"Under these circumstances [ stress-induced hyper-mutation ] , as per EAM , [ above ] , it has been repeatedly demonstrated [ since 1988 , at Corning , by that scientist whose name escapes me ] that the number of adaptive mutations outnumbers the number of of ineffectual or maladaptive mutations by a strongly significant statistical percentage ."
"On the face of it , the implication is that this kind of thing happens all the time ; that everywhere you look , stress-induced hypermutation is occurring , and along with it adaptive mutations are occurring disproportionately often - that this is part and parcel of everyday evolution . The ardour with which this evidence is brandished is , however , misleading . In only a handful of studies , using specific strains of bacteria with specific genetic features under specific environmental circumstances , have specific adaptive mutations seemed to occur with anomalous frequency . There is no suggestion that these cases are in any way generally representative , and even if the results were being interpreted correctly , the idea that they constitute evidence for a pan-species mechanism of internally directed evolution is , unfortunately , wishful thinking . But what of these rare anomalous cases ? The most famous was reported by J. Cairns and P. L. Foster , in which a dish of starving , non-growing E-coli ( a particular strain with a Lac- mutation ) appeared to preferentially induce a reversion mutation ( to Lac+ ) in order to enable growth when the only source of energy was lactose . Moreover , the mutation did not occur with such frequency if lactose was not present , if there was another growth-inhibiting factor in play , or if food sources other than lactose were available . On top of that , although the adapted bacteria showed evidence of accumulating other non-selected mutations , it was nowhere near enough to explain the rate of adaptive mutation , and the bacteria which did n't adapt showed no accumulation of unselected mutations at all ! Understandably , this looked to them , and other people at the time , like a pretty cut'n'dried example of an environmentally-or-organismically induced adaptive mutation . However , the nagging problem remained that this event was completely unprecedented , and was not observed in the general case of bacteria under starvation conditions . Why was this strain of bacteria so good at inducing this particular reversion mutation in just those circumstances ? The answer , as it turned out , was that the experimental assumption of 'no growth ' taking place in the e-coli colony was in error . The strain of e-coli used in the experiment had a 'leaky ' ( inefficient ) mutant Lac allele , with only 1 % to 2 % of the normal ability to process lactose . That 1 % to 2 % was then deliberately 'smothered ' by the experimenters through the addition of scavenger cells which mopped up the product of what little lactose the e-coli could process , effectively halting their growth . Because the later , visible growing colonies of e-coli had a reversion mutation to lac+ , the experimenters deduced that mutation was required for growth to be possible . However , what they did not take into account at the time was that during normal growth prior to incubation on the test medium , a small proportion of the e-coli colony experienced a duplication of the leaky lac gene . This mutation conferred no advantage - until the colony was plated on lactose . Now , the second copy of the gene increased the total amount of lactose they could process beyond the ability of the scavenger cells to inhibit growth , and the e-coli could ( slowly ) grow and divide . Within these slow-growing microcolonies , selection favoured those cells which experienced further lac- duplications . And the more lac- duplications a cell has , the more likely one of them will experience a reversion mutation to lac+ , explaining the apparently anomalous frequency of that particular mutation . When this happens , cell growth rate jumps considerably - but now it is the additional lac- genes which are holding the organism back , destabilising the chromosome and tying up resources which could be more efficiently processed by the lac+ gene . Selection now favours those lac+ revertants who lose the unstable lac- duplications . By the time the microcolonies become visible to the naked eye , they consist almost entirely of lac+ revertants . This hypothesis agrees with all observations related to the earlier experiments , and was verified in a number of ways , including repeating the experiment with a colony composed entirely of duplicate lac- bacteria , increasing the number of microcolonies 100-fold , which tallies with the ~1 % background rate of chromosomal duplications in those bacteria . Also , bacteria in the late-arriving microcolonies were observed to possess residual duplicate lac- genes . In short , the results of the experiment agree completely with classical evolutionary theory . It should be noted , by the way , that in addition to the late-arriving 'directed mutation ' microcolonies that causes such a stir , the original experimenters also observed the expected number of early-appearing colonies from pre-plating revertant mutants , a la L & amp ; D. EDIT : Reading further around the subject , it seems no stress-induced hypermutable state was involved either . Apparently , 10-20 % of the bacteria with lac- duplications also possessed 'dinB ' ( a mutation-promoting gene apparently , though it 's beyond the scope of my research here ) on the same plasmid . The mutagen 'came along for the ride ' so to speak , as selection favoured the duplication of that section of DNA , and induced hgher rates of mutation in - yep - 10-20 % of the adaptive population . So not only was the hypermutational state of that subpopulation not the cause of the adaptive mutation ( clearly , since the other 80-90 % of adaptation happened without it ) , it was actually harmful . Live n learn ! 2ND EDIT : The same experiment yields similar results with lac- situated within the chromosome itself , only with 100-fold fewer colonies , reflecting the lower incidence of chromosomal duplication and reversion events in comparison with plasmids ."
"Under these circumstances [ stress-induced hyper-mutation ] , as per EAM , [ above ] , it has been repeatedly demonstrated"
"On the face of it , the implication is that this kind of thing happens all the time"