JNK protects Drosophila from oxidative stress by trancriptionally activating autophagy

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

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Autophagy*
  • Crosses, Genetic
  • Drosophila melanogaster / embryology*
  • Drosophila melanogaster / metabolism
  • Homozygote
  • MAP Kinase Kinase 4 / metabolism
  • MAP Kinase Kinase 4 / physiology*
  • Models, Biological
  • Oxidative Stress*
  • Phenotype
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Time Factors
  • Transcription, Genetic
  • Transcriptional Activation

Substances

  • MAP Kinase Kinase 4