Unknown

Dataset Information

0

Roles for ROS and hydrogen sulfide in the longevity response to germline loss in Caenorhabditis elegans.


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.

SUBMITTER: Wei Y 

PROVIDER: S-EPMC4878494 | BioStudies | 2016-01-01

REPOSITORIES: biostudies

Similar Datasets

2013-01-01 | S-EPMC3817383 | BioStudies
2021-01-01 | S-EPMC7906160 | BioStudies
2019-01-01 | S-EPMC6710067 | BioStudies
2014-01-01 | S-EPMC3988823 | BioStudies
2012-01-01 | S-EPMC4844853 | BioStudies
2019-01-01 | S-EPMC6694850 | BioStudies
2010-01-01 | S-EPMC2916858 | BioStudies
2020-01-01 | S-EPMC7695986 | BioStudies
1000-01-01 | S-EPMC4658530 | BioStudies
2011-11-15 | GSE25199 | GEO