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Mech Dev. 2009 Aug-Sep;126(8-9):624-37. doi: 10.1016/j.mod.2009.06.1082. Epub 2009 Jun 18.

JNK protects Drosophila from oxidative stress by trancriptionally activating autophagy.

Author information

1
Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, NY 14642, USA.

Abstract

JNK signaling functions to induce defense mechanisms that protect organisms against acute oxidative and xenobiotic insults. Using Drosophila as a model system, we investigated the role of autophagy as such a JNK-regulated protective mechanism. We show that oxidative stress can induce autophagy in the intestinal epithelium by a mechanism that requires JNK signaling. Consistently, artificial activation of JNK in the gut gives rise to an autophagy phenotype. JNK signaling can induce the expression of several autophagy-related (ATG) genes, and the integrity of these genes is required for the stress protective function of the JNK pathway. In contrast to autophagy induced by oxidative stress, non-stress related autophagy, as it occurs for example in starving adipose or intestinal tissue, or during metamorphosis, proceeds independently of JNK signaling. Autophagy thus emerges as a multifunctional process that organisms employ in a variety of different situations using separate regulatory mechanisms.

PMID:
19540338
PMCID:
PMC2750887
DOI:
10.1016/j.mod.2009.06.1082
[Indexed for MEDLINE]
Free PMC Article

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