Transcript LIFE HISTORY EVOLUTION: Why do we get old and die?

LIFE HISTORY EVOLUTION:
Why do we get old and die?
Can life histories evolve through
natural selection?
• An organism’s life history is the stages it goes
through in its lifetime:
birth--> growth --> reproduction --> death
• Life history traits: # and size of offspring, age at
first reproduction, reproductive life span, etc.
• Hence, life histories include many components
that contribute to an individual’s fitness
What life history traits are favored by
natural selection?
• Selection favors genotypes that have higher
fitness: individuals that pass on more of their
genes to future generations
• Natural selection should favor individuals that
mature at birth, produce lots of high quality
offspring and live forever
So why don’t we live forever and
have millions of offspring?
• Energy/resources are limiting!!!
• This sets up TRADE-OFFS between
different life history traits
• Energy/resources devoted to one
function can’t be used for others
The cost of reproduction
• The trade-offs between current reproduction
and other components of fitness is referred to
as the cost of reproduction
• Fundamentally, differences in life histories
concern differences in the allocation of
resources to different life history traits
Evidence for trade-offs
Relationship between
clutch size and
offspring size
Reproductive events per lifetime
Age at first reproduction
Natural selection will act on life histories
to adjust energy/resource allocation to
maximize TOTAL lifetime fitness
• Evolutionary biologists studying life histories are
interested in understanding factors that favor
different LIFE HISTORY STRATEGIES
• The following are some examples of different life
history strategies
Parthenogentic aphids may
carry embryos even before it
is born
A blue whale gives birth
To a single offspring the
Weight of an adult
elephant
Bristlecone pine trees can
live to be 4600 years old
Brown kiwi birds lay a single
egg that can be up to 20% of the
female’s body weight
Let’s look at 2 specific life history
traits:
• Age Schedule of Reproduction
– When and how often should an organism
reproduce?
• Life Span and Senescence
– How long does an organism live?
Age schedule of Reproduction
• Semelparity: individuals reproduce
once and then die (annual plants,
salmon, century plants)
• Iteroparity : individuals reproduce
more than once over their lifetimes
(humans, elephants, perennial
plants, most animals)
When is iteroparity selected for?
When is semelparity selected for?
• If juvenile mortality is high compared to adult
mortality --> i.e., once you make it to
maturity, you have a good chance of living
longer
– Keep on reproducing: iteroparity
• If adult mortality is high compared to juvenile
mortality --> i.e., once you reach maturity,
your time is near
– Go for it why you can: semelparity
Overall: a simplification
• "K"-Selected populations
- If juvenile mortality is high compared to adult mortality:
Iteroparous reproduction
Reproductive delay
Small brood sizes
Large eggs
Characters that result in a low intrinsic rate of increase
Such populations tend to find an equilibrium near K (carrying
capacity)
• “r”-Selected populations
-If populations tend to experience many periods of
exponential growth or high adult mortality selection may favor:
Semelparous (or at least early) reproduction
Fast development
Large brood sizes
Such populations tend to maximize their intrinsic rate of increase,
r
Trinidad Guppies (David Reznick)
Reznick transplanted
guppies from a low
predation stream into
a high predation
stream (w/cichlids) in
Trinadad
High juvenile
mortality
High adult
mortality
Probability of
surviving to next
year is high-->Kselected
Probability of
surviving longer is
low--> r-selected
Surviorship Curves
Evolution of Life Span and
senescence
• We need to distinguish between:
– Senescence/aging: physiological
degeneration and death over time
– Extrinsic mortality: death due to predation,
disease, etc.
• All else being equal, aging should be
opposed by natural selection
A Non-Evolutionary Explanation for Aging
• Hypothesis I: aging is a byproduct of accumulation of
damage to cells and tissues- “RATE OF LIVING” or
“PARTS WEAR OUT”
•Predicts:
– Damage is a byproduct of
metabolism - aging and
metabolic rates should be
positively correlated
–Ability to replace or repair
has been maximized by
selection - species are
constrained from evolving
longer life spans
Selection for longer
life in flies yields
response (2x in 13
generations)contradicts rate of
living hypothesis
No evidence at broad taxonomic levelsmarsupials have lower metabolic rates than
comparably-sized placental mammals. but shorter
life spans
Evolutionary Explanations for Aging
• If selection can produce longer life spans, why don’t
organisms evolve them?
• Hypothesis 2: Accumulation of deleterious mutations
• Medawar (1946) - selection on genes that have negative
effects late in life (“aging genes”) is low because many
individuals are already dead due to environmental causes by
the time they show their effects
• Selection is weak on old individuals, so mutations with
deleterious effects late in life are not removed by selection
Evidence for Mutation-Accumulation Hypothesis
• Inbreeding depression exposes
recessive deleterious alleles
• If mutation-accumulation hypothesis
is true, inbreeding depression
(reduction in fitness due to
inbreeding) should increase with age
(Hughes et al, 2002)
• I.e., there are more mutations that
affect individuals late in life
Evolutionary Explanations for Aging
• Hypothesis 3: Antagonistic Pleiotropy
• Williams (1957) - genes with two effects (pleiotropy)
• “Aging” genes may be those that are advantageous
effect in youth but disadvantageous in old age:
– Such genes would be selected for as many individuals will
benefit from its advantages in youth
– but fewer will suffer its disadvantages in old age
Evolutionary Explanations for Aging
• Hypothesis 3: Antagonistic Pleiotropy
• Genes that exhibit antagonistic pleiotropy:
– Age-1 in C. elegans
• Worms with hx546 mutation live longer, wildtype age-1 allele
increases early reproduction at expense of longevity
– Indy gene in Drosophila
• Indy loss of function mutants have 2x the lifespan as wildtypes
• Under restricted diets, wildtypes have higher fecundity
Evolutionary Explanations for Aging
• An organism’s lifespan is determined by balancing the tradeoff between allocation to repair and allocation to reproduction
• A decrease in extrinsic mortality may favor an increase in
allocation to repair --> delayed senescence (and vice versa)
• Austad (1993) followed opossums on mainland (South
Carolina) and island (Sapelo Island) populations that have
been isolated about 4500 yrs
Life History Evolution- a natural experiment
Virginia opossums
Mainland Population
Island Population
High extrinsic mortalitydogs,bobcats, etc.
Low extrinsic mortalityno mammalian predators
QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
Performance of mainland mothers decreases
in second year (reproductive senescence)
Life History Evolution- a natural experiment
Virginia opossums
Mainland Population
Island Population
High extrinsic mortalitydogs,bobcats, etc.
Low extrinsic mortalityno mammalian predators
QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
Island possums have delayed
senescence and longer lifespans
Island females have slower rate of
physiological aging (collagen
crosslinks reduce flexibility and
increase with age)
Don’t try this at home
• It may reduce your life
expectancy
• Studies have shown
that mating can reduce
the life span of female
Drosophila
• Male sperm induces
female to invest more in
her offspring at cost to
her longevity