Ch 13 Evo Bio (Exam 3)

Life history analysis is the branch of

evolutionary biology that tries to sort out reproductive strategies

No organism can be perfect because there are

tradeoffs in time, size of offspring, and parental investment

Thrips egg mites:

• born already inseminated by mating with brothers inside mothers body

• these offspring eat their way out of their mother

Brown kiwis:

• lay eggs 1/6 of their body weight

• chicks are self-reliant within a week

• takes one month for female to produce each egg

In life history analysis, organisms

may grow to a large size to make large offspring or reproduce earlier at a small size to make

For organisms that wait before reproducing,

the chance of dying is higher

Virginia opossums:

• first litter of ~8 offspring

• months later has a second litter of ~7

• at 20 months theyre killed by predators

Natural selection optimizes energy allocation in a way that

maximizes total lifetime reproduction

Sand crickets are either

short-winged or long-winged

Sand cricket short-winged individuals devote more energy to

reproduction and less to flight

Senescence means

late life decline of fertility and probability of survival

Aging reduces an individual’s

fitness and should be opposed by natural selection

The two hypotheses on aging

• rate-of-living hypothesis

• evolutionary hypothesis of aging

In rate of living hypothesis, senescence is caused by

accumulation of irreparable damage to cells and tissue

All organisms have been selected to resist and repair

damage as much as physiologically possible

• but theres a limit of possible repair

Aging damage is caused by

errors during replication, transcription, translation, and by accumulation of poisonous metabolic byproducts

Two predictions of rate-of-living hypothesis

• because damage is partially caused by metabolic by-products, the aging rate should be correlated to metabolic rate

• because organisms have been selected to repair the maximum possible, species should not be able to evolve longer life spans

In rate-of-living hypothesis, populations lack

genetic variation needed to enable more effective repair mechanisms

Austad and Fischer tested the

first rate-of-living prediction

• because damage is partially caused by metabolic by-products, the aging rate should be correlated to metabolic rate

How did Austad and Fischer test the first rate-of-living hypothesis prediction?

• calculated amount of energy expended per gram of tissue per lifetime for 150+ mammal species

• should expend the same amount regardless of length of life

What did Austad and Fischer find?

that there was great variation in energy expenditure

Luckinbill tested the

second rate-of-living hypothesis prediction

• because organisms have been selected to repair the maximum possible, species should not be able to evolve longer life spans

How did Luckinbill test the second rate-of-living hypothesis prediction?

• artificially selected for longevity in fruit flies

• increased life span from 35 days to 60 days

What did Luckinbill find?

that the long-lived fruit flies have lower metabolic rates during the first 15 days of life

Both predictions in the rate-of-living hypothesis are

not supported by experimentation

Senescence may result from

chromosome damage

Telomeres of chromosomes consist of

tandem repeats that are added by the enzyme telomerase

• overactive in cancer cells

Instead of focusing on the whole organism in the rate of living hypothesis, we should examine

energy expenditure on cells and chromosomes of an organism

Normal animal cells are capable of

a finite number of divisions before death

• all cells except cancer, germ line, and stem cells

Progressive telomere loss is associated with

senescence and death

Cells die because

chromosomes are too damaged to function

In the rate-of-living hypothesis, life spans of mammals are

correlated with life spans of skin and blood cells

Why doesnt natural selection active telomerase to add more telomeres?

because it could be a tradeoff between extending cell life and proliferating cancer

p53 is a

gene that causes cell senescence

Deficiency in p53 causes

cancer susceptibility

In the evolutionary hypothesis of aging, aging is not

caused by damage itself but the failure to repair the damage

Damage isnt repaired in the evolutionary hypothesis because of

deleterious mutations or tradeoffs between repair and reproduction

Evolutionary hypothesis of aging can cause

senescence and death with a few fitness consequences

Evolutionary hypothesis of aging states that

cancers that usually occur late in life only slightly affect fitness of the individual

In evolutionary hypothesis of aging, some individuals reproduce so much earlier that

early death is not selected against

• ex: mutation accumulation hypothesis

Mutation accumulation hypothesis is the

tradeoff between early reproduction and survival late in life

The mutations in the mutation accumulation hypothesis devotes

less to repair and more to reproduce

Example of evolutionary hypothesis of aging

the heat-shocked protein hsp70

The heat-shock protein hsp70

prevents damage due to denaturation

Hsp70 binding interferes with

normal cellular functions

Heat-shocked genes (hsp70) are

only expressed during environmental stress

Expression of hsp70 is seen in Drosophila and

causes longer life span but lower reproduction early in life

The tradeoff between early fecundity and late survival is mediated by

the hsp70 protein

Collard flycatchers in evolutionary hypothesis of aging example

• theyre polymorphic when they begin reproduction

• birds at age 1 have smaller clutch sizes throughout life

• birds at age 2 have larger clutch sizes throughout life

Collard flycatchers first year breeders have

a higher reproductive success

Austad compared Virginia opossums on the

mainland and on an island

• on the mainland, they have high ecological mortality rates

• on island there are no predators

Island female opossums

• showed delayed senescence in month-to-month probability of survival

• showed delayed senescence in reproductive performance

• showed delayed senescence in connective tissue physiology

The opossum island population should have

evolved delayed senescence

Natural experiment in aging is currently

the best explanation for life history variation

The more offspring a parent attempts to raise at once,

the less time and energy the parent can spend on each of them

David Lack’s hypothesis

selection will favor clutch size that produces the most surviving offspring

In David Lack’s hypothesis, the number of surviving offspring

reaches a maximum at intermediate clutch sizes

Boyce and Perrins tested

Lack’s hypothesis

• the tit study

What did Boyce and Perrins find with Lack’s hypothesis?

it wasnt consistent with the hypothesis

Assumptions of Lack’s hypothesis

• no tradeoff between parent’s reproductive effort in one year and survival and reproduction in the future

• the only effect of clutch size on offspring is determining whether offspring survive

• clutch size is fixed by a particular genotype

Lack’s hypothesis serves as a

valuable null model in predicting clutch size

Parasitoid wasps

• inject their eggs into a host insect

• the larvae eats the host, pupate, and emerge

• host insect is analogous to a nest

Lack’s hypothesis for parasitoid wasps

• larger clutches may reduce female fitness

• might be a tradeoff in current and future reproduction and survival

While a female parasitoid wasp searches for a host,

her fitness is 0

• must incorporate fitness gained by the number of eggs laid on one host before leaving

Lack’s hypothesis is a good starting point for

evolutionary analysis of clutch size

Principle of Allocation states that

if organisms use energy for one function, the amount of energy available for other functions is reduced

We have been assuming that size of offspring is constant. true or false

false

Smith and Fretwell’s analysis assumptions

• tradeoff between size and number of offspring

• individual offspring survival is correlated to size

You’re able to test Smith and Fretwall’s analysis if

there is a high polymorphism in offspring size in a population

Optimal offspring size for parents is

often smaller than optimal size for offspring

• offspring always want to be bigger to survive better

• parents want to ration out resources to all offspring

Phenotypic plasticity in beetle egg size

• seed beetle lays eggs on various seeds

• larvae burrow inside, feed, and pupate

Fox studied

seed beetle grown on acacia and palo verde seeds

What did Fox find?

• acacia is a good host (most larvae survive)

• palo verde is a poor host (less than half survive)

• females lay larger eggs on palo verde than acacia

Unless there is pure monogamy,

males are only related to some of the female’s offspring

Genomic imprinting

occurs during gamete production in ovaries and testes

Imprinting affects

transcription in embryo

IGF-II gene is the

insulin-like grown factor II

IGF-II gene only has

the paternal copy transcribed

The paternal hormone is a

cell division stimulant and binds to the IGF-II receptor

The maternal allele codes for

an alternative IGF-II binding site

• CI-MPR receptor

The CI-MPR receptors job is to

bind excess IGF-II and equalize the flow of resources to each embryo

Mother and father have a tug-of-war at the

placental and embryonic levels to devote resources to particular embryos

CI-MPR does not

bind IGF-II in amphibians and birds

CI-MPR evolved after

the placenta

Snowy campions in north America

• evolved since their introduction (invasive species)

• germinate earlier, grew faster, made more flowers, and survived longer

• because they have no predators

Snow Campions in Europe

have higher fitness against predators

As animals increase in body size,

clutch size usually decreases

Small clutches put organisms

at risk of extinction in poor environmental conditions