The discovery of genes that cause aging without any known beneficial effect is one of the most powerful arguments for programmed aging i.e. the idea that aging and associated life span limitation, per se, accomplishes a useful biological function and has therefore evolved and been retained. The need for life span limitation has resulted in the evolution of potentially complex mechanisms for accomplishing that function including, of course, genes. Disabling ("knocking out" by means of genetic engineering) these genes results in delaying symptoms of aging and extending life span substantially.
Opponents of programmed aging claim that these genes must each have some hidden benefit that is compatible with traditional evolutionary mechanics theory, that is, benefiting the ability of individual organisms to survive or reproduce. Proving that such a benefit does not exist in an organism such as a worm or fruit fly or even mouse is difficult. The compensating benefit might involve subtle behaviors or other traits that would only become apparent in a wild context during an extended period and are not obvious in a lab setting.
Genetic engineering has been used to disable genes in order to change some quality of a domesticated species that affects its value in a domesticated context. However, disabling a gene generally does not produce results that would represent a survival or reproductive benefit in a wild context. Opponents therefore have difficulty in finding any case in which disabling a gene produces a traditionally beneficial survival or reproductive advantage. There argument therefore is circular: There must be a hidden traditional benefit entirely because our theory says there must be one.
Because of the nature of genes (see Digital Genetics), there are a very large number of possible mutations that would disable a gene. If a gene did not produce an evolutionary advantage, it would rapidly be disabled. Genomes are full of these pseudogenes that have almost the proper data structure of a functioning gene but are no longer operational.
In any event, studying these genes, their products, and the effect of the products on other biological activity, is obviously of value in understanding aging.
Results of PubMed search for "aging genes."
One of the specific aging genes is P66Shc (shc1). See results of PubMed search for P66Shc. Full text article on P66Shc and aging by Giovambattista Pani describes experiments with P66Shc knock-out mice. The P66KO mice live 30 percent longer and appear to be "phenotypically normal, fertile, and healthy."
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