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 regulationof the nutrient-sensing kinase target of rapamycin(TOR) and its upstream activator, RHEB-1. The increase in lifespan during hypoxia requires theintestinal 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 isrequired for lifespan under hypoxia. These resultsindicate mitochondrial ROS-dependent TOR signaling integrates metabolic adaptations in order to confer survival under hypoxia.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 9-15 |
| Number of pages | 7 |
| Journal | Cell reports |
| Volume | 9 |
| Issue number | 1 |
| DOIs | |
| State | Published - Oct 9 2014 |
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ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
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TOR signaling couples oxygen sensing to lifespan in C.elegans. / Schieber, Michael; Chandel, Navdeep.
In: Cell reports, Vol. 9, No. 1, 09.10.2014, p. 9-15.Research output: Contribution to journal › Article
TY - JOUR
T1 - TOR signaling couples oxygen sensing to lifespan in C.elegans
AU - Schieber, Michael
AU - Chandel, Navdeep
PY - 2014/10/9
Y1 - 2014/10/9
N2 - 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 regulationof the nutrient-sensing kinase target of rapamycin(TOR) and its upstream activator, RHEB-1. The increase in lifespan during hypoxia requires theintestinal 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 isrequired for lifespan under hypoxia. These resultsindicate mitochondrial ROS-dependent TOR signaling integrates metabolic adaptations in order to confer survival under hypoxia.
AB - 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 regulationof the nutrient-sensing kinase target of rapamycin(TOR) and its upstream activator, RHEB-1. The increase in lifespan during hypoxia requires theintestinal 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 isrequired for lifespan under hypoxia. These resultsindicate mitochondrial ROS-dependent TOR signaling integrates metabolic adaptations in order to confer survival under hypoxia.
UR - http://www.scopus.com/inward/record.url?scp=84907993113&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84907993113&partnerID=8YFLogxK
U2 - 10.1016/j.celrep.2014.08.075
DO - 10.1016/j.celrep.2014.08.075
M3 - Article
C2 - 25284791
AN - SCOPUS:84907993113
VL - 9
SP - 9
EP - 15
JO - Cell Reports
JF - Cell Reports
SN - 2211-1247
IS - 1
ER -