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J. Biol. Chem., Vol. 279, Issue 37, 39068-39074, September 10, 2004

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Uth1p Is Involved in the Autophagic Degradation of Mitochondria^*

Ingrid Kissová, Maïka Deffieu, Stéphen Manon, and Nadine Camougrand

From the Unité Mixte de Recherche 5095 CNRS, Université de Bordeaux 2, 33077 Bordeaux, France

The absence of the outer mitochondrial membrane protein Uth1p was found to induce resistance to rapamycin treatment and starvation, two conditions that induce the autophagic process. Biochemical studies showed the onset of a fully active autophagic activity both in wild-type and uth1 strains. On the other hand, the disorganization of the mitochondrial network induced by rapamycin treatment or 15 h of nitrogen starvation was followed in cells expressing mitochondria-targeted green fluorescent protein; a rapid colocalization of green fluorescent protein fluorescence with vacuole-selective FM4-64 labeling was observed in the wild-type but not in the uth1 strain. Degradation of mitochondrial proteins, followed by Western blot analysis, did not occur in mutant strains carrying null mutations of the vacuolar protease Pep4p, the autophagy-specific protein Atg5p, and Uth1p. These data show that, although the autophagic machinery was fully functional in the absence of Uth1p, this protein is involved in the autophagic degradation of mitochondria.

Received for publication, June 22, 2004 , and in revised form, July 9, 2004.

^* This work was supported by grants from the Centre National de la Recherche Scientifique, the Association pour la Recherche contre le Cancer, the Conseil Régional d'Aquitaine, and the Université de Bordeaux 2 and successive post-doctoral fellowships from the Association pour la Recherche contre le Cancer and the Fondation pour la Recherche Médicale (to I. K.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Permanent address: Faculty of Natural Sciences, Comenius University, 84215 Bratislava, Slovak Republic.

To whom correspondence should be addressed: Institut de Biochimie et Génétique Cellulaires/CNRS, 1 Rue Camille Saint-Saëns, F-33077 Bordeaux, France. Tel.: 33-556-99-90-45; Fax: 33-556-99-90-51; E-mail: n.camougrand{at}ibgc.u-bordeaux2.fr.

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