Bio 315 test 6 part 3

In Virginia Oppossum A female might stop allocating energy to growth at an earlier age, thereby reaching sexual maturity more quickly. What are the tradeoffs

◦Trade-off: the female matures at a smaller size, which means that she will produce smaller litters. •Alternatively a female might, after reaching sexual maturity, allocate less energy to reproduction and more to repair damaged tissues, thereby keeping her body in better condition and living longer. ◦Trade-off: Allocating less energy to reproduction means smaller litters. Natural selection acts on life histories to adjust time and energy allocation in a way that, given local environmental conditions, maximizes the total lifetime production of offspring.

What is version B of the rate of living and theory of aging

(F&H Ch. 13.2) Prediction: Aging is caused by the irreversible damage to DNA caused by the division of cells and chromosomes. •Under this hypothesis, normal animal cells are capable of only some limited number of divisions (and duplication of their chromosomes). •As a result, it's not the rate of energy expenditure, but rather the rate of cell division that causes aging. Question: What kind of mechanism might limit the number of divisions in a cell lineage?

Question: Is it surprising that a mutation that causes death is only mildly deleterious? Question: Would a mutation at age 2 be more strongly selected against?

(Yes, is very deleterious). •Mutations causing early death are highly deleterious because lifetime RS is low or even none. •In contrast, mutations causing death late in life, after reproduction has begun, are selected against less strongly.

what are two examples of energy time tradeoffs

1.An individual can maximize size and/or condition at reproduction by allocating energy to growth for a long time. ◦The benefit: Reach a larger a size so that once mature can produce of more or larger offspring. ◦The cost or trade-off: An individual that takes a long time to grow is exposed for a longer time to predators, disease, or accidents, before reaching reproductive maturity, and thus incurs a greater risk of never having reproduced at all. 2.An individual can minimize time to reproductive age by shifting energy to reproduction at a younger age. ◦The benefits: ◦Begin reproduction sooner and perhaps produce more offspring over lifespan. ◦Less likely to die with out having reproduced at all. ◦The costs or trade-offs: ◦Mature at smaller size and so produce smaller or fewer offspring with each bout of reproduction. ◦Early maturation may lead to decreased lifespan, which can limit total reproductive success.

Prediction: Under the Evolutionary Theory of Aging, failure to completely repair damage is ultimately caused by either:

1.Deleterious mutations. 2.Trade-offs between repair and reproduction.

With antagonistic pleiotropy, expected lifetime RS with this mutation is RS = ___ that is 10% better than without the mutation (see Figure 13.10a).

2.66 •The benefits of early reproduction outweigh the cost of early senescence since few individuals live past 10 years. •Therefore, this mutation will be favored by natural selection.

What is an example of mutations that could cause death but only in advanced age in humans?

A form of cellular damage that humans (and other organisms) must repair during the course of their lifetimes is DNA mismatch error. •Mismatched nucleotides can be created during DNA replication (or by chemical mutagens). ◦DNA mismatch error generates point mutations, small insertions and deletions. •Repair of these errors is performed by a suite of special enzymes. •If there are germ-line mutations in the genes that code for these DNA repair enzymes, the result can be the accumulation of mismatch errors in other genes, which in turn can result in cancer. Germ-line mutations in DNA mismatch repair genes in humans can cause a form of cancer called hereditary nonpolyposis colon cancer. •This cancer strikes from age 17 to 92, with a mean age at diagnosis of 48, relatively late in the human reproductive life span. Most people carrying mutations in genes for DNA mismatch repair enzymes do not suffer deleterious consequences of the mutations until well after the age at which reproduction begins. In an evolutionary sense this cancer is a manifestation of senescence that is caused by deleterious mutations. •These mutations persist in populations because they reduce survival only late in life, have relatively small effects on fitness, and so are not strongly selected against, despite ultimately being lethal. Question: Do such mutations accumulate in populations? Answer: They apparently do so quite rapidly. •See, for example, Reed and Bryant's (2000) study documenting the rapid accumulation of late-acting deleterious mutations in populations of houseflies (p.468 and Figure 13.12 of your textbook).

Why do organisms age or die?

Aging, or senescence, is a late-life decline in an individual's fertility and probability of survival. •All else being equal, aging reduces an individual's fitness. •Aging should therefore be opposed by natural selection.

Identifying and Testing the Assumptions of the Lack Hypothesis Assumption 1 AND an Example:

Assumption 1 Lack's hypothesis assumes that there is no trade-off between a parent's reproductive effort in one year and it's survival or reproductive performance in future years. •As we have seen in Section 13.2, however, reproduction often entails exactly such costs. Example - As shown in Figure 13.15b (see preceding lecture), when female collared flycatchers are given an extra egg in their first year, their clutch size in future years is lower than that of control females. When reproduction is costly and natural selection favors withholding energy for the future, the clutch size maximizing lifetime reproductive success will be less than the clutch size maximizing offspring production in any one reproductive bout.

Why is the fitness effect of this deadly mutation so small?

Because few zygotes survive to age 14 anyways, zygotes carrying the mutation do not suffer much of a fitness penalty. Because the reduction in fitness is small, the mutation is not selected against very strongly.

: Why do female wasps lay clutches smaller than predicted by Lack's hypothesis

Charnov and Skinner consider three possible reasons. Reason 1 There may be trade-offs between a female's investment in a particular clutch (e.g., clutch size) and her own future survival or reproductive performance. •This trade-off is similar to that we have discussed for birds. Reason 2 There may be trade-offs between clutch size and offspring quality (survival or reproductive performance). •Again, this trade-off is similar to that we have discussed for birds. Reason 3 There may be trade-offs in clutch size related to the abundance of host insects.

Now lets modify the null model in 13.10a to consider the effect of mutations. •Figure 13.10b depicts life history with a mutation that causes death at age 14 instead of 15 •All other aspects of life history are unchanged from Figure 13.10a.

Deleterious Mutations: The Mutation Accumulation Hypothesis

What kind of mutations result in antagonistic pleiotropy of this type? Describe Example 1:

Example 1 The age-1 gene in the nematode Caenorhabditis elegans Age-1 is one of several recently discovered genes with pleiotropic effects on reproduction and survival. In C. elegans the protein encoded by age-1 plays a role in an intracellular signaling pathway involved in the control of development and the determination of stress resistance. •The age-1 gene product also plays a role in senescence: ◦Mutations in the gene can increase life by as much as 80%! ◦Carriers of the mutation appear to be otherwise normal. Walker et al. (2000) sought more subtle effects on fitness of a mutant age-1 allele called hx546 that causes worms to live longer. •They established lab populations of worms in which the individuals were genetically identical except that some were homozygous for the normal age-1 allele while others were homozygous for hx546. •All worms in the study were hermaphrodites and reproduced by self-fertilization. •This enabled the researchers to measure the relative fitness effects of the hx546 allele by tracking its frequency over 10-12 generations in a mixed population. ◦If the allele was beneficial its frequency would rise. ◦If deleterious its frequency would fall.

What is the paradox of rate of living theory of aging

If natural selection can lead to longer life spans, and the physiological mechanisms for longer life already exist, why has natural selection not produced this result in all species?

Example two of Trade-Offs and Aging: The Antagonistic Pleiotropy Hypothesis :Trade-offs in the collared fly catcher

In brief, •Females that breed in their first year have smaller clutches in years 2, 3, and 4 than females that do not breed until year 2. •Females given extra eggs at age 1 have progressively smaller clutches each year at ages 2, 3, and 4. In contrast, control females do not show a decline in egg production until age 4. These results indicate a cost later in life to breeding early, another example of antagonistic pleiotropy.

Identifying and Testing the Assumptions of the Lack Hypothesis: Assumption 2 and an Example

Lack's hypothesis assumes that the only effect of clutch size on offspring is in determining whether offspring survive. •Being part of a large clutch may, however, impose other costs on an offspring. Example - Schluter and Gustafsson (1993) showed in collared flycatchers (see Figure 13.21) that adding or removing eggs from a nest had a big affect on the reproductive success of the offspring. •Females reared in nests from which eggs had been removed produced larger clutches. •Females reared in nests from which eggs had been added produced smaller clutches. •This indicates that clutch size affects not only offspring survival but offspring performance: there is a trade-off between the quantity and the quality of offspring produced. When larger clutches result in lower offspring reproductive success, the clutch size maximizing lifetime reproductive success will be less than the clutch size maximizing offspring production in any one reproductive bout.

Lack's Hypothesis Applied to Parasitoid Wasps

Lack's hypothesis is a useful null model for other organisms, as well as birds, and helps alert us to interesting patterns that we might not otherwise have noticed. Charnov and Skinner (1985) used Lack's hypothesis to explore the evolution of clutch size in parasitoid wasps. •You are responsible for reading and understanding this example. •See pp. 507-8, Figures 13.22 and 13.23, and Table 13.2. In brief •In the parasitoid wasp Trichogramma embryophagum, female fitness varies as a function of the clutch size it lays in different host insects (see Figure 13.22). •Female wasps shift behavior in a manner appropriate to different hosts: females lay fewer eggs in relatively poor hosts and more eggs in relatively good hosts. •As with many birds, however, female wasps lay smaller clutches than those predicted by Lack's hypothesis (see Table 13.2).

What kind of mutations could cause death but only in advanced age?

One possibility is a mutation that reduces an organism's ability to maintain itself in good repair.

Question: What kind of mechanism might limit the number of divisions in a cell lineage?

One possibility is progressive damage to chromosomes with each cell division. •Each end, or telomere, of a linear eukaryotic chromosome consists of many copies of a repetitive DNA sequence (in humans TTAGGG) that is tagged on to the end of the chromosome by a DNA polymerase enzyme called telomerase. •Telomerase is strongly expressed in the germ line cells (and in cancer cells) but not in most other cells. •A portion of this telomere is lost with each cycle of DNA replication and cell division. •Since telomeres are essential for the stability and the replication of chromosomes, the progressive loss of the telomere with each cell division is associated with senescence and the death of the cell.

There are two variants of this theory, one involving the damaging effects on cells of metabolic byproducts, the other the accumulation of irreparable DNA damage. Version A What are these? what are the predictions

Prediction: Aging is caused by the irreversible damage to cells caused by the accumulation of poisonous metabolic by-products. This theory makes two additional predictions: Prediction 1: The rate of aging should be correlated to an organism's metabolic rate. •All species should expend about the same amount of energy per gram per lifetime, whether they expend it slowly over a long lifetime or rapidly over a short lifetime. Prediction 2: Because of natural selection to resist and repair damage, species should not be able to evolve longer life spans (they are already living as long as is possible).

Describe the prediction and results in The age-1 gene in the nematode Caenorhabditis elegans

Prediction: All else being equal, since the hx546 worms live longer, one would expect that the allele would be advantageous. Results Under Optimal Conditions: As indicated in Figure 13.13a, under optimal conditions with ample food the frequency of hx546 changed little over 10 generations, regardless of starting frequency. •This suggests no fitness benefits to extra longevity or that the benefit of a longer lifespan was balanced by a roughly equivalent cost. Results Under Semi-natural Conditions: As indicated in Figure 13.13b, however, the true cost of carrying the hx546 allele was revealed when populations were reared under conditions that more closely resemble what C. elegans experiences in nature. In these experiments, populations were subject to stress in the form of repeated cycles of starvation: (see p. 497 for experimental details) •For each generation of the experiment, worms are allowed to eat all of the bacteria on their Petri plate. •They are then starved for four days before given more bacteria to eat •Finally, the researchers used only eggs produced in the first 24 hours after feeding resumed to establish the next culture (generation). The Results were Dramatic Under these conditions, in mixed populations of wild-type and mutant worms, the wild-type was strongly favored by natural selection. •The hx546 allele plummeted from a frequency of 0.5 to 0.06 in 12 generations. •To fall so fast the relative fitness of hx546 worms must have been less than 80% that of normal worms. Under natural conditions, the age-1 gene exhibits antagonistic pleiotropy. •Walker et al. isolated worms from cultures that had been starved for four days and then fed. •They examined worms at 12 and 24 hours after feeding had resumed. •They found that only young adults laid eggs during this window, and young adults are much more likely to be homozygous for the wild type allele than the hx546 allele. The normal, wild-type allele acts just as the antagonistic pleiotropy hypothesis predicts: The wild-type allele appears to increase reproductive success in young adulthood at the cost of shorter lifespan.

The Artifact Hypothesis : predictions and verdit

Predictions •Menopause is a non-adaptive artifact of our modern lifestyles. •Menopause cannot be an adaptation because our ancestors never lived long enough to experience it. •Only by living longer, has our modern lifestyle permitted us to see the expression of the late life mutations affecting reproduction. (See preceding lecture on the mutation accumulation hypothesis) The Verdict Anthropological data on current hunter-gatherer societies, presented in Figure 13.18, indicates that women often live well past 40-50 years of age and the onset of menopause. This longevity past menopause is not consistent with the Artifact Hypothesis.

The Grandmother Hypothesis : Predictions and verdict

Predictions •Older women can maximize inclusive fitness by shifting from production of their own offspring (direct fitness) to helping raise grandchildren (indirect fitness). The Verdict The data presented in Figure 13.18 are consistent with available anthropological data on current hunter-gatherer societies. These data support the Grandmother Hypothesis.

what are the tests of the rate of living theory of aging

Test of Prediction 1 Figure 13.5 shows the results of a study testing the hypothesis that total lifetime energy used per gram is the same across species, as predicted by the theory. •In fact, there is substantial variation among mammal groups in lifetime energy expenditure ◦these results do not support the Rate-of-Living theory. For example: ◾Bats have metabolic rates similar to other mammals of similar size but live three times longer. ◾Marsupials have metabolic rates that are significantly lower than those of other mammals of the same size, but life spans that are significantly shorter. Test of Prediction 2 Luckinbill et al. (1984) tested the second prediction, that species cannot evolve longer life spans, by artificially selecting for longevity in lab populations of Drosophila melanogaster. •Luckinbill selected for late reproduction by collecting eggs only from old adults. •Figure 13.6 shows that longevity in these populations increased dramatically during 13 generations of selection. ◦At the beginning of the experiment the average life span was about 35 days. ◦By the end of the experiment, they had increased the average life span to about 60 days! •These results are not consistent with predictions of the theory. Despite the fact that these studies seem to falsify the Rate-of-Living theory of aging, the general idea that organisms who live fast die young has persisted.

Testing the lack model:

Testing Lack's Model Many researchers have tested the assumptions and predictions of David Lack's model in birds by manipulating the number of eggs in a nest. •Assuming that the size of individual eggs is fixed, how many eggs should a bird lay in a single clutch?

Is There an Evolutionary Explanation for Menopause?

The evolutionary theory of senescence has been successful in explaining variation in life history among populations and species. •Can it explain unusual reproductive strategies, such as menopause in human females?

How Many Offspring Should an Individual Produce in a Given Year? : Optimal Clutch Size - The Lack Hypothesis

The simplest model for the evolution of clutch size was first developed by David Lack (1947). •It is based on the hypothesis that selection will favor the clutch size that produces the most surviving offspring. •Figure 13.19 shows a simple mathematical version of this model. ◦The model assumes a fundamental trade-off; that the probability that any individual offspring will survive decreases with increasing clutch size. ◦Why? Because, as stated above, it is intuitive to expect that the more offspring a parent attempts to raise at once, the less time and energy the parent can devote to caring for each one. ◦In Figure 13.19a it is assumed that the relationship between the probability of offspring survival clutch size is linear (a straight line), in this case with the probability of survival declining by 0.1 with each one-egg increment in clutch size. More generally though, the model holds for any continuously decreasing relationship between these two variables. ◦The curve in Figure 13.19b indicates the number of surviving offspring predicted by Lack's model and is obtained from Figure 13.19a by multiplying the clutch size times the probability that an individual will survive. ◦The optimal clutch size predicted by the model is the one that produces the maximum number of surviving offspring, which will occur at some intermediate clutch size. ◦Here, as indicated in Figure 13.19b, the optimal clutch size is five. In this hypothetical case, Lack's model would predict that a clutch of size five is the most productive and so should be favored by natural selection.

Testing the lack model :Example Clutch size in the Great Tit (Parus major

This study exemplifies the many experimental tests of the Lack Hypothesis. In two ways, the results of this study are consistent with Lack's predictions: •Researchers have found that adding eggs to a nest does indeed reduce the survival rate for individual chicks. ◦Presumably this is because the ability for parents to feed any individual offspring declines as the number of offspring increases. •They have also found that the number of surviving offspring reaches a maximum at an intermediate clutch size. However, as indicated in Figure 13.20 the actual mean clutch size observed in nature, 8.53 eggs, is less than that predicted by the number of offspring surviving from clutches of each size. •The number of surviving offspring was highest for natural clutches of size 12. •When researchers added 3 eggs to nests containing 9 eggs, the most productive clutch size was still 12. •In other words, birds that produce smaller clutches could apparently increase their reproductive success for the year by laying 12 eggs. Because the average clutch size is less than the most productive clutch size, these results are not consistent with Lack's Hypothesis.

A second hypothesis falling under the Evolutionary Theory of Aging.

Trade-Offs and Aging: The Antagonistic Pleiotropy Hypothesis: depicts a mutation that affects two different life history characteristics (mutations that affect multiple traits are said to be pleiotropic): •The mutation causes reproduction maturity at age 2 (instead of 3 as in Figures 13.10 a & b) •The mutation causes death at age 10 (instead of 14 or 15). The mutation involves a trade-off between early reproduction and late survival ("live fast and die young"). This mutation's pleiotropic effects are antagonistic (trade-offs are by nature antagonistic...)

example 3 of two of Trade-Offs and Aging: The Antagonistic Pleiotropy Hypothesis : Reproductive allocation in annual versus perennial plants

Truman Young (1990) reviewed data from the literature on the energy allocated to reproduction by closely related pairs of annual plants (Table 12.1). •Annuals, which reproduce once and die, always allocate more energy to their sole bout of reproduction than perennial allocate to any given bout. •This indicates that there is a trade-off in plants between reproduction and survival. Annual plants enjoy enhanced reproduction in their first reproductive season at the cost of drastically accelerated senescence.

senescence is caused by the

accumulation of irreparable damage to cells and tissues.

The Evolutionary Theory of Aging offers two related mechanisms to resolve this parodox

aging isn't due so much to cell tissue damage itself as failure of organisms to completely repair this damage., Although, G. C. Williams argues: •Given that organisms contain the genetic information needed to make complex tissues and organs, then, in principle, basic maintenance should be easier. •Actually, organisms are pretty good at repair at whole part level yet the job is often incomplete at cellular level.

what are some examples of the perfect organism

female thrip mites, , brown kiwi,

different balances will be optimal in different enviroments so we expect__________to be the source of much life history variation among living organisms

local environment variation

explain perfect organism in the thrip mite:

mature at birth, female is already inseminated having hatched inside their mothers both and mater with her brother but she produces just one small clutch of offspring and her life is brief, she dies at the age of 4 days when her own offspring eat her alive from the inside out

when tradeoffs exist we expect natural selection to favor individuals that allocate energy and time with an optimal balance between the benefits and costs so as to ___

maximize lifetime reproductive success

The relationship between fitness, clutch size, and the abundance and spatial distribution of hosts is addressed in a field of study called

optimal foraging theory.

Selection for alleles with pleiotropic effects that are advantageous early in life and deleterious late in life is a _____explanation for aging.

second evolutionary

AS the thrips mite and the brown kiwi suggest the laws of physics and biology impose fundamental trade offs on life histories:

the amount of energy an individual can harvest in finite , and biological processes take time, energy and time devoted to one activity cannot be devoted to another

An organism perfectly adapted for reproduction would : be mature at birth, continuously produce high quality offspring in large numbers, live forever. No organism like this exists even afer 3.8 million years.

the perfect organism " a Darwinian demon". it is possible to maximize one or another of these traits but not all of them in the same organism

explain the perfect organism in the brown kiwi

this bird produces every high quality offspring, females weigh about 6 pounds and lay eggs that weigh 1 lb the chicks that hatch from the huge eggs become highly self relient in about a week, but kiwi parents cannot produce these chicks continuously and they annot produce them in large numbers, it take the female over a month to make each of the eggs in a typical two egg clutch. the male has to incubate the eggs for about 3 months during which time he looses about 20 % of his body weight

Is the longevity of an individual organism associated with the longevity of its cells?

•Again, apparently so: the life span of mammalian species (measured in years) is correlated with the life span of their skin and red blood cells (see Lecture Slides). These results are consistent with Version B of the Rate of Living Theory. However, they also present a fundamental contradiction: •If expressing telomerase increases cell longevity and increased cell longevity causes an organism to live longer, then why doesn't natural selection act to increase individual fitness by increasing telomerase activity so that individuals can live longer? The answer probably involves a trade-off between extending the longevity of cells (through telomerase activity) versus preventing the uncontrolled proliferation of cells (leading to cancer).

All cells contain the gene for telomerase so isn't it possible for cells to live longer by increasing expression of this gene?

•Apparently so: Experiments forcing cell cultures to increase expression of telomerase have been able to increase the longevity of laboratory cell lines by at least an extra 20 cell divisions.

The mutation is obviously deleterious, but how strongly will it be selected against?

•Expected lifetime RS without mutation = 2.419 (Figure 13.10a) •Expected lifetime RS with mutation = 2.34 (Figure 13.10b) The mutant has 96% of the fitness of wild type zygotes!

What is the expected frequency in a population of mutations that are selected against only weakly? Recall that at mutation-selection balance:

•The equilibrium allele frequency is p* ≈ μ/s for dominant mutations and q* ≈ √μ/s for recessive mutations (where μ is the mutation rate and s is the selection coefficient). •Recessive mutations that are only weakly deleterious (s<<1) can accumulate to relatively high levels, for example 0.1 to l% per locus. Weakly deleterious recessive mutations, for example those that affect survival late in life, may be present at many loci.

A Simple Illustrative Null Model Figure 13.10 presents a series of simple genetic and demographic models of a hypothetical population to show how deleterious mutations or trade-offs can lead to evolution of senescence ; This model shows :

•The life histories of individuals in the population from birth until death (e.g., due to accidents, predation, disease). •The probability that an individual will survive is p = 0.8 year from to year (exponential decline). •The maximum life span is 15 years. •The reproduction success of survivors (RS) equals 1 once reproductively mature. •The expected RS = probability of survival x RS. •The expected lifetime RS = expected RS accumulated over the life span. Under the conditions of the model described above, expected lifetime RS = 2.419 for wild type individuals.

If birds can apparently increase their reproductive success by laying more eggs, and natural selection maximizes lifetime reproductive success, then why does research find that the average clutch size is generally smaller than the most productive clutch size?

•The mathematical logic of Lack's model is sound, so the problem must lie with some underlying assumption. The key problem is the implicit assumption that one can extrapolate from the conditions that maximize reproductive success for a single clutch to those that maximize total lifetime reproductive success.

So why do organisms senesce and die?

•They die, at least in part, because their telomeres are lost and their chromosomes become too damaged to function.