Evolution, Chance, and Aging

Abstract

Aging has provided fruitful challenges for evolutionary theory, and evolutionary theory has deepened our understanding of aging. A great deal of genetic and molecular data now exists concerning mortality regulation and there is a growing body of knowledge concerning the life histories of diverse species. Assimilating all relevant data into a framework for the evolution of aging promises to significantly advance the field. We propose extensions of some key concepts to provide greater precision when applying these concepts to age-structured contexts. Secondary or byproduct effects of mutations are proposed as an important factor affecting survival patterns, including effects that may operate in small populations subject to genetic drift, widening the possibilities for mutation accumulation and pleiotropy. Molecular and genetic studies have indicated a diverse array of mechanisms that can modify aging and mortality rates, while transcriptome data indicate a high level of tissue and species specificity for genes affected by aging. The diversity of mechanisms and gene effects that can contribute to the pattern of aging in different organisms may mirror the complex evolutionary processes behind aging.

DNA methylation meta-analysis confirms the division of the genome into two functional groups

“…We regard the ontogenesis program as a strictly defined sequence of IntG gene expression, starting from the zygote stage, for the purpose of organism formation. The main goal of the ontogenesis program is to achieve the maximum competitive advantage by the time the organism reaches the state of fertility, since natural selection is aimed precisely at this stage of metazoan development [26,27,28,29,30]. Genome methylation, as a regulatory tool, is directly involved in the development and implementation of the ontogenesis program, including the processes of cell differentiation in Mammalian [31].…”

Extended lifespan in femaleDrosophila melanogasterthrough late-life caloric restriction

“…Together, our results demonstrate that CS female flies can benefit from late-life caloric shifts with no associated fitness cost and reveal the metabolic adaptations that mediate these events. Traditional evolutionary theory has suggested that caloric restriction is an environmental cue that signals to organisms the need to invest in somatic maintenance rather than reproduction (26). Under this paradigm, organisms would increase survival in order to have the opportunity to reproduce under more favorable conditions.…”

INDY—From Flies to Worms, Mice, Rats, Non-Human Primates, and Humans

“…Some of these additional Indy alleles are intronic P-element insertions ( Rogina and Helfand 2013 ; Rogers and Rogina, 2014 ). In both Drosophila and mice, lifespan is markedly influenced by genetic background, as would be expected for a complex phenotype affected by many pleiotropic genes and epistasis ( Frankel and Rogina, 2021 ). Indy alleles produce longevity extension in several different genetic backgrounds, including the Canton-S wild type strain, the Hyperkinetic , Shaker , drop-dead strains, and the short- and long-lived lines created by Luckinbill ( Luckinbill and Clare, 1985 ; Rogina et al, 1997 ; Rogina et al, 2000 ; Rogina and Helfand, 2013 ).…”

“…Longevity was observed with the Indy 206 /+ allele after 10 generations of backcrossing into the yw genetic background but not after backcrossing into the w 1118 background ( Toivonen et al, 2007 ; Wang et al, 2009 ). The effect of CR upon lifespan, in both flies and mice, is also affected by genetic background ( Frankel and Rogina, 2021 ). CR has a marginal effect upon lifespan in the w 1118 background.…”