Show simple item record

dc.contributor.authorWasko, Brian
dc.date.accessioned2020-10-26T13:49:59Z
dc.date.available2020-10-26T13:49:59Z
dc.date.issued2015
dc.identifier.citationSen P, Dang W, Donahue G, Dai J, Dorsey J, Cao X, Liu W, Cao K, Perry R, Lee JY, Wasko BM, Carr DT, He C, Robison B, Wagner J, Gregory BD, Kaeberlein M, Kennedy BK, Boeke JD, and Berger SL. H3K36 methylation promotes longevity by enhancing transcriptional fidelity. Genes Dev.2015 Jul 1;29(13):1362-1376en_US
dc.identifier.urihttps://hdl.handle.net/10657.1/2533
dc.description.abstractEpigenetic mechanisms, including histone post-translational modifications, control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging phenomenon of shortened life span, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a life span screen in Saccharomyces cerevisiae that is designed to identify amino acid residues of histones that regulate yeast replicative aging. Our results reveal that lack of sustained histone H3K36 methylation is commensurate with increased cryptic transcription in a subset of genes in old cells and with shorter life span. In contrast, deletion of the K36m2/3 demethylase Rph1 increases H3K36me3 within these genes, suppresses cryptic transcript initiation, and extends life span. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to loss of transcriptional precision that is detrimental to life span, and importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity.en_US
dc.publisherGenes & Developmenten_US
dc.subjectaging epigenetics H3K36 methylation cryptic transcriptionen_US
dc.titleH3K36 Methylation Promotes Longevity by Enhancing Transcriptional Fidelityen_US
dc.typeArticleen_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record