Genetics of age-specific mortality in c. Elegans

Mortality increases with chronological age in C. elegans just as in many other species. The standard laboratory wild-type strain, N2, shows age-specific mortality rates (the fraction of worms that die in a 24-hour period) that are highly correlated with age. The normal mortality doubling time is about 4-6 days (Johnson, 1987 and 1990; Brooks et al., 1994).

Mortality of Gerontogene Mutants

The mortality doubling time of strains carrying mutations in age-1 (a gene that can be mutated to increase mean life span 70 percent) has been increased about 3-fold, and this increase is recessive to the normal allele in that individuals with one normal and one mutant allele have mortality doubling times no different from wild type (Johnson, 1990). Males have shorter life spans and a more rapid rate of mortality increase than hermaphrodites (Johnson, 1990). Males carrying age-1 mutations also show a lengthening of life and a slowing of the acceleration rate of mortality, although not as much as hermaphrodites, and age-1 mutant males still have significantly shorter life spans than do hermaphrodites of the same genotype. A major limitation of almost all studies on age-specific mortality rate is the lack of analysis of large populations of nematodes. Only small numbers (200) of worms have been studied, and these results may be modified after larger populations are analyzed.

RI Strains

Both long-lived mutants and RI strains also have been analyzed to see how age-specific mortality rate is altered. Long-lived R1 strains, some having mean and maximum life spans up to 70 percent longer than wild type, still showed exponential rates of increase of mortality with chronological age, as did both wild-type progenitor strains (Johnson, 1987). Longer life results from a slowing of the characteristic increase in mortality rate that had been thought typical of aging populations in most, if not all, species. The lengths of the developmental and reproductive period were unrelated to increased life span but instead were under independent genetic control. Lengthened life resulted entirely from an increase in postreproductive life span. General motor activity decayed linearly with chronological age in all genotypes. The loss of general motor activity was both correlated with and a predictor of life expectancy, suggesting that both share at least one common, rate-determining component (Johnson, 1987).

Mortality of Pure Strains

Because increased mean life expectancy could result from lower initial mortality rate, or from a slower rate of increase in mortality (or to alterations in both),

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