UPDATE: Scott Adams at The Dilbert Blog has become convinced of Intelligent Design! The piece of evidence that tipped him might just be your last straw, too. (H/T: True Ancestor)
Beneficial mutations that advance an organism's fitness are, as we know, rare. Most spontaneous mutations are deleterious. Now, in a finding reported in the journal Heredity that has evolutionary biologists going "WTF??", it appears that the identical mutation is more likely to prove beneficial in less fit organisms than in their fitter cousins, improving the weaklings' chances not to die out. Huh?? Look:
Breed almost any organism under conditions where it is forced to accumulate random mutations, its fitness will invariably decay. The reason is that very few mutations improve an organism's ability to survive or reproduce; the majority are harmful. But a recent study suggests that the size of this majority depends, to a surprising extent, on the [context] in which the mutations occur. The same mutation occurring in a poorly adapted individual, Silander et al. (2007) argue, is more likely to be beneficial than if it occurred in a well-adapted individual.
These results are noteworthy because they suggest that the effects of mutations are dynamic rather than fixed. Such a view is consistent with some models of evolution and not with others. For example, it suggests that very small populations, which tend to accumulate harmful mutations, will be protected from the endless accumulation of more and more harmful mutations by an increasing rate of beneficial mutation. This 'compensatory mutation' view contrasts with the 'mutational meltdown' view, which instead suggests that such populations will suffer a build-up of harmful mutations until they become extinct. [...]
To investigate this, Silander et al. (2007) applied techniques first used decades ago to study the fitness effects of mutations in Drosophila (Mukai, 1964), but instead used a virus system, a DNA bacteriophage known as X174. With the addition of sophisticated statistical tools and computer simulations, they were able to estimate the proportion of beneficial mutations in virus lines with both high and low fitness. For all three high-fitness lines measured, they were unable to detect any beneficial mutations. But for two out of three low-fitness lines, beneficial mutations were clearly evident. In fact, the fraction of mutations inferred to be beneficial was substantial—16%. [...]
One possibility is that low-fitness populations, which suffer from more deleterious mutations, could simply be experiencing a high rate of back mutation—that is, the fitness decline might halt simply because the harmful mutations are changing back to the more benign versions of themselves. Silander et al. (2007) approached this problem by using a mutagen to ensure that nearly all of the mutations in their study were in one direction (from a cytosine nucleotide to a thymine). Another possibility is that selection is working overtime in low-fitness populations, helping them to maintain their fitness: a mutation might well be more harmful in an already sick virus than it is in a healthy individual. Since the worst mutations are quickly eliminated—dead viruses do not replicate—selection would, in this case, more effectively curtail further fitness decline in low-fitness populations. But, as Silander et al. (2007) show, selection is acting only slightly more strongly in low-fitness populations, and the difference is not large enough to explain their results. [...]
[T]he results from this study are consistent with what has been found in some studies of more complex organisms (Estes and Lynch, 2003). Furthermore, the use of viruses for this kind of work opens up exciting future possibilities. Viral genomes are small and easily manipulated, and viral fitness is straightforward to measure. Thus, the main result of Silander et al. (2007), that particular mutations have different effects in high- versus low-fitness virus lines, could potentially be tested directly.
It's as if a species or population, like an individual, is spurred to a desperate creativity by a threat to its existence. A sort of molecular necessity-is-the-mother-of-invention. But wait a minute. We're talking about creativity and invention at the level of DNA molecules.
Kinda makes you go WTF??