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J. Biol. Chem., Vol. 279, Issue 52, 54655-54662, December 24, 2004

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Defective Mitochondrial Protein Translocation Precludes Normal Caenorhabditis elegans Development^*

Sean P. Curran, Edward P. Leverich¶, Carla M. Koehler, and Pamela L. Larsen||**

From the Department of Chemistry and Biochemistry, University of California, Los Angeles, California 90095-1569 and the ^||Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas 78229-3900

We demonstrate biochemically that the genes identified by sequence similarity as orthologs of the mitochondrial import machinery are functionally conserved in Caenorhabditis elegans. Specifically, tin-9.1 and tin-10 RNA interference (RNAi) treatment of nematodes impairs import of the ADP/ATP carrier into isolated mitochondria. Developmental phenotypes are associated with gene knock-down of the mitochondrial import components. RNAi of tomm-7 and ddp-1 resulted in mitochondria with an interconnected morphology in vivo, presumably due to defects in the assembly of outer membrane fission/fusion components. RNAi of the small Tim proteins TIN-9.1, TIN-9.2, and TIN-10 resulted in a small body size, reduced number of progeny produced, and partial embryonic lethality. An additional phenotype of the tin-9.2(RNAi) animals is defective formation of the somatic gonad. The biochemical demonstration that the protein import activity is reduced, under the same conditions that yield the defects in specific tissues and lethality in a later generation, suggests that the developmental abnormalities observed are a consequence of defects in mitochondrial inner membrane biogenesis.

Received for publication, August 20, 2004 , and in revised form, October 12, 2004.

^* This work was supported in part by the Damon Runyon-Walter Winchell Cancer Research Foundation Grant DRS18, Burroughs Wellcome Fund New Investigator Award 1001120 in the Toxicology Sciences, Beckman Foundation scholar award, National Institutes of Health Grant 1R01GM61721, and the Ellison Medical Foundation. 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.

Supported by United States Public Health Service Grant GM07185. Present address: Dept. of Molecular Biology, Massachusetts General Hospital and Dept. of Genetics, Harvard Medical School, Boston, MA 02114.

^¶ Supported by United States Public Health Service Grant

^** To whom correspondence should be addressed: Dept. of Cellular and Structural Biology, University of Texas Health Science Center, 7703 Floyd Curl Dr., San Antonio, TX 78229. Tel.: 210-567-0608; Fax: 210-567-3803; E-mail: larsenp{at}uthscsa.edu.

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