학술논문

Autophagy genes are essential for dauer development and life-span extension in C. elegans
Document Type
Academic Journal
Source
Science. September 5, 2003, Vol. 301 Issue 5638, p1387, 5 p.
Subject
Caenorhabditis elegans -- Physiological aspects -- Research -- Genetic aspects
Developmental genetics -- Research -- Physiological aspects -- Genetic aspects
Science and technology
Physiological aspects
Genetic aspects
Research
Language
English
ISSN
0036-8075
Abstract
Both dauer formation (a stage of developmental arrest) and adult life-span in Caenorhabditis elegans are negatively regulated by insulin-like signaling, but little is known about cellular pathways that mediate these processes. Autophagy, through the sequestration and delivery of cargo to the lysosomes, is the major route for degrading long-lived proteins and cytoplasmic organelles in eukaryotic cells. Using nematodes with a loss-of-function mutation in the insulin-like signaling pathway, we show that bec-1, the C. elegans ortholog of the yeast and mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal dauer morphogenesis and life-span extension. Dauer formation is associated with increased autophagy and also requires C. elegans orthologs of the yeast autophagy genes APG1, APG7, APG8, and AUT10. Thus, autophagy is a cellular pathway essential for dauer development and life-span extension in C. elegans.
The regulation of dauer entry in C. elegans shares similarities with the induction of autophagy in other eukaryotes. The environmental cues that promote dauer morphogenesis in C. elegans are also [...]