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J. Biol. Chem., Vol. 281, Issue 7, 4035-4041, February 17, 2006

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Excess Peroxisomes Are Degraded by Autophagic Machinery in Mammals^*

Jun-ichi Iwata¹, Junji Ezaki¹, Masaaki Komatsu, Sadaki Yokota^¶, Takashi Ueno, Isei Tanida, Tomoki Chiba, Keiji Tanaka, and Eiki Kominami²

From the Department of Biochemistry, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, the Department of Molecular Oncology, Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku, Tokyo 113-8613, and the ^¶Biology Laboratory, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Tamaho-machi, Yamanashi 409-38, Japan

Peroxisomes are degraded by autophagic machinery termed "pexophagy" in yeast; however, whether this is essential for peroxisome degradation in mammals remains unknown. Here we have shown that Atg7, an essential gene for autophagy, plays a pivotal role in the degradation of excess peroxisomes in mammals. Following induction of peroxisomes by a 2-week treatment with phthalate esters in control and Atg7-deficient livers, peroxisomal degradation was monitored within 1 week after discontinuation of phthalate esters. Although most of the excess peroxisomes in the control liver were selectively degraded within 1 week, this rapid removal was exclusively impaired in the mutant liver. Furthermore, morphological analysis revealed that surplus peroxisomes, but not mutant hepatocytes, were surrounded by autophagosomes in the control. Our results indicated that the autophagic machinery is essential for the selective clearance of excess peroxisomes in mammals. This is the first direct evidence for the contribution of autophagic machinery in peroxisomal degradation in mammals.

Received for publication, November 15, 2005

^* This work was supported by Grants-in-aid 15032263, 16790195, 15590254, 09680629, and 1270040 from the Ministry of Education, Culture, Sports, Science and Technology of Japan. 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.

¹ Both authors contributed equally to this work.

² To whom correspondence should be addressed: Dept. of Biochemistry, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan. Tel.: 81-3-5802-1031; Fax: 81-3-5802-5889; E-mail: komilabo{at}med.juntendo.ac.jp.

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