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Research
To the disciple of Natural Selection, aging presents itself as a paradox. How does a process that favors reproductive success and survival overlook a decline in fitness so great as to have death as its endpoint? In 1957, George C. Williams published his theory of Antagonistic Pleiotropy, in which he suggested that a gene will face positive selective pressure and be maintained in the gene pool as long as its net effect on fitness is positive. Ergo, a gene exerting detrimental effects on fitness after the reproductive period would persevere in the gene pool so long as it also imbued a beneficial effect. The earlier said trait is expressed, the more heavily it is weighted.
Our research implicates the phenomenon now known as alternative splicing as a validating, molecular mechanism for the Antagonistic Pleiotropy model. We now investigate the relationships between alternative splicing events, functional diversity, connectivity, expression, mutation susceptibility and mutation impact in aging related versus non-aging related gene sets. An examination of these functional and structural characteristics may reveal pervading features exclusive to the otherwise motley collection of AR genes, enabling their identification a priori by characteristic features rather than by mutant models, substantially hastening our understanding of the aging process.
