The evolution of senescence under curtailed life span in laboratory populations of Musca domestica (the housefly).

The evolution of senescence may be explained by two different, but not mutually exclusive, genetic mechanisms. The antagonistic pleiotropy hypothesis predicts that senescence is a consequence of the fixation of alleles with pleiotropic effects favouring early life fitness, but bearing a cost in later life. The mutation-accumulation hypothesis attributes senescence to the accumulation of deleterious mutations with late-acting effects on fitness in mutation-selection balance. Experiments were carried out on the housefly, Musca domestica, in which large and small populations were maintained so that reproduction was limited to four or five days after reaching sexual maturity. Longevity declined significantly under the husbandry protocol and was largely the same in large and small populations; this is consistent with the random accumulation of deleterious alleles affecting longevity under curtailed life span, although laboratory adaptation cannot be ruled out entirely as a causal mechanism. An analysis of life-history data did not provide evidence for a trade-off between longevity and age at sexual maturity, developmental time, or dry body weight, but there was an apparent trade-off between longevity and early progeny production, in support of antagonistic pleiotropy.