed expression?
I guess this confirms my suspicion that it would not be beneficial for both genes to be pumping out the same protein as a normal course of events and that the general result would be the shut-down of one of the genes.
The two questions that arise from this line of thought would be 1) basically asked above - what is it that allows that tis gene will be expressed under stress?
2) If it is being suppressed and mutates what would cause its new product to be expressed?
Thanks.
I'm sure this line of questioning will die a fairly quick and painless death.
Comment by Pez — August 25, 2008 @ 9:06 pm
August 25th, 2008 at 9:15 pm
Pez,
It can be thought of as a form of functional specialization. The two copies start out to be functionally identical, completely redundant. Either one copy is mutated to non-function, as Steve noted, or it is mutated to a form that offers the cell more adaptability. This involves mutational changes in the promoter (among other things) that render one copy of the gene subject to new regulation, whatever the need might be. In any case, this is a very common theme among duplicated genes studied in yeast (about 12% of the duplicates remain). The cool thing about this is that there are yeast species that diverged from other yeast species prior to the whole genome duplication. They have only one copy of each gene (on half the number of chromosomes). Such pre-duplication species serve as a control for the "housekeeping" functions as a contrast to the derived function of a duplicate.
Comment by David E Levin — August 25, 2008 @ 9:15 pm
August 25th, 2008 at 9:16 pm
Hi Steve,
I take it your position is then that there is no reason that both copies will not be equally and continually expressed.
How is this balanced with the fact that the original gene itself was under expression control? Having the second copy and an immediate doubling of the output without any means of suppression would defeat the purpose of any regulation in the first place, would it not?
I see David brings up the evidence which occurs to me first - the cases of trisomy argue against the acceptance of mass duplications. But I would have no idea whatsoever if that had anything to do with over-expression of gene products.
Comment by Pez — August 25, 2008 @ 9:16 pm
August 25th, 2008 at 9:17 pm
I see another response from david.
To avoid the appearance of mere contrariness I'm going to rest this for a bit, but would appreciate if you guys will check back for further thoughts.
Thanks again.
Comment by Pez — August 25, 2008 @ 9:17 pm
August 25th, 2008 at 9:24 pm
Pez,
Complete redundancy will not be maintained by functional selection for the obvious reason. The second copy will either be lost through inactivating mutations (because of the absence of functional selection), or will mutate to acquire a new function (deviate from the redundant state). In the latter case, the new function provides the means for selection to maintain the second copy.
Comment by David E Levin — August 25, 2008 @ 9:24 pm
August 25th, 2008 at 10:20 pm
Pez, there's no appearance of contrariness at all. If there's a problem, it's just that you've asked a reasonable question that requires more than a brief answer. You are assuming that extra copies of genes will experience negative selection due to their wastefulness, and the evidence strongly suggests that this is not the case. As David explained, extra copies of some genes might very well lead to negative selection due to specifics of their function, but not (as far as we know) due to the mere wastefulness of the excess. This is not to say that pseudogenes last forever, only to note that duplicates don't tend to be the target of negative selection. (Some, in fact, have been positively selected.)
David, thanks for clarifying the fact that alterations in gene copy number can lead to selectable defects. What I had in mind was widespread copy-number variation, or CNV, in the human genome, a source of variation that rivals the point mutations we all love to talk about. Given the prevalence of CNV in the human genome, and the recent demonstration that increased copy number underlies a key human adaptation, the suggestion that duplicate genes are of necessity under negative selection is plainly incorrect. As you will surely agree.
Comment by SteveMatheson — August 25, 2008 @ 10:20 pm
August 26th, 2008 at 12:32 am
Hi Dave and Steve,
I didn't quite mean to do this, but I ended up posting my responses on the Sherman thread where I first posed my question.
Comment by Pez — August 26, 2008 @ 12:32 am
August 26th, 2008 at 7:34 am
Bacterial genome size tends to be proportional to the organism's metabolic and reproductive complexity, and seems to be optimized for maximum complexity with minimum genes. This implies that reproductive efficiency is selectively important in bacteria leading to trim genomes. This is much less a factor in eukaryotes.
Comment by Zachriel — August 26, 2008 @ 7:34 am
August 26th, 2008 at 8:30 am
That doesn't mean there are no duplicated genes in bacteria genomes—there are—just that they tend to be deleted over time if they fail to provide a benefit.
Comment by Zachriel — August 26, 2008 @ 8:30 am
August 26th, 2008 at 11:33 am
David said:
So then what do you make of that link that you posted here that attempted to discredit Behe's claims about the blood clotting cascade? It included Christmas Factor, but Behe never said that Christmas Factor was part of the portion of the blood clotting cascade that he believed to be IC. Same with proaccelerin. It's not like there was nothing there, in the chart.
Was that dishonest of you, David? Or just uninformed?
Comment by Doug — August 26, 2008 @ 11:33 am
August 26th, 2008 at 1:02 pm
Doug,
Go back and read the section in DBB. There is no conceptual reason to exclude the components above the branch point. Behe doesn't include these factors simply because, in his words, less is known about the upper part of the pathway. However, this is not true. This is a cascade of proteolysis using a series of related factors. We have had a good understanding of this pathway for many years. Besides which, he goes on to mention that mutations in the upper part of the pathway, which he inexplicably excludes from the part he declares as IC, are the major causes of hemophilia in humans. I can't think of a good reason why he would have excluded the upper part of the pathway, unless it was to give himself an out in case a simpler form of the pathway was identified. Can you think of any reason the upper part of the pathway is mechanistically different from the lower part? Why would you say the upper part of the pathway doesn't appear to be IC, but the lower part does? Let's think this through, shall we?
Comment by David E Levin — August 26, 2008 @ 1:02 pm
August 26th, 2008 at 1:49 pm
Assuming this study says what you say it says (and what it seems to be saying to me, also), then I would say that Hall's prediction was wrong. But apparently his premise, that if it takes more than two mutations to increase resistance then it won't happen, is assumed by everyone around here to be correct, which is what I originally wanted to find out.
So whether or not anyone wants to admit it, when Hall and Behe were saying that if it requires more than two mutations to confer selectivity, then Darwinian evolution won't do it, they were right.
I would like to know what Hall's reaction to this study was, since it seems to throw into doubt his method for testing the potential for evolution.
And since I found out what I wanted to know about Behe's premise about evolution having difficulty when more than two unselected mutations are required — he's right, I'll move on to the next topic — his two-binding site rule, hopefully tomorrow.
Comment by Bilbo — August 26, 2008 @ 1:49 pm
August 26th, 2008 at 2:44 pm
Bilbo,
Of course he's right. This was never the issue. As has been noted by many here, Behe's logical failing is in his assertion that evolution generally, or at least often, requires the skipping of multiple steps. There is no reason to impose such a requirement.
Comment by David E Levin — August 26, 2008 @ 2:44 pm
August 26th, 2008 at 3:19 pm
@Bilbo
1.) Can in some cases the resistance to a certain antibiotic be increased by single or double point mutation? - Yes, see meripenem
2.) Can in all cases the resistance to a certain antibiotic be increased by single or double point mutation? - No, see imipenem
3.) Is it impossible to increase resistance to an antibiotic by single or double point mutation? - No, see meripenem
4.) Is every increase in the resistance to an antibiotic due to singele or double point mutation? No, see TPs example for blaIMP-1
You cannot draw the general conclusion from Halls paper, that single or double point mutation will never suffice to improve resistance to any antibiotic. It states very clearly that sometimes it works (meripenem) and sometimes it does not (imipenem).
So Hall never claimed, or even suggested anything, that could be interpreted as a general limitation to effectiveness of single and double point mutations.
Hall never said anything to that effect, so you cannot conclude that he agrees with or condones this view, which is entirely Behes interpretation.
All the best
Karla
Comment by Karla — August 26, 2008 @ 3:19 pm
August 26th, 2008 at 5:25 pm
Karla says:
Neither did Behe, nor anybody in this thread. So your point is?
Comment by RogerRabbitt — August 26, 2008 @ 5:25 pm
August 26th, 2008 at 5:40 pm
RR,
The whole point of EoE was Behe's claim that many important evolutionary adaptations require multiple, simultaneous mutations (skipping steps in Behe-speak), which presents an impediment to evolution because of their improbability.
Comment by David E Levin — August 26, 2008 @ 5:40 pm
August 26th, 2008 at 5:50 pm
Zachriel says:
I don't think Behe is speaking of "simultaneous" mutations, but "cumulative but unselected" mutations.
Comment by RogerRabbitt — August 26, 2008 @ 5:50 pm
August 26th, 2008 at 5:59 pm
David,
Yes, "many", not "all", not "most", not a general limitation on the effectiveness of single or double mutations, only that not all "problems" are solved by such solutions.
Comment by RogerRabbitt — August 26, 2008 @ 5:59 pm
August 26th, 2008 at 6:01 pm
David,
He admitted, as you stated, that prior to the fork it was murky.
But the fact remains he only included those 4 elements in his IC protion of the blood clotting cascade.
And of course it's possible for there to have been an IC core that was further developed with more factors via unguided (possibly as well as front loaded)evolutionary methods. Behe doesn't deny that.
And this is being honest?
David, if you can't understand how he could have conceived of a small set of IC components that were later to be developed upon…. without you having to fall back on your consistent claims of insidious intentions on the part of Behe then what worth is it to discuss this?
It's always going to be that dishonest Behe. Even when he admits that the understanding isn't complete…. then that's just a ticket out years down the line.
You're something.
Comment by Doug — August 26, 2008 @ 6:01 pm
August 26th, 2008 at 6:05 pm
Zachriel says,
Yes, that's possible, but an appeal to random good luck in fixing that first mutation. The more appeals to good luck one must make, the less appealing the argument.
Comment by RogerRabbitt — August 26, 2008 @ 6:05 pm
August 26th, 2008 at 6:08 pm
RogerRabbitt, I thought her point was very clear, perhaps because I read her entire comment.
Evolutionary biology is being severely mangled in this conversation, and the intellectual integrity of some of the conversants is becoming harder to take for granted.
Hall's findings don't do Behe any good, because Behe's claim (when teased away from some confusion) is that complex mutations can't happen at all (non-randomly) because they're too unlikely. Hall applied what everyone already knows: that complex mutations (>2 nucleotides) almost never arise in a single generation. He applied it to one enzyme, to probe the capacities of that enzyme, and concluded that a particular level of activity is out of likely mutational reach of that particular enzyme. He didn't show a problem with Darwinian assumptions or hypotheses, he applied them to his experiment.
Now, why would any ID theorist bring this up? There seem to be two things going on here, and I'm starting to wonder why they are being consistently conflated. 1) One might bring this up to demonstrate the way in which Darwinian principles might be applied at the nucleotide level. So in this example, Hall – knowing what Orr and others have established (that >2 mutations at a time is highly improbable) – set up an experiment in which he sampled the possibilities surrounding a particular enzyme, and found that those possibilities do not include a certain level of activity. 2) One might bring this up in an attempt to fool people into thinking that evolution cannot generate >2 mutations in a particular gene, and that any evolutionary change that requires >2 mutations is the work of the Intelligent Designer.
Scenario number one is called "stating the obvious," and is tiresome as well as a little suspicious when repeated. Scenario number two is called "dishonesty."
Comment by SteveMatheson — August 26, 2008 @ 6:08 pm
August 26th, 2008 at 6:24 pm
RR,
There is no functional distinction between these two occurances. Whether both mutations happen in one individual, or one in a parent and the next in that individual's offspring, without the benefit of selection to expand the first mutation within the population, the probability is the same.
Comment by David E Levin — August 26, 2008 @ 6:24 pm
August 26th, 2008 at 6:43 pm
David says:
I don't disagree with that. But I'm curious as to why several of your allies inserted "simultaneous" when that isn't in Behe's book. Because it seems to have confused one of your other allies, who I don't remember you challenging:
Seems like he is hangning a lot on simultaneous.
Comment by RogerRabbitt — August 26, 2008 @ 6:43 pm
August 26th, 2008 at 6:50 pm
SteveMatheson Says:
As did I. And I read yours as well. Still nothing that explained why she made a point of what she posted, that apparently has no relevance to the actual conversation.
Now I get the impression that English is not her native tongue, so maybe it is just a misunderstanding. But if you are able to explain it, feel free. Don't want a recap of the thread from your perspective, just the relevance of that conclusion she felt the need to post, that nobody appeared to be asserting.
Comment by RogerRabbitt — August 26, 2008 @ 6:50 pm
August 26th, 2008 at 6:50 pm
From where did you get this false idea? Are you unaware of all the mutations that aren't substitutions?
Hall tested for increased resistance. You're really twisting a relatively simple paper.
If that's true (that Hall is only doing applied medical research), why is his grant from NIGMS instead of NIAID?
Comment by richcheese — August 26, 2008 @ 6:50 pm
August 26th, 2008 at 7:27 pm
Behe is badly muddled on the topic of multiple mutations, but when it came time to calculate probabilities and to discuss the silly "double CCC" illustration, he showed his cards. (Or he made an elementary mistake, of huge impact.)
He came up with a probability for something called a CCC. It doesn't matter what that probability is or how he estimated it. Let's call the probability X. Then he said that the probability of two of them occurring is X squared. That, my friends, is the probability that both occur simultaneously. He makes this "mistake" more than once in EoE, and it's one reason the book is not taken seriously by any expert on genetics or evolution.
RR, I thought that Karla was trying, as I and others are, to put Hall's results into their scientific context…to tease apart scenario one from scenario two, as my previous comment explained.
Friends, exploring and discussing design is fun and interesting and I want to be a part of it. But you are unwise to follow Behe. His book is an embarrassment, and he has set you back by making huge mistakes of fact and of judgment. There may be a non-random component to evolution, even a huge non-random component, but EoE doesn't get you there.
Comment by SteveMatheson — August 26, 2008 @ 7:27 pm
August 26th, 2008 at 7:53 pm
Karla says:
Hall says:
Sounds like Hall is saying that which many folks here accuse Behe of. Saying that it is a practical barrior to "evolve increased activity against imipenem", and that "It is important to consider the effects of only one or two independent amino acid substitution mutations".
Why doesn't Hall say, "only one or two independent amino acid substitution mutations might not do it, but it can probably evolve using other mechanisms". That seems to be the position of many here, but Hall clearly did not say that when he had the opportunity to do so.
Comment by RogerRabbitt — August 26, 2008 @ 7:53 pm
August 26th, 2008 at 7:58 pm
Steve says:
No, that is the probability that both occur independently. If the first one is fixed by NS, then the odds improve. If not, it is also subject to mutation, and that decreases the odds.
Comment by RogerRabbitt — August 26, 2008 @ 7:58 pm
August 26th, 2008 at 8:13 pm
RR,
to essentially the same probability as simultaneous occurance of both mutations. What is the argument here?
Comment by David E Levin — August 26, 2008 @ 8:13 pm
August 26th, 2008 at 8:27 pm
Steve doesn't agree with you and I. I thought a smart guy like you would figure that out and attempt to correct him.
Is there a reason you took time to address a post to me and not him, when he is the guy who disagrees with you?
Comment by RogerRabbitt — August 26, 2008 @ 8:27 pm
August 26th, 2008 at 8:47 pm
Actually, Behe was talking about simultaneous point mutations, exploring the statistical probability of a double point mutation conferring chloroquine restance. Steve was correct about that, though I can't figure out why he thinks this is a "mistake". The math seems correct to me.
Comment by chunkdz — August 26, 2008 @ 8:47 pm
August 26th, 2008 at 8:55 pm
chunkdz,
There's nothing wrong with the math, it's where Behe tries to take it that isn't valid.
Comment by David E Levin — August 26, 2008 @ 8:55 pm
August 26th, 2008 at 10:42 pm
David Levin,
Behe's math is correct, but you said that theoretical stepwise point mutation was
How did you calculate this?
Why is limiting point mutation to one at a time "not valid"?
Comment by chunkdz — August 26, 2008 @ 10:42 pm
August 26th, 2008 at 11:19 pm
RR, "independently" doesn't explain the multiplication of the probabilities, at least not in genetic terms. The probability of rolling snake eyes in a single roll is 1/6 x 1/6 = 36. We multiplied because the events occur together, independently. Now what's the probability of getting snake eyes 3 times in a row? Those aren't simultaneous, but we're AND-ing them together, saying that they must happen together, so we cube 1/36 and get a small probability. Behe makes this assumption, that the events must happen together, and so he multiplies. (This, chunkdz, is the "mistake" I was referring to.) What he seems to ignore is the probability that we get the same results – in the dice example it would be 6 1's on dice – cumulatively. As I explain elsewhere, the probability of rolling snake eyes in X rolls is not the same as the probability of getting two 1's, not necessarily simultaneously, in X rolls.
I'm done on this thread; I'll look forward to Bilbo's discussion of the "two binding-sites rule."
Comment by SteveMatheson — August 26, 2008 @ 11:19 pm
August 27th, 2008 at 5:02 am
@Roger Rabbitt
The point I am trying to thrash out with Bilbo is still related to the initial question, wether Behe´s interpretation of Halls results are correct and therefore merrit using Hall as a reference. Bilbo assumes this is the case which results in statements like:
The problem I was trying to alert him to was, considering the entire content of Halls paper and not a few sentences taken out of context, it is easy to see that Halls paper is unsutible to serve as a reference for a general statement like Behes.
You yourself adress this in you last comment to me:
Sorry, but that is exactly what Hall takes the opportunity to say in his paper. Halls paper is about the application of a technique he developed to establish, if problems with resistance for a range of existing or evern newly developed carbapenem might arise by the very simple mechanismen of one or double mutation. Hall discusses clinical implications and not general mechanisms and their limits.
To anyone familiar with the sience, native english-speaker or not, this is obvious.
And no, I am not a native english-speaker and addionally I live in a different time zone, so my comment may seem rather belated. I hope you take no offence
@Steve an others:
Thank you for giving support to and recently clarifing points I was trying to make. I suppose it will be more prudent to refrain from commenting here in future since a lack of language skills on my part could easily lead to misunderstandings and possible damage to the efforts to clarify, what the science really tells us. If have already blundered, I am sorry - I did not mean to make your job even more difficult
Comment by Karla — August 27, 2008 @ 5:02 am
August 27th, 2008 at 6:16 am
Hi Karla,
A non-native english speaking dude here. I thought your original posts did an excellent job of clarifying Hall's paper without launching in to a vociferous attack on Behe. So thanks for that and keep commenting.
Comment by samsen — August 27, 2008 @ 6:16 am
August 27th, 2008 at 7:45 am
Hi Samsen,
thank you for your kind comment, I do feel encouraged to give it another try. On the other hand I shudder at spelling desasters like "offence" and "unsutible"
I will try to concentrate more when posting.
But thanks again for your support.
all the best
Karla
Comment by Karla — August 27, 2008 @ 7:45 am
August 27th, 2008 at 9:00 am
Ha! spelling checkers ftw!
Comment by samsen — August 27, 2008 @ 9:00 am
August 27th, 2008 at 12:03 pm
Hi Steve,
You've insinuated that someone is not being honest here. I'm guessing you mean me. I assure you that I am being honest. Perhaps I'm incompetent or lacking in communication skills, but not honesty.
Comment by Bilbo — August 27, 2008 @ 12:03 pm
August 27th, 2008 at 12:11 pm
Agreed.
Inconclusive.
Agreed.
Disagree. What TP showed, if we understand the paper she cited, is that Hall's prediction was wrong, not that more than two mutations were required to increase resistance to imipenem. I think most or all of the other commenters here would agree that if resistance to imipenem increased, it was because of one or two mutations, not three. Why was Hall's prediction wrong, then? Either because his method was not sensitive enough to pick up the increase, or because a sub-family of the enzyme had increased resistance in one or two mutations and passed it on to blaIMP-1 by horizontal gene transfer.
Agreed.
Agreed. What Hall did claim was that if more than two mutations were required, then it probably wouldn't evolve.
Comment by Bilbo — August 27, 2008 @ 12:11 pm
August 27th, 2008 at 12:14 pm
By the way, are TP and I interpreting this paper correctly, as showing that Hall's prediction was wrong? Anybody?
And now I'll try to write up Behe's two-binding site rule. But I'll have to quote him at length, so I don't know if I'll get it done today.
Comment by Bilbo — August 27, 2008 @ 12:14 pm
August 27th, 2008 at 12:35 pm
Steve,
No, he says that if the events happen together, then that is their probability.
No, he was quite careful to leave room for alternate pathways.
Take care.
Comment by chunkdz — August 27, 2008 @ 12:35 pm
August 27th, 2008 at 2:22 pm
Hi Bilbo,
we are finally getting there!
Both the
and
are conected by Mendez et al. They descibe the fact that the original blaIMP-1 was not modified by point mutation but has become fused to additional proteins aac(6')-31 and aadA1, thus aquiring increased resistance. The ancestor for aac(6')-31 seems to be IMP-16 (figure 2 in the paper) but shows 28 and 27 amino-acid changes to both presented variants of this molecule (the change of one amino-acid residue you seem to allude to and which reportedly changed substrate-specifity referes to the two variants of IMP-16).
So the mechanism to improve resistance to imipenem in this case seems to be beg, borrow, steal and cobble together whatever it take to survive.
But it does not look like simple horizontal gene transfer of a slightly modified subclass of IMP as you suggested.
The realy disconcerting point here is, that the bacteria have strated to combine different subclasses of IMPs - keep one, fool around with the other and see where it gets you. Serious wild-life, it seems to me.
Halls prediction was not wrong - he was completly right in expecting trouble with imipenem comming from a diffrent direction than simply modifiing an exsiting IMP.
all the best
Karla
Comment by Karla — August 27, 2008 @ 2:22 pm
August 28th, 2008 at 10:21 am
This is fascinating. How many mutations did this require?
And previously you wrote:
I scanned it too quickly and thought you were saying that more than two mutations were needed. On second reading I see misunderstood.
Comment by Bilbo — August 28, 2008 @ 10:21 am
August 28th, 2008 at 4:38 pm
Bilbo–
I am not insinuating that you are being dishonest. I am saying that there are only a few outcomes of harping on trajectories that involve >2 mutations. One outcome is to state what is already obvious to those who are not completely ignorant. Another is to suggest that these phenomena cannot occur randomly. This is a falsehood. In my opinion, those who repeatedly utter (or type) falsehoods are being dishonest. Elsewhere I've mulled the implications of using this term to describe the actions of others, and so I will not refer to the misleading aspects of this discussion as 'lying.' But I'm concerned by the pattern I've seen here. You have, in my view, repeatedly presented us with a very misleading picture, in which trajectories of 2 or less mutations can be driven by darwinian mechanisms, and those of 3 or more cannot. In my view, the misleading and inaccurate nature of this line of argument has been made very clear by others. And yet, it seems to me, it persists. Perhaps you have clearly disclaimed the falsehood, and I have missed it; this is likely since I have read only a few threads on the blog. I don't believe you to be a dishonest person, but I am uncomfortable with your approach here. It's not always easy to distinguish ignorance from duplicity, and since you are an official poster on a widely-read website, it's fair to hold you to some fairly high standards regarding the accuracy of your words and the effort you have expended in actually trying to understand the topics on which you hold forth. Word to the wise.
In any case, I do find Behe's book to be intellectually dishonest. Whether Behe himself believes that he has assembled a reasonable or coherent challenge to evolutionary biology, I don't know. But I find his work to lack integrity, and I have concluded that he is someone who should not be trusted to provide accurate or complete information on population genetics.
Comment by SteveMatheson — August 28, 2008 @ 4:38 pm
August 29th, 2008 at 10:51 am
I place myself in that category. Before this thread, I was under the impression that people were objecting to Behe's claim that Darwinian evolution normally can't handle more than two unselected (and I guess I should add non-neutral) mutations. Hall seemed to confirm what Behe was saying.
Yeah…I guess I don't follow you. If Darwinian evolution normally can't handle more than two unselected, non-neutral mutations, then the phenomena seems to be non-random. Or at least abnormal. And either I'm dishonest for repeating it, or I'm not. Which is it? I prefer thinking of myself as completely ignorant. It's less morally repugnant.
It's still not clear to me why this is misleading. And if it has been made clear by others, then I've been too dense to see it, which wouldn't surprise me.
But in your case, you know from personal experience that I was ready, willing and able to take on one of the world's greatest Christian philosophers when he claimed that Christian scientists must reject "unguided" Darwinism. (And if I had been allowed a follow up question, I would have succeeded in pinning his hide to the wall.) So you should know that in my case it's not duplicity. So from now on just assume it's ignorance.
I try to be accurate. But in another thread here, I already admitted that I am just another member of the peanut gallery, with only a BA in philosophy. With no disrespect to the other TTers, I think Mike Gene was the chief reason for the high quality of this blog. Without him, we try to fill in as best we can.
Yeah, there you go throwing around moral judgments, again.
He has often claimed that he has. Why not just take his word for it and explain why he has failed? Why the need to attack his moral character?
See, you could say that without having to attack his character.
Now let me defend my view of Hall and Behe:
Hall says:
Clearly, Hall wants to know if the continued used of imipenem will result in increased resistance of the enzyme. It is important to know this as a public health concern. After using the Barlow-Hall model, he concludes:
He states his reason:
This seems to reflect exactly what Behe had argued in the earlier part of EoE. And Behe rephrases Hall's conclusion, saying
From the context it's clear that Behe means effectively ruling out Darwinian evolution of the IMP-1 enzyme.
How is Behe's rephrasing any different from Hall's conclusion, other than the fact that he includes the word "Darwinian"? What? Was Hall referring to Lamarckian evolution?
Now it appears that Hall's prediction was wrong, and the IMP-1 enzyme increased resistance. According to Karla it was because it fused with another protein.
According to Karla, Hall wasn't wrong, but only talking about evolution by point mutation. But if that were the case, I would expect Hall to say something like, "This study is only of point mutations. It's quite possible that IMP-1 will evolve by some other form of mutation." He does say that it is necessary to study the sub-families of the enzyme. But no indication that other forms besides point mutation need to be considered.
Meanwhile, I have asked Karla if the fusion of IMP-1 with other proteins took more than two unselected steps. If so, I would consider that to be significant, and rethink the conclusion I've drawn from this thread.
Now if you think I'm wrong here, please don't attribute it to my dishonesty. If you do, I'll take that as a sign of your immaturity and inability to respect other people, even if you disagree with them. Perhaps that's the great advantage I've gained from ID discussions over the past seven years — an ability to respect people that I disagree with.
Comment by Bilbo — August 29, 2008 @ 10:51 am