Let's face it, this thread was going to happen sooner or later.
Mike Behe's new book The Edge of Evolution is out, and he basically has two points.
1. In the case of malaria, with generation sizes in the trillion trillions, all evolution has done is basically make advantageous changes that are destructive to DNA. Basically making a house safer by breaking the doorlocks.
2. Proteins, in order to bind need multiple bonding sites, and when considering tests done with antibodies, it takes, again, astronomical numbers to randomly produce these sites in matching pairs.
Both of these things he says, prove that evolution is, outside of the sorts of changes that malaria has made, not possible.
To hear the other side of the story, I went over to P.Z. Meyers' website. Very quickly PZ, Stephen Wells, and other very bright people steered my to what I think is the root of the argument. As best as I can tell, it amounts to saying 'it's not impossible' and 'look at the fossil record.'
Meyers suggested this article by Steve Carroll to counter Behe's claim:
http://www.sciencemag.org/cgi/conten.../316/5830/1427
... his two objections are:
and...
I think Carroll is dodging Behe's point. First, he ducks the Behe's probabilities in the first quote, and Behe's observation that all we see in nature are the destructive, avantageous changes. Second, he dodges the point that while there are proteins out there that need only a couple binding sites, in reality there are many proteins that do need the 6 or so sites, and can't 'wait around' to build themselves one-by-one. And if you are evolving from a chimp,or higher organism, we are past evolving in the context of only those simple proteins.
So, where's the beef?
Mike Behe's new book The Edge of Evolution is out, and he basically has two points.
1. In the case of malaria, with generation sizes in the trillion trillions, all evolution has done is basically make advantageous changes that are destructive to DNA. Basically making a house safer by breaking the doorlocks.
2. Proteins, in order to bind need multiple bonding sites, and when considering tests done with antibodies, it takes, again, astronomical numbers to randomly produce these sites in matching pairs.
Both of these things he says, prove that evolution is, outside of the sorts of changes that malaria has made, not possible.
To hear the other side of the story, I went over to P.Z. Meyers' website. Very quickly PZ, Stephen Wells, and other very bright people steered my to what I think is the root of the argument. As best as I can tell, it amounts to saying 'it's not impossible' and 'look at the fossil record.'
Meyers suggested this article by Steve Carroll to counter Behe's claim:
http://www.sciencemag.org/cgi/conten.../316/5830/1427
... his two objections are:
Quote:
Behe states correctly that in most species two adaptive mutations occurring instantaneously at two specific sites in one gene are very unlikely and that functional changes in proteins often involve two or more sites. But it is a non sequitur to leap to the conclusion, as Behe does, that such multiple-amino acid replacements therefore can't happen. Multiple replacements can accumulate when each single amino acid replacement affects performance, however slightly, because selection can act on each replacement individually and the changes can be made sequentially.
Behe begrudgingly allows that only "rarely, several mutations can sequentially add to each other to improve an organism's chances of survival." Rarely? This, of course, is the everyday stuff of evolution. Examples of cumulative selection changing multiple sites in evolving proteins include tetrodotoxin resistance in snakes (3), the tuning of color vision in animals (4), cefotaxime antibiotic resistance in bacteria (5), and pyrimethamine resistance in malarial parasites (6)--a notable omission given Behe's extensive discussion of malarial drugresistance.
Behe begrudgingly allows that only "rarely, several mutations can sequentially add to each other to improve an organism's chances of survival." Rarely? This, of course, is the everyday stuff of evolution. Examples of cumulative selection changing multiple sites in evolving proteins include tetrodotoxin resistance in snakes (3), the tuning of color vision in animals (4), cefotaxime antibiotic resistance in bacteria (5), and pyrimethamine resistance in malarial parasites (6)--a notable omission given Behe's extensive discussion of malarial drugresistance.
and...
Quote:
This lack of quantitative thinking underlies a second, fatal blunder resulting from the mistaken assumptions Behe makes about protein interactions. The author has long been concerned about protein complexes and how they could or, rather, could not evolve. He argues that the generation of a single new protein-protein binding site is extremely improbable and that complexes of just three different proteins "are beyond the edge of evolution." But Behe bases his arguments on unfounded requirements for protein interactions. He insists, based on consideration of just one type of protein structure (the combining sites of antibodies), that five or six positions must change at once in order to make a good fit between proteins--and, therefore, good fits are impossible to evolve. An immense body of experimental data directly refutes this claim. There are dozens of well-studied families of cellular proteins (kinases, phosphatases, proteases, adaptor proteins, sumoylation enzymes, etc.) that recognize short linear peptide motifs in which only two or three amino acid residues are critical for functional activity [reviewed in (7-9)]. Thousands of such reversible interactions establish the protein networks that govern cellular physiology.
Very simple calculations indicate how easily such motifs evolve at random. If one assumes an average length of 400 amino acids for proteins and equal abundance of all amino acids, any given two-amino acid motif is likely to occur at random in every protein in a cell. (There are 399 dipeptide motifs in a 400-amino acid protein and 20 20 = 400 possible dipeptide motifs.) Any specific three-amino acid motif will occur once at random in every 20 proteins and any four-amino acid motif will occur once in every 400 proteins. That means that, without any new mutations or natural selection, many sequences that are identical or close matches to many interaction motifs already exist. New motifs can arise readily at random, and any weak interaction can easily evolve, via random mutation and natural selection, to become a strong interaction (9). Furthermore, any pair of interacting proteins can readily recruit a third protein, and so forth, to form larger complexes. Indeed, it has been demonstrated that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution.
Very simple calculations indicate how easily such motifs evolve at random. If one assumes an average length of 400 amino acids for proteins and equal abundance of all amino acids, any given two-amino acid motif is likely to occur at random in every protein in a cell. (There are 399 dipeptide motifs in a 400-amino acid protein and 20 20 = 400 possible dipeptide motifs.) Any specific three-amino acid motif will occur once at random in every 20 proteins and any four-amino acid motif will occur once in every 400 proteins. That means that, without any new mutations or natural selection, many sequences that are identical or close matches to many interaction motifs already exist. New motifs can arise readily at random, and any weak interaction can easily evolve, via random mutation and natural selection, to become a strong interaction (9). Furthermore, any pair of interacting proteins can readily recruit a third protein, and so forth, to form larger complexes. Indeed, it has been demonstrated that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution.
I think Carroll is dodging Behe's point. First, he ducks the Behe's probabilities in the first quote, and Behe's observation that all we see in nature are the destructive, avantageous changes. Second, he dodges the point that while there are proteins out there that need only a couple binding sites, in reality there are many proteins that do need the 6 or so sites, and can't 'wait around' to build themselves one-by-one. And if you are evolving from a chimp,or higher organism, we are past evolving in the context of only those simple proteins.
So, where's the beef?
In our desire to impose form on the world we have lost the capacity to see the form that is there;
and in that lies not liberation but alienation, the cutting off from things as they really are. --...
In our desire to impose form on the world we have lost the capacity to see the form that is there;
and in that lies not liberation but alienation, the cutting off from things as they really are. --...
