- May 19, 2006
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In the thread called "The appearance of design" Shernen wrote:
From the first link:
Through a combination of experimental evidence, genome research, and mathematical law, Behe analyzes three key case studies of the tens of thousands of generations of malaria, E. coli, and the HIV virus, and the human genomic response to those invaders. We now know exactly what mutations have occurred in the struggle between these parasites and their human hosts. We know their rate of occurrence. We know all possible types of mutations, and their natural rate of occurrence. Armed with all this, it is a simple matter of extrapolation to determine the limits of Darwinian randomness in the entire tree of life on earth.
I think I've found what I'm going to ask for for Father's day.... Michael Behe has a brand new book due out today, June 5, 2007: THE EDGE OF EVOLUTION: The Search for the Limits of Darwinism Amazon apparently has it in stock...About bacterial resistance: http://www.ncbi.nlm.nih.gov/sites/en...t_uids=9332013Policies aimed at alleviating the growing problem of drug-resistant pathogens by restricting antimicrobial usage implicitly assume that resistance reduces the Darwinian fitness of pathogens in the absence of drugs. While fitness costs have been demonstrated for bacteria and viruses resistant to some chemotherapeutic agents, these costs are anticipated to decline during subsequent evolution. This has recently been observed in pathogens as diverse as HIV and Escherichia coli. Here we present evidence that these genetic adaptations to the costs of resistance can virtually preclude resistant lineages from reverting to sensitivity. We show that second site mutations which compensate for the substantial (14 and 18% per generation) fitness costs of streptomycin resistant (rpsL) mutations in E. coli create a genetic background in which streptomycin sensitive, rpsL+ alleles have a 4-30% per generation selective disadvantage relative to adapted, resistant strains. We also present evidence that similar compensatory mutations have been fixed in long-term streptomycin-resistant laboratory strains of E. coli and may account for the persistence of rpsL streptomycin resistance in populations maintained for more than 10,000 generations in the absence of the antibiotic.(emphases added) There goes your point about antibiotic resistance. Which is shredded in a far less friendly way over at http://mikethemadbiologist.blogspot....evolution.html .
From the first link:
Through a combination of experimental evidence, genome research, and mathematical law, Behe analyzes three key case studies of the tens of thousands of generations of malaria, E. coli, and the HIV virus, and the human genomic response to those invaders. We now know exactly what mutations have occurred in the struggle between these parasites and their human hosts. We know their rate of occurrence. We know all possible types of mutations, and their natural rate of occurrence. Armed with all this, it is a simple matter of extrapolation to determine the limits of Darwinian randomness in the entire tree of life on earth.