Title: “Endogenous Epigenetic Silencing and Aging”

Abstract: Human monozygotic twins develop nearly identical features at the same rate, but age at different rates, usually dying seven to ten years apart. The same is true for animals. Hundreds of genetically identical nematodes will all develop the same number of somatic cells, yet, there will be an order of magnitude between the first and last deaths. Understanding the mechanisms underlying this heterogeneity is critical for achieving personalized geroscience. Growing evidence suggests that stochastic epigenetic silencing is among the greatest contributors to individual variation during aging. Differences in endogenous epigenetic silencing create individual physiological states. These distinct physiological states cause isogenic individuals to age at different rates and have differences in disease/sickness outcomes. Understanding how to control and account for these stochastic endogenous silencing events is critical for manipulating the aging process in humans, who will have both genetic and epigenetic differences affecting response to aging interventions. We have developed C. elegans as a model to study how to control and account for endogenous epigenetic silencing. We focus on germline and somatic transposon control systems that also control stochastic, endogenous silencing of native genes. By studying a biomarker of aging and mutation penetrance, we found that the pleiotropic, endogenously, RDE-3-silenced chaperone, hsp-17/HSPB5, affects variation in lifespan after heat shock, and the penetrance of the Ras G13E gain of function mutation. We also found that a somatic, endogenous silencing system controls variation in gene expression at the level of the individual allele, thereby controlling the degree of monoallelic expression in tissues


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