title: Loss of function of KRE5 suppresses temperature sensitivity of mutants lacking mitochondrial anionic lipids.
abstract: 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 pgs1Delta mutant exhibits severe growth defects at 37 degrees C. To understand the essential functions of mitochondrial anionic lipids at elevated temperatures, we isolated suppressors of pgs1Delta that grew at 37 degrees C. One of the suppressors has a loss of function mutation in KRE5, which is involved in cell wall biogenesis. The cell wall of pgs1Delta 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 pgs1Delta and suppressed the temperature sensitivity of all CL-deficient mutants. Evidence is presented suggesting that the previously reported inability of pgs1Delta 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.
authors.affiliation: Department of Biological Sciences, Wayne State University, Detroit, MI 48202, USA.
authors.forename: Quan
authors.initials: Q
authors.lastname: Zhong
authors.forename: Jelena
authors.initials: J
authors.lastname: Gvozdenovic-Jeremic
authors.forename: Paul
authors.initials: P
authors.lastname: Webster
authors.forename: Jingming
authors.initials: J
authors.lastname: Zhou
authors.forename: Miriam L
authors.initials: ML
authors.lastname: Greenberg
mesh_terms: D000483:Alleles; D000595:Amino Acid Sequence; D000617:Aminoglycosides / Q000494:pharmacology; D000838:Anions / Q000378:metabolism*; D000942:Antigens, Bacterial / Q000633:toxicity; D016667:Bacterial Capsules; D002308:Cardiolipins / Q000235:genetics / Q000378:metabolism* / Q000648:ultrastructure; D002470:Cell Survival / Q000235:genetics; D002473:Cell Wall / Q000737:chemistry / Q000648:ultrastructure; D002686:Chitin / Q000032:analysis / Q000378:metabolism; D018389:Codon, Nonsense; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005456:Fluorescent Dyes; D017353:Gene Deletion; D005800:Genes, Fungal; D016153:Genes, Suppressor; D006023:Glycoproteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism* / Q000648:ultrastructure; D007211:Indoles; D008928:Mitochondria / Q000737:chemistry* / Q000378:metabolism; D010715:Phosphatidylglycerols / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D011135:Polysaccharides, Bacterial / Q000633:toxicity; D012441:Saccharomyces cerevisiae / Q000235:genetics / Q000378:metabolism / Q000648:ultrastructure; D029701:Saccharomyces cerevisiae Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism* / Q000648:ultrastructure; D013696:Temperature; D047071:beta-Glucans / Q000032:analysis / Q000737:chemistry
chemical_list: D000617:Aminoglycosides; D000838:Anions; D000942:Antigens, Bacterial; D002308:Cardiolipins; D018389:Codon, Nonsense; D004791:Enzyme Inhibitors; D005456:Fluorescent Dyes; D006023:Glycoproteins; D007211:Indoles; C064198:KRE5 protein, S cerevisiae; D010715:Phosphatidylglycerols; D011135:Polysaccharides, Bacterial; D029701:Saccharomyces cerevisiae Proteins; D047071:beta-Glucans; C036962:capsular polysaccharide K1; D002686:Chitin; C007293:DAPI; C033363:beta-1,3-glucan; C011952:nikkomycin