Oxidation as a Post-Translational Modification that Regulates Autophagy

Ruth Scherz-Shouval, Elena Shvets and Zvulun Elazar

volume 3 | issue 4

July/August 2007
Pages: 371 - 373

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The toxicity associated with accumulation of reactive oxygen species (ROS) has led to the evolution of various defense strategies to overcome oxidative stress, including autophagy. This pathway is involved in the removal and degradation of damaged mitochondria and oxidized proteins. At low levels, however, ROS act as signal transducers in various intracellular pathways. In a recent study we described the role of ROS as signaling molecules in starvation-induced autophagy. We showed that starvation stimulates formation of ROS, specifically H₂O₂, in the mitochondria. Furthermore, we identified the cysteine protease HsAtg4 as a direct target for oxidation by H₂O₂, and specified a cysteine residue located near the HsAtg4 catalytic site as critical for this regulation. Here we focus on Atg4, the target of regulation, and discuss possible mechanisms for the regulation of this enzyme in the autophagic process.

Addendum to:
Reactive Oxygen Species Are Essential for Autophagy and Specifically Regulate the Activity of Atg4
R. Scherz-Shouval, E. Shvets, E. Fass, H. Shorer, L. Gil and Z. Elazar
EMBO J 2007; doi: 10.1038/sj.emboj.7601623

Authors

Ruth Scherz-Shouval

Weizmann Institute

Elena Shvets

Department of Biological Chemistry; The Weizmann Institute of Science; Rehovot Israel

Zvulun Elazar