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首页> 外文期刊>eLife journal >Epigenetic drift of H3K27me3 in aging links glycolysis to healthy longevity in Drosophila
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Epigenetic drift of H3K27me3 in aging links glycolysis to healthy longevity in Drosophila

机译：H3K27me3在衰老中的表观遗传漂移将糖酵解与果蝇的健康长寿联系起来

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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.
机译：表观遗传改变与衰老有关。然而，表观遗传变化影响衰老的机制仍有待了解。 H3K27me3，一种高度保守的组蛋白修饰，代表转录抑制，由Polycomb Repressive Complexes（PRC）标记和维护。在这里，我们探讨了H3K27me3的年龄调节增加影响成人寿命的机制。使用果蝇，我们发现衰老导致表观遗传标记的保真度损失和H3K27me3的漂移以及糖酵解基因表达的减少，从而对能量产生和氧化还原状态产生负面影响。我们表明，通过PRCs缺乏症减少H3K27me3会促进糖酵解和健康的寿命。虽然干扰糖酵解会减少由PRCs缺乏介导的延长寿命的益处，但野生型动物中糖酵解基因的转基因增加会延长寿命。在一起，我们建议H3K27me3的表观遗传漂移是导致衰老的分子机制之一，而糖酵解的刺激促进了代谢健康和长寿。

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