Regulation of cytoplasmic stress granules by apoptosis-inducing factor
Author:
Candé Céline1, Vahsen Nicola1, Métivier Didier1, Tourrière Hélène2, Chebli Karim2, Garrido Carmen3, Tazi Jamal2, Kroemer Guido1
Affiliation:
1. CNRS-UMR8125, Institut Gustave Roussy, 39 rue Camille-Desmoulins, 94805 Villejuif, France 2. CNRS-UMR5535, Université de Montpellier II, 34293 Montpellier CEDEX 5, France 3. INSERM U-517, Faculty of Medicine and Pharmacy, 7 Boulevard Jeanne d'Arc, 21033 Dijon, France
Abstract
Stress granules (SG) are dynamic cytoplasmic foci in which stalled translation initiation complexes accumulate. In conditions of acute cellular redox, stress cells manipulated to lose the expression of apoptosis-inducing factor (AIF) nucleate SG signature proteins (e.g. TIA-1, PABP1) more efficiently than AIF-positive controls. AIF also inhibited SG formation induced by the RasGAP-associated endoribonuclease G3BP. Retransfection of mouse AIF into cells subjected to human AIF-specific siRNA revealed that only AIF imported into mitochondria could repress SGs and that redox-active domains of AIF, which are dispensable for its apoptogenic action, were required for SG inhibition. In response to oxidative stress, AIF-negative cells were found to deplete non-oxidized glutathione more rapidly than AIF-expressing cells. Exogenous supplementation of glutathione inhibited SG formation elicited by arsenate or G3BP. Together, these data suggest that the oxidoreductase function of AIF is required for the maintenance of glutathione levels in stress conditions and that glutathione is a major regulator of SG.
Publisher
The Company of Biologists
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