How To BE FiT 281
functions reduce fitness less, the later in life they exert these effects. That is, selec-
tion against these mutations is weaker, and so they persist at higher frequencies in
the population than if they affected younger individuals (see Chapter 5). Mutation
accumulation will cause the genetic variance for reproductive success to be greater
for older than for younger age classes. Exactly that pattern was found in a study of
a laboratory population of Drosophila melanogaster (FIGURE 11.5A) [27]. Studies in
several species of birds and mammals have found that mating between relatives
results in greater inbreeding depression expressed at later than at earlier ages [32].
Because inbreeding depression is caused by homozygosity for partially recessive
deleterious alleles, this pattern is consistent with mutation accumulation.
Because of allocation trade-offs, alleles that increase reproduction early in life
are likely to have a pleiotropic effect on reproduction or survival later in life. The
greater fitness impact of early reproduction causes the advantage of reproducing
when young to outweigh the pleiotropic disadvantages at greater ages. Therefore,
reproduction will be expected to dwindle with age, and perhaps to cease alto-
gether. The selective value of surviving to later ages likewise declines, finally to
zero. Based on this principle, George Williams proposed a second factor that can
explain senescence and limited life span: antagonistic pleiotropy [62]. Williams
suggested that a great many genes are likely to affect allocation to reproduction
versus self-maintenance—that is, they incur a cost of reproduction. Alleles that
increase allocation to reproduction (reproductive effort) early in life will thus
reduce function later in life.
Antagonistic pleiotropy can cause a negative relationship between early repro-
duction and both longevity and later reproduction. This has been found in many
selection experiments with Drosophila. For example, several investigators have
selected Drosophila populations for higher reproduction late in life (and therefore
were also selecting for long life) (FIGURE 11.5B) [43]. The flies evolved higher late-
life fecundity, but their egg production at younger ages was lowered—exactly as
expected under the pleiotropy hypothesis.
Although both antagonistic pleiotropy and mutation accumulation contribute to
senescence, many biologists think antagonistic pleiotropy is often the more impor-
tant factor. Both factors can affect many genes, so it is unlikely that a single cause
of senescence can ever be found.Evolution of the Population Growth Rate
and DensityThe values of survival and fecundity in a life table are affected by ecological
conditions. We have seen that mutations that increase R will spread through aFutuyma Kirkpatrick Evolution, 4e
Sinauer Associates
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Evolution4e_11.05.ai Date 11-22-2016Genetic variance forreproductive success 00.040.080.120.16(A) (B)Fecundity1 2 3 4 5
Age (weeks)4081216Baseline
populationSelected to reproduce at young age
Selected to reproduce at old age7 14 21 28
Age (days)FIGURE 11.5 Evidence for two hypotheses
for the evolution of senescence and life span.
(A) The genetic variance for reproductive
success increases with age in Drosophila me-
lanogaster, as expected under the mutation
accumulation hypothesis. (B) Several labora-
tory populations of Drosophila were selected
for reproduction at a young age (by propa-
gating offspring only from young parents) or
for reproduction at an older age (by growing
flies only from eggs laid by old females). Flies
from the old-selected populations laid fewer
eggs when they were young (1 week after
reaching adulthood), relative to the nonse-
lected baseline populations. This effect is
expected under the antagonistic pleiotropy
hypothesis. (A after [27]; B after [44].)11_EVOL4E_CH11.indd 281 3/22/17 1:11 PM