Abstract:
:Cells can enter quiescent states in which cell cycling and growth are suspended. We find that during a long developmental arrest (quiescence) induced by starvation, newly hatched C. elegans acquire features associated with impaired proteostasis and aging: mitochondrial fission, ROS production, protein aggregation, decreased proteotoxic-stress resistance, and at the organismal level, decline of mobility and high mortality. All signs of aging but one, the presence of protein aggregates, were reversed upon return to development induced by feeding. The endoplasmic reticulum receptor IRE-1 is completely required for recovery, and the downstream transcription factor XBP-1, as well as a protein kinase, KGB-1, are partially required. Interestingly, kgb-1(-) mutants that do recover fail to reverse aging-like mitochondrial phenotypes and have a short adult lifespan. Our study describes the first pathway that reverses phenotypes of aging at the exit of prolonged quiescence.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Roux AE,Langhans K,Huynh W,Kenyon Cdoi
10.1016/j.cmet.2016.05.024subject
Has Abstractpub_date
2016-06-14 00:00:00pages
1113-1126issue
6eissn
1550-4131issn
1932-7420pii
S1550-4131(16)30246-7journal_volume
23pub_type
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