Reproductive Lifespan
& Ageing
Reproductive Value
•
Expectation of offspring from a female of age A to the end of
her life
RV weighs contribution of individuals of different age to pop growth
beyond that age
1.
•
Has into account having survived to age A to reproduce, prob of
surviving beyond A and associated fecundity
2.
RV compares sensitivity of fitness to events at different ages
3.
When pop grows, offspring produced later contribute less to fitness,
because older offspring may be reproducing already (new offspring
is discounted by rate of pop growth and delay of their birth)
RV is defined relative to newborn females which is 1
4.
Cole’s Paradox (1954)
“101 offspring at age 1 = 100 offspring forever”
•
•
•
•
•
Annual vs perennial (semelparous vs iteroparous)
No mortality
Charnov & Shaffer 1973: allow for varying juvenile and adult
mortality:
Ba = Bp + (P/C)
P = adult mortality
C = juvenile mortality
“Degree of Itoreparity”
Cole’s Paradox (1954)
Stearns 1976
Physiological Trade-offs: Cost of reproduction
(Lifespan vs Reproduction)
r is maximized when the trade-off curve
of births vs survival intersects with the
straight line farthest to the right
Stearns 1976
Vi = reproductive value at age I
r, pop growth rate is constant
r is maximized when the trade-off curve
of births vs survival intersects with the
straight line farthest to the right
Stearns 1976
Stearns 1976
Senescence
• Why do organisms age and die?
• Senescence – deteriorative changes that occur in an
individual with increasing age
– A decline in age-specific survival probability
– A decline in age-specific reproductive rate
• Senescence is a life history phenomenon
Senescence
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Senescence
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Senescence
•
•
Aging reduces fitness!
Why isn’t there strong
selection against aging?
• The “rate-of-living” hypothesis
for aging
– Aging is caused by irreparable
damage to cells and tissues
– Organisms have been selected
to repair damage to the
maximum extent
physiologically possible
• i.e., there is no genetic variation
left to select for “better” repair
mechanism
Predictions:
• Cell and tissue damage is
caused in part by metabolic byproducts, therefore the aging
rate should be correlated with
metabolic rate
• If species have no genetic
variation to enhance repair
mechanisms, species should
not be able to evolve longer
life spans due to either natural
or artificial selection
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Senescence
•
•
•
•
•
Tests of the 1st prediction by
Austad and Fischer (1991):
Does lifespan correlate with
metabolic rate?
Calculated energy expended
per gram of tissue per lifetime
For 164 mammal species from
14 Orders
If the hypothesis is true, this
value should be constant
among species
No support for the “rate-of-living” hypothesis
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Senescence
•
•
•
•
Test of second prediction
(inability to select for longer life
spans)?
Data from Luckinbill et al.
(1984) for Drosophila
melanogaster
Artificial selection for: Early
reproduction (2-6 days after
emergence)
Late reproduction (22 days
after Emergence or more)
No support for the “rate-of-living” hypothesis
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
http://ic.ucsc.edu/~whs68/bio150/07LifeTableLifeHistory.pdf#search=%22life%20history%20strategies%20age%20size%20at%20maturity%22
Evolutionary hypothesis
• Aging is not necessarily due to cellular and tissue damage, but is
instead associated with failures to completely repair damage
• Argues that complete repair should be feasible?
• Incomplete repair may be due to
– Deleterious mutations
– A trade off between repair and reproduction
http://ic.ucsc.edu/~whs68/bio150/07LifeTableLifeHistory.pdf#search=%22life%20history%20strategies%20age%20size%20at%20maturity%22
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Evolution of senescence
fecundity, mx
Pr(survival), lx
•Mutation accumulation
•Antagonistic pleiotropy
reproductive value, Vx
age, x
age, x
age, x
A life-history
table example
Because few
individuals survive to
age 14 anyway, there
is little selection
against the late-acting
deleterious allele:
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
…the forces of natural selection weakens with
increasing age …. If a genetical disaster… happens
late enough in individual life, its consequences may
be completely unimportant.
Even in such a crude and unqualified form, this
dispensation may have a real bearing on the origin
of innate deterioration with increasing age.
Medawar, 1952
Inbreeding depression more pronounced at
older ages. (from Hughes et al. 2002)
Inbreeding depression calc: (Wout −Win) /Wout
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Williams 1957
reproductive value, Vx
Mutation Accumulation
•effect of deleterious
mutations on fitness depends
on the age at which they are
expressed
•weight by Vx
frequency of mutations
age, x
•Mutations accumulate
later in life because little
detrimental effect on
fitness
•Selection on interacting
loci to shift time of
expression
age, x
Stearns 1990
Antagonistic Pleiotropy
Trade-offs between early- and late- age effects
fecundity
survival
age, x
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Evidence for Antagonistic Pleiotropy
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Evidence for Antagonistic Pleiotropy
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
Evidence for Antagonistic
Pleiotropy
A natural experiment on the
evolution of aging with the
Virginia Opossum (Austad 1993)
• Sources of mortality:
– Ecological
– Intrinsic
• In populations with low
ecological mortality, selection
may favor delayed senescence
(and eliminate deleterious lateacting alleles)
• Study compared island
population (low ecological
mortality) to mainland
population (high ecological
mortality)
http://www.biology.usu.edu/courses/biol5250-miller/pdfs/Lecture%2021-22%20Aging%20and%20life%20history%20attributes.pdf#search=%22life%20history%20aging%20lecture%22
mutation
survival
onset of
reproduction
effect on fitness
---
negative
---
positive
---
negative
---
positive
positive
no pleiotropy
no trade-off
negative
trade-off
favored
because of
effects on fitness
Evidence of Antagonistic Pleiotropy in
Drosophila
Rose and Charlesworth 1984 Genetics
•select for increased early (day 1-5) or late (day 21-25) fecundity
•did not select directly on lifespan
•Lines selected for late fecundity had significantly less early oviposition
and significantly higher late oviposition than lines selected for early fecundity
Rose 1984