Mitochondrial clearance and increased HSF-1 activity are coupled to promote longevity in fasted Caenorhabditis elegans

被引:0
|
作者
Tataridas-Pallas, Nikolaos [1 ]
Aman, Yahyah [1 ]
Williams, Rhianna [1 ]
Chapman, Hannah [1 ]
Cheng, Kevin J. H. [1 ]
Gomez-Paredes, Casandra [2 ,3 ]
Bates, Gillian P. [2 ,3 ]
Labbadia, John [1 ]
机构
[1] UCL, Inst Hlth Ageing, Dept Genet Evolut & Environm, Div Biosci, London WC1E 6BT, England
[2] UCL, Dept Neurodegenerat Dis, Huntingtons Dis Ctr, London WC1N 3BG, England
[3] UCL, UK Dementia Res Inst UCL, Queen Sq Inst Neurol, London WC1N 3BG, England
基金
英国生物技术与生命科学研究理事会; 英国医学研究理事会;
关键词
HEAT-SHOCK RESPONSE; LIFE-SPAN; DIETARY RESTRICTION; PROTEOSTASIS; REGULATOR; AUTOPHAGY; COLLAPSE; PATHWAY; SYSTEM; HEALTH;
D O I
10.1016/j.isci.2024.109834
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Fasting has emerged as a potent means of preserving tissue function with age in multiple model organisms. However, our understanding of the relationship between food removal and long-term health is incomplete. Here, we demonstrate that in the nematode worm Caenorhabditis elegans, a single period of early -life fasting is sufficient to selectively enhance HSF-1 activity, maintain proteostasis capacity and promote longevity without compromising fecundity. These effects persist even when food is returned, and are dependent on the mitochondrial sirtuin, SIR -2.2 and the H3K27me3 demethylase, JMJD-3.1. We find that increased HSF-1 activity upon fasting is associated with elevated SIR -2.2 levels, decreased mitochondrial copy number and reduced H3K27me3 levels at the promoters of HSF-1 target genes. Furthermore, consistent with our findings in worms, HSF-1 activity is also enhanced in muscle tissue from fasted mice, suggesting that the potentiation of HSF-1 is a conserved response to food withdrawal.
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页数:20
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