
Cairns added lactose either immediately after spreading the bacteria on agar plates, 24 hours later or 72 hours later. The graph shows the number of colonies that appeared, on the left in real time and on the right relative to the time at which the lactose was added. Lactose causes the late mutants to appear Delaying the lactose delays their appearance, but does not affect the number of mutants.
The final experiment that Cairns and his colleagues report comes even closer to the sort of selection one might expect in the real world. It exploits a technique developed early this century for classfying bacteria according to their ability to use certain sugars. Wild E coli, for example, can ferment lactose whereas shigella and salmonella cannot. Some species, however, are so-called “late” fermenters of certain sugars. That is, it may take a week or more before bacteria start using an unusual food source. Shigella sonnei, for example, is a late fermenter of lactose.
In fact, bacteria possess several such cryptic genes, which are brought into play only when needed. The mechanism of activation varies. Sometimes, another piece of DNA is inserted upstream of the desired gene and switches that gene on.
In other cases, The DNA sequence needs several specific changes before the cryptic gene will function properly. Cairns and his group studied one such cryptic gene which allows E coli to ferment lactose even when its beta-galactosidase gene is not working.
The gene is called ebg, and it needs at least two mutations to turn it on. The first is a change in the repressor, a DNA sequence which codes for a protein that normally keeps ebg inactive. The second is a change to ebg itself. The enzyme produced by the usual version of the gene cannot, in fact, break down lactose. It needs a mutation to make it effective. Under normal circumstances, each of these two mutations happens roughly once in every 100 million generations. Both mutations are needed, which would happen by chance roughly once every 10 million billion generations. Cairns says:
That such events ever occur seems almost unbelievable.
Yet colonies do appear after about two weeks. That they do, without at the same time gathering a lot of neutral and outright harmful mutations, suggests to Cairns that bacteria must have access to some reversible process of trial and error.
A Mechanism Needed
Cairns stresses that the main purpose of his paper is “to show how insecure is our belief in the spontaneity of most mutations”. But he realizes that the experiments he reports are not going to settle the issue. What seems to be missing, at the moment, is a mechanism that would use what we already know about the workings of the cell to achieve the sorts of directed mutations that the group at Harvard has demonstrated.
Cairns suggests that the cell might make a set of variable RNA messages—which carry the genetic instructions from the DNA to the machinery that makes proteins according to those instructions—and reverse transcribe the most effective of these back into DNA.
It would need some way of monitoring “effective” RNA, but if it reverse transcribed only those messages present when it started to grow again, it would most likely capture the message that had indeed enabled growth to resume.
Critics of Darwinism have already leapt on Cairns’s work to support their belief that there is something rotten in the state of evolutionary biology. Biologists, however, are being more circumspect. They would like to see further demonstrations of the phenomenon—and preferably a mechanism too—in bacteria before they embrace it wholeheartedly. They also doubt that it could apply when the biochemical link between adaptation and gene is longer and more complex than that between an enzyme and its substrate.
Report by Jeremy Cherfas, New Scientist, 22 September 1988.
Originally posted 2009-06-17 01:14:34. Republished by Blog Post Promoter



