Dh. Reed et Eh. Bryant, The evolution of senescence under curtailed life span in laboratory populations of Musca domestica (the housefly), HEREDITY, 85(2), 2000, pp. 115-121
The evolution of senescence may be explained by two different, but not mutu
ally exclusive, genetic mechanisms. The antagonistic pleiotropy hypothesis
predicts that senescence is a consequence of the fixation of alleles with p
leiotropic effects favouring early life fitness, but bearing a cost in late
r life. The mutation-accumulation hypothesis attributes senescence to the a
ccumulation 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 th
at reproduction was limited to four or five days after reaching sexual matu
rity. Longevity declined significantly under the husbandry protocol and was
largely the same in large and small populations; this is consistent with t
he random accumulation of deleterious alleles affecting longevity under cur
tailed life span, although laboratory adaptation cannot be ruled out entire
ly 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, deve
lopmental time, or dry body weight, but there was an apparent trade-off bet
ween longevity and early progeny production, in support of antagonistic ple
iotropy.