RRC ID 53264
Author Wei Y, Kenyon C.
Title Roles for ROS and hydrogen sulfide in the longevity response to germline loss in Caenorhabditis elegans.
Journal Proc. Natl. Acad. Sci. U.S.A.
Abstract In Caenorhabditis elegans, removing germ cells slows aging and extends life. Here we show that transcription factors that extend life and confer protection to age-related protein-aggregation toxicity are activated early in adulthood in response to a burst of reactive oxygen species (ROS) and a shift in sulfur metabolism. Germline loss triggers H2S production, mitochondrial biogenesis, and a dynamic pattern of ROS in specific somatic tissues. A cytoskeletal protein, KRI-1, plays a key role in the generation of H2S and ROS. These kri-1-dependent redox species, in turn, promote life extension by activating SKN-1/Nrf2 and the mitochondrial unfolded-protein response, respectively. Both H2S and, remarkably, kri-1-dependent ROS are required for the life extension produced by low levels of the superoxide-generator paraquat and by a mutation that inhibits respiration. Together our findings link reproductive signaling to mitochondria and define an inducible, kri-1-dependent redox-signaling module that can be invoked in different contexts to extend life and counteract proteotoxicity.
Volume 113(20)
Pages E2832-41
Published 2016-5-17
DOI 10.1073/pnas.1524727113
PII 1524727113
PMID 27140632
PMC PMC4878494
MeSH Active Transport, Cell Nucleus Aging* Animals Caenorhabditis elegans / cytology Caenorhabditis elegans / physiology* Caenorhabditis elegans Proteins / metabolism DNA-Binding Proteins / metabolism Germ Cells / physiology Hydrogen Sulfide / metabolism* Intracellular Signaling Peptides and Proteins / metabolism Longevity Mitochondrial Dynamics Organelle Biogenesis Oxidation-Reduction Reactive Oxygen Species / metabolism* Signal Transduction Transcription Factors / metabolism
IF 9.58
C.elegans tm1011 tm3676 tm760