This Article Full Text (PDF) Other Versions of this Article: AEM.02843-06v1 73/18/5919    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Cheng, V. Articles by Bakalinsky, A. T. Search for Related Content PubMed PubMed Citation Articles by Cheng, V. Articles by Bakalinsky, A. T. Agricola Articles by Cheng, V. Articles by Bakalinsky, A. T.

 Previous Article  |  Next Article 

Appl. Environ. Microbiol. doi:10.1128/AEM.02843-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Genome-wide screen for oxalate-sensitive mutants of Saccharomyces cerevisiae

Department of Food Science and Technology, Wiegand Hall, Oregon State University, Corvallis, OR 97331-6602; Environmental and Molecular Toxicology, Agricultural and Life Sciences Building, Oregon State University, Corvallis, OR; Department of Horticulture, Agricultural and Life Sciences Building, Oregon State University, Corvallis, OR

	Abstract

Oxalic acid is an important virulence factor produced by phytopathogenic filamentous fungi. In order to discover yeast genes whose orthologs in the pathogen may confer self-tolerance and whose plant orthologs may protect the host, a Saccharomyces cerevisiae deletion library consisting of 4,827 haploid mutants harboring deletions in non-essential genes was screened for growth inhibition and survival in a rich medium containing 30 mM oxalic acid at pH 3. A total of 31 mutants were identified that had significantly lower cell yields in oxalate medium relative to yields in an oxalate-free medium. About 35% of these mutants had not previously been detected in published screens for sensitivity to sorbic or citric acids. Mutants impaired in endosomal transport, rgp1, ric1, snf7, vps16, vps20, and vps51, were significantly overrepresented relative to their frequency among all verified yeast ORFs. Oxalate exposure to a subset of 5 mutants, drs2, vps16, vps51, ric1, and rib4, was lethal. With the exception of rib4, all of these mutants are impaired in vesicle-mediated transport. Indirect evidence is provided suggesting that the sensitivity of the rib4 mutant, a riboflavin auxotroph, is due to oxalate-mediated interference with riboflavin uptake by the putative monocarboxylate transporter Mch5.