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Cell Rep. 2014 Oct 9;9(1):9-15. doi: 10.1016/j.celrep.2014.08.075. Epub 2014 Oct 2.

TOR signaling couples oxygen sensing to lifespan in C. elegans.

Author information

1
Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
2
Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. Electronic address: nav@northwestern.edu.

Abstract

Metazoans adapt to a low-oxygen environment (hypoxia) through activation of stress-response pathways. Here, we report that transient hypoxia exposure extends lifespan in C. elegans through mitochondrial reactive oxygen species (ROS)-dependent regulation of the nutrient-sensing kinase target of rapamycin (TOR) and its upstream activator, RHEB-1. The increase in lifespan during hypoxia requires the intestinal GATA-type transcription factor ELT-2 downstream of TOR signaling. Using RNA sequencing (RNA-seq), we describe an ELT-2-dependent hypoxia response that includes an intestinal glutathione S-transferase, GSTO-1, and uncover that GSTO-1 is required for lifespan under hypoxia. These results indicate mitochondrial ROS-dependent TOR signaling integrates metabolic adaptations in order to confer survival under hypoxia.

PMID:
25284791
PMCID:
PMC4194168
DOI:
10.1016/j.celrep.2014.08.075
[Indexed for MEDLINE]
Free PMC Article

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