文献类型：期刊文献

英文题名：Developmental ROS individualizes organismal stress resistance and lifespan

作者：Bazopoulou, Daphne[1];Knoefler, Daniela[1];Zheng, Yongxin[2,3];Ulrich, Kathrin[1];Oleson, Bryndon J.[1];Xie, Lihan[1];Kim, Minwook[1];Kaufmann, Anke[1];Lee, Young-Tae[4];Dou, Yali[4];Chen, Yong[5];Quan, Shu[2,3];Jakob, Ursula[1]

机构：[1]Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA;[2]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[3]SCICB, Shanghai, Peoples R China;[4]Michigan Med, Dept Pathol, Ann Arbor, MI USA;[5]Chinese Acad Sci, Shanghai Inst Biochem & Cell Biol, CAS Ctr Excellence Mol Cell Sci, State Key Lab Mol Biol,Natl Ctr Prot Sci Shanghai, Shanghai, Peoples R China

年份：2019

卷号：576

期号：7786

起止页码：301

外文期刊名：NATURE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000502792400061)】；

基金：We thank M. Malinouski and T. Mullins for assistance with the reconfiguration of the Biosorter; G. Csankovszki for antibodies, C. elegans RNAi feeding clones and comments; B. Braeckman for the N2jrIs2[Prpl-17::Grx-1-roGFP2] strain; J. Nandakumar for HeLa (EM-2-11ht) cells; the Caenorhabditis Genetics Center (funded by National Institutes of Health Infrastructure Program P40 OD010440) for C. elegans strains; the DNA Sequencing Core (BRCF), R. Tagett, W. Wu and the Bioinformatics Core of University of Michigan for RNA sequencing and data analysis; K. Wan for protein purification; R. Sawarkar and J. Labbadia for important suggestions; Jakob laboratory members for comments on the manuscript and J. Bardwell for critically reading the manuscript. Mass spectrometry was performed by MS Bioworks. This work was supported by NIH grants GM122506 and AG046799 as well as the Priority Program SPP 1710 of the Deutsche Forschungsgemeinschaft (Schw823/3-2) to U.J., a NIH T32 Career Training in the Biology of Aging grant to D.B., a NIH T32 Career Training in the Biology of Aging grant and a Bright Focus ADR Fellowship (A2019250F) to B.J.O., and the National Natural Science Foundation of China (31470737) to Y.C.

语种：英文

摘要：A central aspect of aging research concerns the question of when individuality in lifespan arises(1). Here we show that a transient increase in reactive oxygen species (ROS), which occurs naturally during early development in a subpopulation of synchronized Caenorhabditis elegans, sets processes in motion that increase stress resistance, improve redox homeostasis and ultimately prolong lifespan in those animals. We find that these effects are linked to the global ROS-mediated decrease in developmental histone H3K4me3 levels. Studies in HeLa cells confirmed that global H3K4me3 levels are ROS-sensitive and that depletion of H3K4me3 levels increases stress resistance in mammalian cell cultures. In vitro studies identified SET1/MLL histone methyltransferases as redox sensitive units of the H3K4-trimethylating complex of proteins (COMPASS). Our findings implicate a link between early-life events, ROS-sensitive epigenetic marks, stress resistance and lifespan.