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Theories of Aging MCB135k, 2/10/03

Evolution Theory of Aging

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Problems with the Mutation Accumulation Theory

The basic problem is that mutation accumulation is too simple a mechanism to explain the detail in the observed aging processes of different species.

 does not support the mutation accumulation theory.

Mutation rate varies within and among taxa, including among individuals within the same population (; ; ). In principle, mutation rate may vary among groups descended from a common ancestor for three general reasons. First, the respective environments inhabited by the different groups may differ in mutagenicity (e.g., incident UV radiation), in which case the difference in mutation rates is solely due to environmental effects and does not represent evolutionary divergence, except incidentally. Second, non-adaptive processes (mutation, genetic drift, hitchhiking) may have caused the different groups to evolve different mutation rates. Third, natural selection may have favored different mutation rates in the different groups - i.e., the difference represents the adaptive outcome of divergent optimizing selection.

(Rate-of-Living theory of aging)

2)Reproductive state determines the rate of physiological aging

Background: Non-random segregation of DNA strands during stem cell replication has been proposed as a mechanism to minimize accumulated genetic errors in stem cells of rapidly dividing tissues. According to this hypothesis, an "immortal" DNA strand is passed to the stem cell daughter and not the more differentiated cell, keeping the stem cell lineage replication error-free. After it was introduced, experimental evidence both in favor and against the hypothesis has been presented. Principal findings: Using a novel methodology that utilizes cancer sequencing data we are able to estimate the rate of accumulation of mutations in healthy stem cells of the colon, blood and head and neck tissues. We find that in these tissues mutations in stem cells accumulate at rates strikingly similar to those expected without the protection from the immortal strand mechanism. Significance: Utilizing an approach that is fundamentally different from previous efforts to confirm or refute the immortal strand hypothesis, we provide evidence against non-random segregation of DNA during stem cell replication. Our results strongly suggest that parental DNA is passed randomly to stem cell daughters and provides new insight into the mechanism of DNA replication in stem cells.

Understanding why individuals express a given level of immune competence is necessary for predicting the incidence, spread, and evolution of disease. It is often observed that males have weaker immune systems than females and thus get sick more often. Sex-biases in susceptibility, both before and during infection, can affect pathogen prevalence and host-parasite coevolution. One potential cause of sexual dimorphism in immunity could be differential effects of infection on fitness between the sexes, i.e. females may be selected to invest more in immunity because the fitness costs of infection are greater. When individuals differ in their ability to maintain fitness during infection they are said to express different levels of tolerance. Most eco-immunology studies assess resistance, which involves those responses that prevent, restrict, or clear infection by parasites, rather than tolerance mechanisms. Distinguishing between resistance and tolerance is important as they predict markedly different evolutionary and epidemiological outcomes. Tolerance has long been acknowledged as a mechanism of managing stressors in the plant literature, but few studies have investigated tolerance in animals. To date, no comparison of tolerance in male and female animals has been undertaken. Using males and females from several Drosophila melanogaster genotypes, we assessed resistance and tolerance to the common bacterial pathogen Pseudomonas aeruginosa. Across all lines, resistance and tolerance was significantly lower in females. There was a significant negative correlation between male and female tolerance. In addition, we observed a genetic trade-off between resistance and tolerance. Our results suggest that antagonistic pleiotropy can maintain genetic variation in immunity. Implications for the genetics of immune function and sex-specific immunocompetence will be discussed.

Mutation Accumulation Hypothesis - Programmed Aging

Ohta T (1992) The nearly neutral theory of molecular evolution. Annual Review of Ecology and Systematics 23: 263–286.

- Aging results from a decline in the force of natural selection, therefore genes that promote aging should not exist (can not be selected for).

If we assume a species (e.g. elephant) that has relatively few predators and therefore lives a relatively peaceful existence in the wild, then presumably death of old age is a fitness factor. These issues led to the subsequent development of the antagonistic pleiotropy theory and other competing theories that suppose that aging is an unavoidable adverse side-effect of some beneficial function.

However, there are problems with the idea that such mutations cause aging as put forth in the mutation accumulation theory:
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Mutation accumulation hypothesis – …

The ‘cost of males’ reduces the fitness of sexuals relative to asexuals. Sex is common, implying that the existence of males may generate indirect fitness benefits. One proposal is that deleterious alleles may be subject to stronger selection in males than females, due to sexual selection. This would eliminate harmful mutations at the expense of males and reduce the mutation load of sexual females. We performed competitive fitness assays to estimate selection on male and female fruit flies bearing chromosomes that accumulated spontaneous mutations. We found that selection on males was 75% stronger than on females, suggesting that sexual selection can reduce mutation load. We then asked whether the presence of parasites can enhance this effect. To examine the interaction of mutations and parasites, we assessed the fitness of mutant and non-mutant males and females that were inoculated with either sterile media or an opportunistic insect pathogen. Infection seemed to cause selection to be stronger in males and weaker in females. This interaction could increase the benefits of sexual selection. However, the presence of males could also reduce female fitness if many alleles are subject to sexually-antagonistic selection. When sexually-antagonistic alleles are common, a large fraction of the genetic variance in reproductive fitness should be due to intermediate-frequency alleles rather than rare deleterious mutations. We compared the contribution of deleterious mutations to standing genetic variance in male and female reproductive fitness and juvenile viability. We found that the fraction of standing variance explained by mutation varied among traits, but there was little evidence for sexual antagonism. Our experiments suggest that sexual selection can have a net positive impact on population mean fitness, with the potential to offset the cost of males in sexual populations.

Theories of Aging MCB135k, 2/10/03

Although “death of old age” in the wild probably only occurs frequently in species that have few predators, aging in mammals obviously has effects other than death that would affect fitness and therefore death rate. Aging in mammals affects strength, speed, agility, and other factors that affect fitness even in relatively young animals. It therefore does not appear plausible that aging has a negligible effect on fitness.

Theories of Aging MCB135k, 2/10/03 ..

AB - Reactive oxygen species have been implicated as a cause of cancer and aging in mammals. Mice deficient for the antioxidant enzyme CuZn-superoxide dismutase (Sod1) have a decreased life span and an elevated incidence of liver cancer. To test the hypothesis that the cancer-prone phenotype in such mice is due to accelerated spontaneous mutation accumulation, we crossed these mutants with mice harboring a neutral lacZ mutation reporter gene. At 2 months of age, the lacZ mutation frequency in the liver of the hybrid animals was already twice as high as in littermate controls of the same age. This difference in mutation frequency increased to >3-fold at 6 months of age, after which it did not increase any further. Characterization of the mutation spectra in liver of the Sod1-null mice indicated mainly GC-to-TA transversions and GC-to-AT transitions, signature mutations of oxidative stress. The accelerated mutation accumulation in liver was accompanied by an increased frequency of apoptotic cells, as indicated by an increase in both terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling- and caspase 3-stallied cells at 6 and 12 months of age. In kidney, an elevated mutation frequency above controls of ∼2.5-fold was found not earlier than at 6 months. No increased mutation accumulation was observed in brain or spleen. These results support the hypothesis, that oxidative stress is an important causal factor of cancer in mammals.

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