You did. And you said it was “all over the front page of a google search or even a yahoo one” and then you accused me of being intellectually dishonest.
So, once again, I ask you to provide me with a link to this study that you claim disproves Behe.
Behe didn’t perform a study. Why should we have to? Again, you should actually look for the response before you suggest no one has responded.
Yeah, I looked. Can’t find “it.” Whatever “it” really is. Since you brought “it” up I thought you might be able to to point me in the right direction. Perhaps I am asking too much.
And yes, Behe crafted a powerful argument against Darwinian Evolution based on the observational data available from the studies of HIV, Malaria and E.Coli.
For example, Behe did not study E.Coli directly. Richard Lenski did. But Behe, who is a biochemist, was able to see the obvious negative implications Lenski’s study has for Darwinian Evolution:
"The studies of malaria and HIV provide by far the best direct evidence of what evolution can do. The reason is simple: numbers. The greater the number of organisms, the greater the chance that a lucky mutation will come along, to be grabbed by natural selection. But other results with other organisms can help us find the edge of evolution, especially laboratory results where evolutionary changes can be followed closely. The largest, most ambitious, controlled laboratory evolutionary study was begun more than a decade ago in the laboratory of Professor Richard Lenski at Michigan State University. Lenski wanted to follow evolution in real time. He started a project to watch the unfolding of cultures of the common gut bacterium Escherichia coli. E. coli is a favorite laboratory organism that has been studied by many scientists for more than a century. The bug is easy to grow and has a very short generation span of as little as twenty minutes under favorable conditions. Like those of P. falciparum, H. sapiens, and HIV, the entire genome of E. coli has been sequenced.
Unlike malaria and HIV, which both have to fend for themselves in the wild and fight tooth and claw with the human immune system, the E. coli in Lenski’s lab were coddled. They had a stable environment, daily food, and no predators. But doesn’t evolution need a change in the environment to spur it on? Shouldn’t we expect little evolution of E. coli in the lab, where its environment is tightly controlled? No and no. One of the most important factors in an organism’s environment is the presence of other organisms. Even in a controlled lab culture where bacteria are warm and well fed, the bug that reproduces fastest or outcompetes others will dominate the population. Like gravity, Darwinian evolution never stops.
But what does it yield? In the early 1990s Lenski and coworkers began to grow E. coli in flasks; the flasks reached their capacity of bacteria after about six or seven doublings. Every day he transferred a portion of the bugs to a fresh flask. By now over thirty thousand generations of E. coli, roughly the equivalent of a million years in the history of humans, have been born and died in Lenski’s lab. In each flask the bacteria would grow to a population size of about five hundred million. Over the whole course of the experiment, perhaps ten trillion, 1013, E. coli have been produced. Although ten trillion sounds like a lot (it’s probably more than the number of primates on the line from chimp to human), it’s virtually nothing compared to the number of malaria cells that have infested the earth. In the past fifty years there have been about a billion times as many of those as E. coli in the Michigan lab, which makes the study less valuable than our data on malaria.
Nonetheless, the E. coli work has pointed in the same general direction. The lab bacteria performed much like the wild pathogens: A host of incoherent changes have slightly altered pre-existing systems. Nothing fundamentally new has been produced. 25 No new protein-protein interactions, no new molecular machines. As with thalassemia in humans, some large evolutionary advantages have been conferred by breaking things. Several populations of bacteria lost their ability to repair DNA. One of the most beneficial mutations, seen repeatedly in separate cultures, was the bacterium’s loss of the ability to make a sugar called ribose, which is a component of RNA. Another was a change in a regulatory gene called spoT, which affected en masse how fifty-nine other genes work, either increasing or decreasing their activity. One likely explanation for the net good effect of this very blunt mutation is that it turned off the energetically costly genes that make the bacterial flagellum, saving the cell some energy. Breaking some genes and turning others off, however, won’t make much of anything. After a while, beneficial changes from the experiment petered out. 26 The fact that malaria, with a billion fold more chances, gave a pattern very similar to the more modest studies on E. coli strongly suggests that that’s all Darwinism can do."