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Vol. 16, Issue 2, 665-675, February 2005
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* Department of Biological Sciences, Wayne State University, Detroit, MI 48202;
House Ear Institute, Los Angeles, CA 90057
Submitted September 15, 2004;
Revised November 9, 2004;
Accepted November 14, 2004
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
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 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 contained markedly reduced 
-1,3-glucan, which was restored in the suppressor. Stabilization of the cell wall with osmotic support alleviated the cell wall defects of pgs1 and suppressed the temperature sensitivity of all CL-deficient mutants. Evidence is presented suggesting that the previously reported inability of pgs1 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.
Abbreviations used: CFW, calcoflour white; CL, cardiolipin; CSIII, chitin synthase III; GS, glucan synthase; mtDNA, mitochondrial DNA; PGP, phophatidylglycerolphosphate; PG, phosphatidylglycerol; Ura-, synthetic drop out medium without uracil; YPD, yeast extract, peptone, and dextrose; YPGE, yeast extract, glycerol and ethanol; YPDS, YPD supplemented with 1 M sorbitol.
These authors contributed equally to this study.
Corresponding author. E-mail address: mlgreen{at}sun.science.wayne.edu.
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