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

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Presentation on theme: "LIFE HISTORY EVOLUTION : Why do we get old and die?"— Presentation transcript:

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

2 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

3 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 What life history traits are favored by natural selection?

4 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

5 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

6 Evidence for trade-offs Reproductive events per lifetime Relationship between clutch size and offspring size Age at first reproduction

7 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

8 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

9 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

10 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?

11 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)

12 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

13 "K"-Selected populations - If juvenile mortality is high compared to adult mortality: Iteroparous reproductionReproductive delay Small brood sizesLarge 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 Overall: a simplification

14 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

15 Surviorship Curves Probability of surviving to next year is high-->K- selected Probability of surviving longer is low--> r-selected

16 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

17 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 levels- marsupials have lower metabolic rates than comparably-sized placental mammals. but shorter life spans

18 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

19 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

20 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

21 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

22 Evolutionary Explanations for Aging An organism’s lifespan is determined by balancing the trade- off 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

23 Life History Evolution- a natural experiment Virginia opossums Mainland Population High extrinsic mortality- dogs,bobcats, etc. Island Population Low extrinsic mortality- no mammalian predators Performance of mainland mothers decreases in second year (reproductive senescence)

24 Life History Evolution- a natural experiment Virginia opossums Mainland Population High extrinsic mortality- dogs,bobcats, etc. Island Population Low extrinsic mortality- no mammalian predators Island possums have delayed senescence and longer lifespans Island females have slower rate of physiological aging (collagen crosslinks reduce flexibility and increase with age)

25 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

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