Regulation of anoxic death in Caenorhabditis elegans by mammalian apoptosis signal-regulating kinase (ASK) family proteins.

Content Provider	Semantic Scholar
Author	Hayakawa, Teruyuki Kato, Kumiko Hayakawa, Ryoichi Hisamoto, Naoki Matsumoto, Kunihiro Takeda, Kohsuke Ichijo, Hidenori
Copyright Year	2011
Abstract	Cells and organisms face anoxia in a wide variety of contexts, including ischemia and hibernation. Cells respond to anoxic conditions through multiple signaling pathways. We report that NSY-1, the Caenorhabditis elegans ortholog of mammalian apoptosis signal-regulating kinase (ASK) family of MAP kinase (MAPK) kinase kinases (MAP3Ks), regulates viability of animals in anoxia. Loss-of-function mutations of nsy-1 increased survival under anoxic conditions, and increased survival was also observed in animals with mutations in tir-1 and the MAPK kinase (MAP2K) sek-1, which are upstream and downstream factors of NSY-1, respectively. Consistent with these findings, anoxia was found to activate the p38 MAPK ortholog PMK-1, and this was suppressed in nsy-1 and tir-1 mutant animals. Furthermore, double-mutant analysis showed that the insulin-signaling pathway, which also regulates viability in anoxia, functioned in parallel to NSY-1. These results suggest that the TIR-1-NSY-1-SEK-1-PMK-1 pathway plays important roles in the reponse to anoxia in C. elegans.
File Format	PDF HTM / HTML
DOI	10.1534/genetics.110.124883
PubMed reference number	21212236
Journal	Medline
Volume Number	187
Issue Number	3
Alternate Webpage(s)	http://www.genetics.org/content/genetics/early/2011/01/06/genetics.110.124883.full.pdf
Alternate Webpage(s)	https://doi.org/10.1534/genetics.110.124883
Journal	Genetics
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article