Evolution, 4th Edition

280 CHAPTER 11

patches before becoming extinct. This lifestyle favors the evolution of early repro-

duction, so many weeds have evolved to mature at a young age. Common ragweed

(Ambrosia artemisiifolia), an American plant that is invading Europe and produces

pollen that is a major cause of hay fever, colonizes road edges and other disturbed

soils. Its seeds germinate in late spring and it flowers in early fall, just 4–5 months

later. In contrast, some oak trees do not mature for several decades.

In a sexually reproducing population, we can also use a life table to find the

fitness of an allele. For the survivorship (lx) and fecundity (mx) entries, we use the

average values in males and females for individuals that carry the allele. Alleles

with larger values of R have higher fitness and will spread. (Again, a correction

is needed if R is much different than 1.) Suppose a mutation appears in a popula-

tion that has the life table we just looked at. The mutation increases the average

fecundity of both males and females at age 2 from 1 to 1.2 offspring. That increases

l 2 m 2 from 0.5 to 0.6, and so R increases from 1 to 1.1. The mutation has higher fit-

ness than the other allele at the same locus (which has R = 1). The mutation will

increase in frequency, causing the life history of the population to evolve and the

growth rate R to increase.

Senescence

Our life table illustrates a general point: natural selection does not act to prolong survival

beyond the last age of reproduction. In the life table above, a mutation that increases

the chance of survival to age 4 from 0 to 0.25 has no effect on R, because females

do not reproduce at that age. (There are a small number of interesting exceptions.

In humans and orca whales, postreproductive parents care for their offspring, so

postreproductive survival may be advantageous [15, 19].) But why should reproduc-

tion cease? Why do women experience menopause, and older men have lowered

sperm production and sex drive? The answer is that, all else being equal, the selec-

tive advantage of reproducing declines with age.

Increasing survival and fecundity at earlier ages has a larger effect on fitness

than at later ages, simply because predators, disease, and all sorts of accidents

make individuals less likely to survive to the later ages. In the discussion of the life

table above, we saw that a mutation that increases fecundity at age 2 from 1 to 1.2

increases fitness, R, from 1 to 1.1. Now consider a second mutation that increases

fecundity by the same amount at age 3 instead of age 2, increasing l 3 m 3 from 0.5 to

0.55. Comparing the life tables for the two mutations, we have:

First mutation Second mutation

x lx mx lx mx lx mx lx mx

0

1

2

3

4

1

0.75

0.5

0.25

0

0

0

1.2

2

0

0

0

0.6

0.5

0

1

0.75

0.5

0.25

0

0

0

1

2.2

0

0

0

0.5

0.55

0.00

R: 1.1 R: 1.05

We see that the second mutation increases R from 1 to 1.05. This is a smaller

increase in fitness than that for the first mutation, because a smaller number of

individuals survive to age 3 than to age 2.

The principle that increasing survival and fecundity at earlier ages has a larger

effect on fitness than at later ages is the basis of the two major factors respon-

sible for the evolution of senescence and life span. One, first identified by Peter

Medawar [36], is mutation accumulation: mutations that compromise biological

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