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M403275200v1
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Papers In Press, published online ahead of print May 29, 2004
J. Biol. Chem, 10.1074/jbc.M403275200
Submitted on March 24, 2004
Revised on May 12, 2004
Accepted on May 29, 2004

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

Biological Sciences, Wayne State University, Detroit, MI 48202

Corresponding Author: mlgreen{at}sun.science.wayne.edu

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 (J. Biol.Chem. 278, 35204-35210) suggested that defects associated with CL deficiency may result from reduced expression of PET56 in crd1[delta] 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 temperature. The observed mutant phenotypes are characteristic of crd1[delta] 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 nonfermentable carbon sources, although the extent of increase is higher in non-fermentable 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 temperature.


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