Modalities of Gene Action Predicted by the Classical Evolutionary Biological Theory of Aging
What might now be referred to as the classical evolutionary biological theory of why we age has had a number of serious challenges in recent years. While the theory might therefore have to be modified under certain circumstances, in the author's opinion, it still provides the soundest theoretical basis for thinking about how we age. Nine modalities of gene action that have the potential to modulate processes of aging are reviewed, including the two most widely reviewed and accepted concepts (antagonistic pleiotropy and mutation accumulation). While several of these nine mechanisms can be regarded as derivatives of the antagonistic pleiotropic concept, they frame more specific questions for future research. Such research should pursue what appears to be the dominant factor in the determination of intraspecific variations in longevitystochastic mechanisms, most likely based upon epigenetics. This contrasts with the dominant factor in the determination of interspecific variations in longevitythe constitutional genome, most likely based upon variations in regulatory loci
antagonistic pleiotropy epigenetics evolutionary biology of aging longevity assurance adaptive silencing adaptive expression nonadaptive loss of silencing nonadaptive loss of expression somatic mutation paradoxical antagonistic pleiotropy late-acting constitutional mutations stochastics