In this chapter we have described the uniquely high level of phenotypic plasticity in aging in Strongyloides ratti, corresponding to an 80-fold difference in lifespan, accompanied by a 400-fold difference in maximum fecundity. While these represent something of a comparative gerontological party trick, does it provide any real insight into the biology of aging? Arguably, the existence of plasticity of this sort has implications for the genetic mechanisms underlying lifespan evolution.
Evolutionary theory predicts that organisms in environments with a low rate of extrinsic mortality will evolve slower rates of aging than those in environments with a high rate of extrinsic mortality (Medawar, 1952; Williams, 1957). This is because high levels of extrinsic mortality reduce selection against alleles which produce deleterious effects later in life. As a consequence, populations experiencing higher extrinsic mortality will accumulate such late-acting deleterious alleles, which cause aging. If alleles are pleiotropic, and capable of producing phenotypic effects at different time in an animal's life, there may be selection for alleles which enhance fitness due to early effects, despite later deleterious effects (antagonistic pleiotropy).
The relationship between extrinsic mortality rate and aging has been supported by numerous comparative studies. For example, bats generally live longer than rodents of a similar size, presumably since flight aids predator evasion, reducing extrinsic mortality (Wilkinson and South, 2002). Evolution results in intraspecific as well as interspecific differences in lifespan. For example, in social insect species there are intercaste differences in lifespan which may reflect the evolutionary effects of different levels of extrinsic mortality on rates of aging (Page and Peng, 2001; Chapuisat and Keller, 2002). However, the extent to which these lifespan differences are the result of differences in the rate of aging remains unclear. For example, Chapuisat and Keller (2002) compared survival in large and small worker ants, and found that the smaller workers lived significantly longer, which they hypothesized was because the larger morphs were fighting and getting killed more quickly.
Thus, here lifespan differences are not due to differences in aging but rather, just differences in extrinsic mortality rates.
Although the evolutionary theory of aging provides an explanation for how different aging rates evolve, in terms of molecular or developmental genetics, the concept of ''late-acting deleterious mutations'' remains frustratingly abstract. Potentially, the pattern of aging in S. ratti provides a clue as to the molecular genetic basis of lifespan evolution, as follows. Free-living nematodes are typically much shorter lived than parasitic nematodes, some of which have lifespans of over a decade (Gems, 2001). These evolved differences are likely to reflect differences in extrinsic mortality experienced by free-living versus parasitic species. Hence the difference in lifespan of free-living and parasitic S. ratti seems consistent with the evolutionary theory of aging. What is interesting about S. ratti is that the two adult forms have evolved such a vast difference in aging rate, despite the fact that they are the same species, sharing a common genome.
That this is possible sheds some light on the nature of ''late-acting deleterious mutations.'' According to an evolutionary interpretation, free-living S. ratti have evolved a short lifespan due to high extrinsic mortality rate and accumulation of alleles with deleterious late-acting effects. However, one might expect that these alleles would be purged from the population by selection against them in the parasitic adult. The nature of S. ratti clearly demonstrates that this has not happened, and in this sense its evolution represents a useful experiment of nature. What is also clear from S. ratti is that the evolved difference in lifespan between the two adult forms is the product of differential gene expression. This tells us that, at least in this one species, ''late-acting deleterious mutations'' actually reflect regulated differences in gene expression leading to shorter lifespan.
Aging is a trait which shows remarkable evolutionary plasticity and is able to evolve rapidly. For example, humans and chimpanzees have evolved a difference in maximum lifespan of some 50 years since divergence from a common ancestor only 6-7 million years ago. It has been suggested that there are ''lifespan regulatory modules,'' which are regulated sets of genes which control the rate of aging (Kenyon, 2005). The existence of these makes possible the observed rapid rates of evolutionary change in aging rates. Some clues to the possible nature of the genes involved in lifespan are emerging from new genetic studies of aging in model organisms.
Was this article helpful?
For centuries, ever since the legendary Ponce de Leon went searching for the elusive Fountain of Youth, people have been looking for ways to slow down the aging process. Medical science has made great strides in keeping people alive longer by preventing and curing disease, and helping people to live healthier lives. Average life expectancy keeps increasing, and most of us can look forward to the chance to live much longer lives than our ancestors.