Aging and Other Life History Characters

1
Aging and Other Life History Characters

• Chapter 12

2
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

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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)

4
The life history of a hypothetical female
Virginia opossum (Austad 1988, 1993) (fig. 12.2)
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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?

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Aging and life spanwhat is aging?

• Mortality senescence
• Decrease in the probability of survival, per unit
  time, as age increases
• Reproductive senescence
• Decrease in reproduction with increasing age

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Survivorship Patterns

• px is the probability of surviving from age x to
  x1

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Survivorship Patterns

• px is the probability of surviving from age x to
  x1

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Survivorship Patterns

• px is the probability of surviving from age x to
  x1

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Mortality Patterns

• qx is the probability of dying in the age
  interval x to x1 ( 1 - px)

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Aging in collared flycatchers natural population
(Gustafsson Part 1990) (Fig. 12.4 a)
12
Aging in red deer natural population
(Clutton-Brock et al. 1988) (Fig. 12.4 b)
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Aging in D. melanogaster laboratory population
(Rose 1984) (Fig. 12.4 c)
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Rate-of-living theory of aginglive 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.

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Predictions of the rate-of-living theory of aging

• 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
• 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

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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

17
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.
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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

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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

20
Life span of cells and whole organisms (Rhome
1981) (Fig. 12.7)
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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?

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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
  doesnt natural selection reduce or eliminate
  aging?
• To answer this question, we need an evolutionary
  theory of senescence

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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. 1212-45

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A verbal argument

• 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.)

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A hypothetical non-senescent life history
(constant survivorship, constant reproduction for
ages 3, all individuals die before age 16)
(Fig. 12.9 a)
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A hypothetical non-senescent life history
(constant survivorship, constant reproduction for
ages 3, all individuals die before age 14)
(Fig. 12.9 b)
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A hypothetical non-senescent life history
(constant survivorship, constant reproduction for
ages 2, all individuals die before age 10)
(Fig. 12.9 c)
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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

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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).

30
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)
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Evolution of life span in laboratory populations
of D. melanogaster (Service, Michieli, and
McGill. 1998. Evolution 521844-1850). 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 lt 0.0001 b F 94.82, P lt
0.0001 Population Cohort Life
span b size (days) Short-generation
B1 231 26.3 0.280 B2 167 26.2 0.318 B3 231 22.4
0.309 B4 196 24.8 0.274 B5 235 27.4 0.243 B
mean 25.4 0.285 Long-generation
O2 263 53.6 0.072 O3 289 65.2 0.062 O4 409 60.9
0.101 O5 307 63.7 0.128 O mean 60.9 0.091
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Mortality rate vs. age in fly populations that
have evolved different life spans

• B flies are selected on short generation times
  O flies are selected on long generation times
• (Service, Michieli, and McGill. 1998. Evolution
  521844-1850)

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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

• 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
  521844-1850)

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Laboratory evolution of life span in D.
melanogaster (Luckinbill et al. 1984) (Fig. 12.6)
35
Increase in inbreeding depression with age is
consistent with the mutation accumulation
mechanism of senescence (Hughes et al. 2002)
(Fig. 12.10)
36
Decrease in life span in houseflies when adults
live 4 days is consistent with mutation
accumulation (Reed and Bryant 2000) (Fig. 12.11)
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Antagonistic pleiotropy in the age-1 gene of C.
elegans (Walker et al. 2000) (Fig. 12.12)

• Frequency of life-extending hx546 allele with no
  food shortage
• Frequency of hx546 allele when environment is
  degraded

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A phenotypic trade-off between early age and
later age reproduction in collared flycatchers
(Gustafsson Part 1990) (Fig. 12.13)

• 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

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How many offspring should an individual produce
in a given year?

• Clutch size in birds and Lacks hypothesis (David
  Lack 1947)
• Clutch size should be such that it maximizes the
  number of surviving offspring

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A mathematical treatment of Lacks 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

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Most birds lay smaller clutches than predicted by
Lacks hypothesis
Clutch size and number of young per clutch in
great tits (Boyce and Perrins 1987) (Fig. 12.17)
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Reasons why birds may not behave according to
Lacks hypothesis

• Lacks hypothesis assumes that there is no
  trade-off between reproduction in one year and
  the next
• Lacks 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)