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J. Biol. Chem., Vol. 279, Issue 31, 32294-32300, July 30, 2004

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Absence of Cardiolipin Results in Temperature Sensitivity, Respiratory Defects, and Mitochondrial DNA Instability Independent of pet56^*

Quan Zhong, Vishal M. Gohil, Lining Ma, and Miriam L. Greenberg

From the Department of Biological Sciences, Wayne State University, Detroit, Michigan 48202

Cardiolipin (CL) is a dimeric phospholipid localized primarily in the mitochondrial membrane. Previous studies have shown that yeast cells containing a disruption of CRD1, the structural gene encoding CL synthase, exhibit temperature-sensitive colony formation and multiple mitochondrial defects. A recent report (Zhang, M., Su, X., Mileykovskaya, E., Amoscato, A. A., and Dowhan, W. (2003) J. Biol. Chem. 278, 35204–35210) suggested that defects associated with CL deficiency may result from the reduced expression of PET56 in crd1 mutant backgrounds and should be reevaluated. In the current study, we present evidence that CL deficiency leads to mitochondrial DNA instability, loss of viability, and defects in oxidative phosphorylation at elevated temperatures. The observed mutant phenotypes are characteristic of crd1 mutant cells of both PET56 and pet56 backgrounds and are complemented by an episomal copy of CRD1 but not by expression of the PET56 gene. Phosphatidylglycerol is elevated in crd1 mutant cells when grown in the presence of fermentable and non-fermentable carbon sources, although the extent of the increase is higher in nonfermentable medium. An increase in the ratio of phosphatidylethanolamine to phosphatidylcholine was also apparent in the mutant. These findings demonstrate that CRD1, independent of PET56, is required for optimal mitochondrial function and for an essential cellular function at elevated temperatures.

Received for publication, March 24, 2004 , and in revised form, May 12, 2004.

^* This work was supported by National Institutes of Health Grant HL62263. 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.

These authors contributed equally to this work.

To whom correspondence should be addressed: Dept. of Biological Sciences, Wayne State University, 5047 Gullen Mall, Detroit, MI 48202. Tel.: 313-577-5202; Fax: 313-577-6891; E-mail: mlgreen{at}sun.science.wayne.edu.

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