Developmental ROS individualizes organismal stress resistance and lifespan

Daphne Bazopoulou, Daniela Knoefler, Yongxin Zheng, Kathrin Ulrich, Bryndon J. Oleson, Lihan Xie, Minwook Kim, Anke Kaufmann, Young-Tae Lee, Yali Dou, Yong Chen, Shu Quan and Ursula Jakob ()
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Daphne Bazopoulou: University of Michigan
Daniela Knoefler: University of Michigan
Yongxin Zheng: East China University of Science and Technology
Kathrin Ulrich: University of Michigan
Bryndon J. Oleson: University of Michigan
Lihan Xie: University of Michigan
Minwook Kim: University of Michigan
Anke Kaufmann: University of Michigan
Young-Tae Lee: Michigan Medicine
Yali Dou: Michigan Medicine
Yong Chen: National Center for Protein Science Shanghai, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences
Shu Quan: East China University of Science and Technology
Ursula Jakob: University of Michigan

Nature, 2019, vol. 576, issue 7786, 301-305

Abstract: Abstract A central aspect of aging research concerns the question of when individuality in lifespan arises1. 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.

Date: 2019
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DOI: 10.1038/s41586-019-1814-y

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