Calorie restriction breaks an epigenetic barrier to longevity
Résumé
It is becoming increasingly evident that aging is controlled by both genetic and epigenetic factors. Histone modifying enzymes and their modifications comprise one of the main components of epigenetic mechanisms which have been directly linked to lifespan regulation in many organisms. Studies in diverse species have highlighted changes in the distribution or abundance of certain histone marks during the lifespan of a cell or an organism, leading to alterations in gene expression. In some cases, this aging-dependent patterning of histone modifications affects the expression of key longevity genes while, in other cases, they drive large-scale transcriptome changes that eventually contribute to functional decline and other hallmarks of aging. Since epigenetic factors, including histone modifications, are malleable to environmental signals, it was reasonably hypothesized that the epigenome could act as a platform through which external signals control lifespan via gene regulation. However, evidence connecting an environmental stimulus to a specific histone modification and the subsequent alteration of a particular gene expression program influencing lifespan was lacking. Using the genetically tractable eukaryote Saccharomyces cerevisiae we have recently reported that histone H4 N-terminal acetylation (N-acH4), a modification catalyzed by the N-terminal acetyltransferase Nat4, responds to calorie restriction (CR) in order to enable the expression of genes which directly delay aging
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Molina-Serrano et Kirmizis - 2017 - Calorie restriction breaks an epigenetic barrier t.pdf (1.34 Mo)
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