The last century marked a success for public health, defined by achieving a dramatic increase in human life expectancy. However, aging can be accelerated by several factors and, by itself, is the principal risk factor for multiple chronic health conditions, including cancer, diabetes, and neurodegeneration. Epigenetic modifications are an emerging mechanism by which the aging process can be regulated. For example, methyltransferase complexes that modify trimethylation in histones (H3K4me3, H3K27me3, and H3K36me3) influence lifespan in yeast, worms, and flies. But little is known about the molecular mechanisms linking these chromatin alterations to longevity. Recently, we described a non-cell autonomous mechanism by which a deficiency of the H3K4me3 regulates longevity in C. elegans. Thus, transcriptional regulation in the nervous system, which depends on the CRTC-1/AP-1 transcriptional complex, maintains histone acetylation levels in peripheral tissues to promote longevity in H3K4me3-deficient animals. We also demonstrated that activation of this histone acetylation is sufficient to promote longevity in wild-type animals. Since epigenetic noise is causal to aging, epigenetic modifiers are ideal targets to improve the aging process. Moreover, epigenetic changes are reversible. Therefore, manipulation of epigenetic enzymes could prove to be crucial in reversing epigenetic aberrations that are a hallmark of aging and thus provide the basis for developing novel therapeutics to target a range of human age-related pathologies.
Join us on Monday, November 20 in Stephens Room (3503 Thomas Hall) and ZOOM for the Genetics and Genomics Seminar Series. Link: https://ncsu.zoom.us/j/91741454918?pwd=U0drVUpPdGJiSXVpcnVUZDNwaHVUZz09