Aging and Sex, DNA Repair in
79
complex in humans and these are vulnera-
ble to such problems as ectopic pregnancy
and venereal diseases. Further, courtship
activities are costly. Even at the micro-
scopic level in humans, genetic processes
for determining sexual development are
easily perturbed with one sex chromo-
some too few or too many, or a shift in
the hormone balance of a fetus, causing
abnormalities in physiology and behavior.
Clearly sex has large costs.
3.4
Benefts oF Sex
Sex must have a large bene±t to make up
for its large costs. A major function of sex
is to counteract two types of ‘‘noise’’ in
the transmission of genetic information
from parent to progeny: DNA damage and
mutation.
As pointed out in Section 1.1, about
95,000 DNA damages occur, on aver-
age, per day per cell in the rat. Most
of these are single-strand damages that
can be removed by excision repair or
other repair processes that only need the
redundant information present on the op-
posite strand of DNA. However, excision
repair of single-strand damages is not
100% ef±cient, and double-strand dam-
ages also occur at signi±cant frequencies
(Table 1). Such DNA damages remaining
in germ cells (e.g. egg and sperm, in mam-
mals) would cause the death of zygotes
and loss of potential progeny. During the
meiotic stage of the sexual process, how-
ever, HRR is strongly enhanced by the
systematic homologous pairing of chro-
mosomes, the major feature of meiosis.
This enhanced HRR repair is one ma-
jor bene±t that can compensate for the
costs of sex, since clearing the germ line
of lingering damages can greatly increase
viability of progeny.
The other type of noise in the transmis-
sion of genetic information from parent to
progeny is mutation. Mutation is quite dif-
ferent from DNA damage. A mutation is a
change in the DNA sequence rather than
a change to a deformed DNA structure
(DNA damage). Mutation and DNA dam-
age have distinctly different consequences.
Mutations can be replicated (when DNA
replicates) and thus can be inherited,
w
h
i
l
ead
am
a
g
ec
a
n
n
o
tb
er
e
p
l
i
c
a
t
e
d
.
However, damages can be recognized by
enzymes and repaired, whereas mutation
cannot be recognized and thus cannot
be repaired.
Genes carrying mutations often code
for nonfunctional proteins. If one of a
pair of chromosomes in a diploid cell
carries a mutation in a given gene, and
the second chromosome carries the ho-
mologous gene in a functional form, this
second gene can usually provide an ad-
equate level of gene expression for the
organism to function normally. This mask-
ing of the expression of mutant genes
by wild-type genes is called
complementa-
tion
. Complementation is available in the
diploid phase of the life cycle of organ-
isms. However, complementation is most
bene±
c
ia
lwhenano
rg
an
i
smunde
rgoe
s
outcrossing.
To see why mutation makes it ben-
e±cial to have outcrossing, consider a
hypothetical population of diploid organ-
isms that is strictly inbreeding (all of the
organisms are self-fertilizing) and assume
that the population has been long estab-
lished. In such a population, the rate at
which new mutations arise will be bal-
anced by the rate at which they are lost
from the population by natural selection.
In this self-fertilizing population, each mu-
tation present in an individual will have a
one in four chance of being paired with
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