Aging and Other Life History
Characters
Chapter 12
1
What is life history?
• Life histories describe:
–
–
–
–
–
Age at maturity (age of 1st reproduction) (early or late)
Reproductive patterns (reproduce once or many times)
Number of offspring (many or few)
Size of offspring (large or small)
Life span (short or long)
• Life history is a description of the way in which
organisms realize their fitness
– “Life history components” are “fitness components”
2
Life histories and trade-offs
• Because the amount of energy than an organism
can harvest is finite, life histories inevitably
involve trade-offs:
– many small vs. few large offspring
– rapid reproduction and shorter life span vs. slower
reproduction and longer life span
• Natural selection should attempt to adjust the
allocation of energy between growth, metabolism,
repair, and reproduction in such a way as to
maximize total lifetime reproduction (= fitness)
3
The life history of a hypothetical female Virginia
opossum (Austad 1988, 1993) (fig. 12.2)
4
Life history theory attempts to answer
questions such as the following:
• Why do we age (senesce)?
• Why do some species reproduce only once while
other reproduce repeatedly?
• Why do some species have many small offspring
while others have only a few relatively large ones?
• Why do some take a long time to reach
reproductive maturity, others only a short time?
5
Aging and life span:
what is aging?
• Mortality senescence
Decrease in the probability of survival, per unit
time, as age increases
• Reproductive senescence
Decrease in reproduction with increasing age
6
Probability of survivorship, p
x
Survivorship Patterns
1
Senescent
0
Age
px is the probability of surviving from age x to x+1
7
Probability of survivorship, p
x
Survivorship Patterns
1
Senescent
Non-senescent
0
Age
px is the probability of surviving from age x to x+1
8
Probability of survivorship, p
x
Survivorship Patterns
1
Senescent
Anti-senescent
Non-senescent
0
Age
px is the probability of surviving from age x to x+1
9
Probability of mortality, q
x
Mortality Patterns
1
Senescent
0
Age
qx is the probability of dying in the age interval x to x+1 (= 1 - px)
10
Aging in collared flycatchers: natural population
(Gustafsson & Part 1990) (Fig. 12.4 a)
11
Aging in red deer: natural population
(Clutton-Brock et al. 1988) (Fig. 12.4 b)
12
Aging in D. melanogaster: laboratory population
(Rose 1984) (Fig. 12.4 c)
13
Rate-of-living theory of aging:
“live fast, die young”
• Aging is caused by accumulation of irreparable
damage to cells and tissues
• Damage is caused by errors in replication,
transcription and translation; and by toxic
metabolic by-products (oxidative damage, etc.)
• All organisms have been selected to resist and
repair cell and tissue damage to the maximum
extent physiologically possible. They lack the
genetic variation that would enable them to evolve
more effective repair mechanisms than they
already have.
14
Predictions of the rate-of-living theory of
aging
1) Because cell and tissue damage is caused in part
by the by-products of metabolism, the aging rate
should be correlated with the metabolic rate, or,
equivalently, different species (within broad
taxonomic groups) should have similar per gram
total lifetime energy expenditures
2) Because organisms have been selected to resist
and repair damage to the maximum extent
possible, species should not be able to evolve
longer life spans
15
The data suggest that prediction (1) is not upheld
(Austad & Fischer 1991) (Fig. 12.5)
Bats, in particular,
live almost 3
times longer
than other
mammals of
similar size and
metabolic rate
Marsupials have
significantly
lower
metabolic rates
than other
mammals of
the same size,
but also have
significantly
shorter life
spans
16
Experiments show that prediction (2) is not upheld
(Luckinbill et al. 1984) (Fig. 12.6)
Life span of D.
melanogaster is
easily increased
by selection in
the laboratory.
This means that
there is heritable
genetic variation
for life span.
17
The “telomere” theory of aging
• Telomeres are tandemly repeated nucleotide sequences that
are placed on the ends of eukaryotic chromosomes by the
enzyme telomerase (TTAGGG in humans)
• Telomeres are necessary because linear chromosomes
shorten with each round of replication. Without them,
chromosomes would erode away
• Telomerase is not expressed in most somatic cells
• This means that somatic cells can undergo a limited
number of mitotic divisions
• Under this theory, individuals age because they can no
longer replace damaged and worn-out cells
18
A prediction based on the “telomere” theory
of aging
• If life span is limited by the number of cell divisions, and
different species have similar numbers of cell divisions
before telomeres are eroded away, then the life spans of
whole organisms should be correlated with the life spans of
their constituent cells
19
Life span of
cells and
whole
organisms
(Rhome 1981)
(Fig. 12.7)
20
The paradox of aging – 1
• The rate-of-aging and telomerase theories address the
physiological, cellular and molecular causes of aging —
whether correct or not, they leave an important question
unanswered:
• If laboratory fruit fly populations can evolve longer life
spans, and bats have evolved longer life spans than other
mammals of similar size and metabolic rate, and genetic
engineers can increase the number of times cells can divide
by artificially increasing telomerase expression, why has
natural selection not produced longer life spans in all
species?
21
The paradox of aging – 2
• All other things being equal, longer life span and
high levels of reproduction into late age will equal
greater fitness. Given that aging (senescence)
reduces individual fitness and given that there is
genetic variance for life span, why doesn’t natural
selection reduce or eliminate aging?
• To answer this question, we need an evolutionary
theory of senescence
22
The evolutionary theory of
senescence
• Senescence occurs because the “force of
selection” declines with advancing age.
W. D. Hamilton 1966. The moulding of senescence by natural
selection. J. Theoret. Biol. 12:12-45
23
A verbal argument
1.
2.
3.
4.
Death before reproduction = zero fitness
Death after reproduction begins = greater than zero
fitness
Therefore: natural selection will work most effectively
against lethal mutations that kill before reproduction
begins, but less effectively against lethals that act later in
life.
If harmful genetic effects are expressed late enough in
life, selection against them will be negligible because
most individuals carrying the harmful alleles will already
have died from other causes (predation, accident, etc.)
24
A hypothetical non-senescent life history (constant
survivorship, constant reproduction for ages ≥ 3, all
individuals die before age 16) (Fig. 12.9 a)
25
A hypothetical non-senescent life history (constant
survivorship, constant reproduction for ages ≥ 3, all
individuals die before age 14) (Fig. 12.9 b)
26
A hypothetical non-senescent life history (constant
survivorship, constant reproduction for ages ≥ 2, all
individuals die before age 10) (Fig. 12.9 c)
27
Evolutionary genetic mechanisms
• Mutation accumulation
Peter Medawar (1952) — senescence due to
deleterious alleles with effects confined to late
ages — senescence evolves because natural
selection is powerless to prevent it
• Antagonistic pleiotropy (trade-offs)
George Williams (1957) — senescence due to
alleles with beneficial effects early in life but
deleterious pleiotropic effects late in life —
senescence is selectively advantageous
28
An implication of the evolutionary
analysis
• The rate of senescence of an organism
should evolve by natural selection in
response to environmental changes that alter
the schedule of survivorship and fecundity
— e.g., if the environmental force of mortality
declines so that survivorship to later ages is
increased, then selection should favor reduced
rates of senescence (and vice versa).
29
Experimental evolution of life span in D.
melanogaster
Wild population (S. Amherst, MA)
Laboratory population (IV)
(B. Charlesworth, 1975)
B selection
5 replicate populations (B1 – B5)
2 -wk discrete generations
O selection
5 replicate populations (O1 – O5)
10 – 12 wk discrete generations
(M. Rose, 1984)
30
Evolution of life span in laboratory populations of D. melanogaster (Service,
Michieli, and McGill. 1998. Evolution 52:1844-1850). “B” populations are maintained on
a 2-wk generation time and “O” populations are maintined on 10 – 12 wk generation times, which selects
for longer life span. The “b” parameter describes the rate of increase in mortality rate with age: higher
values equal more rapid mortality senescence. One-way ANOVA (df = 1, 7) was used to test for
differences between selection regimes. Life span: F = 207.36, P < 0.0001; b: F = 94.82, P < 0.0001;
Population
Cohort
size
Life span
(days)
b
Short-generation B1
B2
B3
B4
B5
B mean
231
167
231
196
235
26.3
26.2
22.4
24.8
27.4
25.4
0.280
0.318
0.309
0.274
0.243
0.285
Long-generation O2
O3
O4
O5
O mean
263
289
409
307
53.6
65.2
60.9
63.7
60.9
0.072
0.062
0.101
0.128
0.091
31
Mortality rate vs. age in fly populations that have
evolved different life spans
QuickTime™ and a
decompressor
are needed to see this picture.
•
•
QuickTime™ and a
decompressor
are needed to see this picture.
“B” flies are selected on short generation times; “O” flies are selected
on long generation times
(Service, Michieli, and McGill. 1998. Evolution 52:1844-1850)
32
Female egg laying vs. age in fly populations that have
evolved different life spans - evidence for antagonistic
pleiotropy between early age reproduction and life span
QuickTime™ and a
decompressor
are needed to see this picture.
•
•
“B” flies (solid squares) are selected on short generation times; “O”
flies (open squares) are selected on long generation times
(Service, Michieli, and McGill. 1998. Evolution 52:1844-1850)
33
Laboratory evolution of life span in D. melanogaster
(Luckinbill et al. 1984) (Fig. 12.6)
34
Increase in inbreeding depression with age is consistent with
the mutation accumulation mechanism of senescence (Hughes
et al. 2002) (Fig. 12.10)
35
Decrease in life
span in
houseflies
when adults
live ≥ 4 days is
consistent with
mutation
accumulation
(Reed and
Bryant 2000)
(Fig. 12.11)
36
Antagonistic pleiotropy in the age-1 gene of C.
elegans (Walker et al. 2000) (Fig. 12.12)
a) Frequency of life-extending hx546 allele with no food
shortage
b) Frequency of hx546 allele when environment is degraded
37
A phenotypic trade-off between early age and later
age reproduction in collared flycatchers (Gustafsson
& Part 1990) (Fig. 12.13)
a)
b)
Females that reproduce at age 1, have fewer offspring later in life
Females given extra offspring to raise at age 1, lay fewer eggs in
subsequent years
38
How many offspring should an individual produce in
a given year?
• Clutch size in birds and Lack’s hypothesis
(David Lack 1947)
• Clutch size should be such that it maximizes
the number of surviving offspring
39
A mathematical treatment of Lack’s
hypothesis (Fig. 12.16)
•
Given the relationship between clutch size and the probability of survival of individual
offspring, the clutch size that maximizes the number of surviving offspring is 5
40
Most birds lay smaller clutches than predicted by
Lack’s hypothesis
Clutch size and
number of young
per clutch in great
tits (Boyce and
Perrins 1987) (Fig.
12.17)
41
Reasons why birds may not behave according to
Lack’s hypothesis
• Lack’s hypothesis assumes that there is no trade-off between
reproduction in one year and the next
• Lack’s hypothesis assumes that the only effect of clutch size on the
offspring is through their survivorship
Clutch size of mothers
affects clutch size of
daughters in collared
flycatchers (Schluter &
Gustafsson 1993) (Fig.
12.18)
42