Hormetic heat shock and HSF-1 overexpression improve C. elegans survival and proteostasis by inducing autophagy. Issue 6 (3rd June 2017)

• Record Type: Journal Article
• Authors: Kumsta, Caroline; Hansen, Malene
• Is Part Of: Autophagy. Volume 13:Issue 6(2017)
• Page Start: 1076
• Page End: 1077
• Publication Date: 2017-06-03
• Subjects: aging -- autophagy -- C. elegans -- heat shock -- HLH-30 -- hormesis -- HSF-1 -- polyQ aggregation -- proteostasis -- stress resistance; Autophagic vacuoles -- Periodicals; Apoptosis -- Periodicals; Cell death -- Periodicals; Lysosomes -- Periodicals; Degeneration (Pathology) -- Periodicals; Autophagy -- Periodicals; Cell Death -- Periodicals; Lysosomes -- Periodicals; Periodicals; 571.936
• DOI: 10.1080/15548627.2017.1299313
• Languages: English
• ISSNs: 1554-8627

Abstract

ABSTRACT: The cellular recycling process of macroautophagy/autophagy is an essential homeostatic system induced by various stresses, but it remains unclear how autophagy contributes to organismal stress resistance. In a recent study, we report that a mild and physiologically beneficial ("hormetic") heat shock as well as overexpression of the heat-shock responsive transcription factor HSF-1 systemically increases autophagy in C. elegans . Accordingly, we found HSF-1- and heat stress-inducible autophagy to be required for C. elegans thermoresistance and longevity. Moreover, a hormetic heat shock or HSF-1 overexpression alleviated PolyQ protein aggregation in an autophagy-dependent manner. Collectively, we demonstrate a critical role for autophagy in C. elegans stress resistance and hormesis, and reveal a requirement for autophagy in HSF-1 regulated functions in the heat-shock response, proteostasis, and aging.