Abstract
A universal theory of aging remains elusive despite decades of research. Traditional gerontological research has focused on genetic alterations as the driving unit of the aging processes. Recent breakthroughs in cellular reprogramming, transgenerational epigenetic inheritance, and molecular aging clocks have motivated theories proposing that the disruption of epigenetic regulation is the proximal cause of aging. The claim that aging is fundamentally an epigenetic process, however, is largely based on studies using clonal cell populations and genetically identical organisms. Consequently, there has been limited experimental evidence demonstrating the correlation between epigenetic differences and longevity differences among genetically diverse populations. To address this gap in literature we leveraged laboratory populations of the model organism Drosophila melanogaster. Using sister populations with evolved differences in longevity after more than 1 500 generations of divergent life history selection, we measured the methylation at the H3K27 and H3K9 sites which have previously been shown to become dysregulated with age. Here we report that there were no differences in the amount of H3K27me3 or H3K9me2 between 3 replicate population pairs of the divergent lines. These results do not support that epigenetic dysregulation is the underlying cause of aging. Future studies investigating additional indicators of epigenetic dysregulation are required to clarify the role of epigenetics in aging.
Published Version
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