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• W1535702947 abstract "Understanding the mechanism whereby the aging process is controlled has proven to be a uniquely difficult biological problem. Many theories have been put forth offering explanations for the phenomenon of senescence on a variety of different levels ranging from cellular, biochemical, and physiological to genetic and evolutionary. Many of these explanations are nonexclusive, which adds redundancy to confusion in considering the whole body of theory. Many of the cellular and/or biochemical mechanisms proposed amount to little more than detailed discussions of various possible gene end-products, which are themselves the subject of genetic and evolutionary theories. And even among these, no single theory predominates. J. B. S. Haldane (1941) and P. B. Medawar (1952) advanced the first theory of senescence incorporating a modem genetic and evolutionary perspective on the aging process. Their theory postulates the existence of specialized age-of-onset modifier genes which repress the action of other genes that are deleterious until an advanced age has been reached. Little harm results from the expression of the mutations then, however, and senescence gradually ensues with their derepression. In this theory, selection modifies life span by simply increasing or decreasing the period over which such modifiers are effective. Williams (19 57) later expanded on this, introducing the notion that the genes influencing senescence might themselves act pleiotropically with reciprocal effects at early and late ages. In this theory, the beneficial effects of genes early in life are weighed in evolution against their late life effects; youthful vigor must be accompanied by an early senescence and short life, while a delayed senescence and long life occur at the cost of youthful vitality. Apart from further extension of these ideas by Hamilton (1966) and Emlen (1 970), no new major theories of the evolution of senescence have arisen since Williams (1957). One reason for this may be that until recently, the few experimental tests performed contributed comparatively little substantiating information toward these theories. Early attempts at modifying life span through artificial selection include that of Glass (1960), who withheld mating in Drosophila to enforce an early versus late age-specific pattern of reproduction. This produced a slight increase in the longevity of late-reproducing lines. Wattiaux (1968) also found an increase in longevity in Drosophila under selection for an agespecific pattern of reproduction. This was followed by Sokal's (1970) study showing that continuous reproduction at an early age reduced median life span in Tribolium. Mertz (1975) found similar trends in an even later study. Taylor and Condra (1980) and Barclay and Gregory (1982) report changes in the longevity of Drosophila populations under rand K-selection or when exposed to predation. Concurrently with these, Lints and Hoste (1974, 1977) published the results of a well designed and extensive experiment that also selected for increased longevity in D. melanogaster through an early or late age-specific schedule of reproduction. But life span fluctuated wildly throughout the 13 generations of selection here, declining by 70% in the first few generations and then recovering. Further experiments (Lints et al., 1979)" @default.
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• W1535702947 date "1984-09-01" @default.
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• W1535702947 title "Selection for Delayed Senescence in Drosophila melanogaster" @default.
• W1535702947 doi "https://doi.org/10.2307/2408433" @default.
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