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MBC in Press, published online ahead of print November 24, 2004
Mol. Biol. Cell 10.1091/mbc.E04-09-0808

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Submitted on September 15, 2004
Revised on November 9, 2004
Accepted on November 14, 2004

Loss of Function of KRE5 Suppresses Temperature Sensitivity of Mutants Lacking Mitochondrial Anionic Lipids

Quan Zhong,*{dagger} Jelena Gvozdenovic-Jeremic,*{dagger} Paul Webster,{ddagger} Jingming Zhou,* and Miriam L. Greenberg*{sect}

*Department of Biological Sciences, Wayne State University, Detroit, MI 48202; {ddagger}House Ear Institute, Los Angeles, CA 90057

Monitoring Editor: Howard Riezman

Disruption of PGS1, which encodes the enzyme that catalyzes the committed step of cardiolipin (CL) synthesis, results in loss of the mitochondrial anionic phospholipids phosphatidylglycerol (PG) and CL. The pgs1{Delta} mutant exhibits severe growth defects at 37°C. To understand the essential functions of mitochondrial anionic lipids at elevated temperatures, we isolated suppressors of pgs1{Delta} that grew at 37°C. One of the suppressors has a loss of function mutation in KRE5, which is involved in cell wall biogenesis. The cell wall of pgs1{Delta} contained markedly reduced {beta}-1,3-glucan, which was restored in the suppressor. Stabilization of the cell wall with osmotic support alleviated the cell wall defects of pgs1{Delta} and suppressed the temperature sensitivity of all CL deficient mutants. Evidence is presented suggesting that the previously reported inability of pgs1{Delta} to grow in the presence of ethidium bromide was due to defective cell wall integrity, not from "petite lethality". These findings demonstrated that mitochondrial anionic lipids are required for cellular functions that are essential in cell wall biogenesis, the maintenance of cell integrity and survival at elevated temperature.

{dagger}These authors contributed equally to this study.

{sect}Corresponding author. E-mail: MLGREEN{at}sun.science.wayne.edu






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