I hope this isn't too substantial a lift from the paper.
Maresca and Schwartz, 2006 writes:
If an organism’s features are not adaptations to specific environmental circumstances, we can decouple “evolution” and “adaptation.” The apparent “order” with which organisms seem to be distributed in nature results from the elimination of the “wrong” phenotypes, not necessarily the selection of better adapted ones. Phenotypes do not change to “fit” their environment as a result of “correct” sequences of mutation. Rather, the environment provokes organismal (plant and animal) change via stress. Since the cause of cell function disruption is random, the resultant mutation’s effects on the regulation of development and its ultimate phenotypic expression are also random. In short, if a newly emergent phenotypic property does not kill you, you have it [...]
We can see a number of straw man representations of evolutionary theory here.
The apparent “order” with which organisms seem to be distributed in nature results from the elimination of the “wrong” phenotypes, not necessarily the selection of better adapted ones
What the distinction is between eliminating 'wrong' phenotypes and selecting 'right' phenotypes is is beyond me, it seems purely semantic. This is especially a problem since what is the 'wrong' phenotype is determined by a number of environmental factors one of which is the rest of your population, so there is nothing to stop the criteria for a 'wrong' phenotype shifting as one might expect in some form of directional selection.
Phenotypes do not change to “fit” their environment as a result of “correct” sequences of mutation
This isn't a claim which is made, there is no hypothetical "correct" sequence, there is just what works and what doesn't and some things work better than other in certain conditions.
Rather, the environment provokes organismal (plant and animal) change via stress. Since the cause of cell function disruption is random, the resultant mutation’s effects on the regulation of development and its ultimate phenotypic expression are also random.
This could apply to almost any scale of mutation. The only 'unique' thing about this theory seems to be the blending of the stress induced mutation models common in bacterial studies with some sort of large scale make or break level of catastrophic mutation, such as you might see with large scale chromosomal rearrangements or wholesale duplications.
TTFN,
WK
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