期刊
ELIFE
卷 7, 期 -, 页码 -出版社
eLIFE SCIENCES PUBL LTD
DOI: 10.7554/elife.35368
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资金
- National Natural Science Foundation of China [81770143, 31671428, 31500665, 31530041, 21575151, 31371326]
- National Institutes of Health [GM120033]
- National Science Foundation [DMS-1263932]
- Cancer Prevention and Research Institute of Texas [RP170387]
- Robert A and Renee E Belfer Family Foundation
- Chao Family Foundation
- National Program on Key Research Projects of China [2016YFA0501900]
- 100 Talents Program of the Chinese Academy of Sciences
Epigenetic alteration has been implicated in aging. However, the mechanism by which epigenetic change impacts aging remains to be understood. H3K27me3, a highly conserved histone modification signifying transcriptional repression, is marked and maintained by Polycomb Repressive Complexes (PRCs). Here, we explore the mechanism by which age-modulated increase of H3K27me3 impacts adult lifespan. Using Drosophila, we reveal that aging leads to loss of fidelity in epigenetic marking and drift of H3K27me3 and consequential reduction in the expression of glycolytic genes with negative effects on energy production and redox state. We show that a reduction of H3K27me3 by PRCs-deficiency promotes glycolysis and healthy lifespan. While perturbing glycolysis diminishes the pro-lifespan benefits mediated by PRCs-deficiency, transgenic increase of glycolytic genes in wild-type animals extends longevity. Together, we propose that epigenetic drift of H3K27me3 is one of the molecular mechanisms that contribute to aging and that stimulation of glycolysis promotes metabolic health and longevity.
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