From these theoretical arguments, it appears that a theory involving deleterious mutation pressure alone as the cause for senescence is not consistent with mortality plateaus far below 100%.
Further, classic ideas about mutation pressure (Mukai et al.
Further, female early-age mortality increased nearly 2% per generation under mutation pressure (Pletcher et al.
They do not imply that the mortality curve will no longer change under mutation pressure, but when mutational effects are small it will always tend to converge on these values.
Thus, the decline of early age mortality results in a net mutation pressure in favor of increasing mortality rates at older ages.
Perhaps the most conspicuous of these is the nature of the directed mutation pressure. In Osawa's view, G+C content is a neutral trait that reflects the mutation spectum.
much of the variation in codon usage between species is due to mutation pressure. He does not discuss or even cite any of the work of Michael Bulmer, Adam Eyre-Walker, Paul Sharp, Hiroshi Akashi, and others, which has shown that codon usage evolution is quite complex, involving translation efficiency, accuracy, and various pleiotropic effects collectively called "conficting selection" by Eyre-Walker.
Mutation pressure is not the only force that could maintain variation in viability, and we do not discount the possibility of temporal or spatial variation in selection pressures.
Following the logic in previous paragraphs, it is clear that deleterious
mutation pressure in the origin of replication could produce such a situation, because the relationship between !Mathematical Expression Omitted^ and s is U-shaped.
