TY - JOUR
T1 - A Saccharomyces cerevisiae genome-wide mutant screen for altered sensitivity to K1 killer toxin
AU - Pagé, Nicolas
AU - Gérard-Vincent, Manon
AU - Ménard, Patrice
AU - Beaulieu, Maude
AU - Azuma, Masayuki
AU - Dijkgraaf, Gerrit J P
AU - Li, Huijuan
AU - Marcoux, José
AU - Nguyen, Thuy
AU - Dowse, Tim
AU - Sdicu, Anne-Marie
AU - Bussey, Howard
N1 - Keywords: Cell Wall; Fungal Proteins; Gene Expression Regulation, Fungal; Genome, Fungal; Glucans; Killer Factors, Yeast; Mutagenesis; Mycotoxins; Open Reading Frames; Phenotype; Ribosomes; Saccharomyces cerevisiae; Sequence Deletion; beta-Glucans
PY - 2003
Y1 - 2003
N2 - Using the set of Saccharomyces cerevisiae mutants individually deleted for 5718 yeast genes, we screened for altered sensitivity to the antifungal protein, K1 killer toxin, that binds to a cell wall beta-glucan receptor and subsequently forms lethal pores in the plasma membrane. Mutations in 268 genes, including 42 in genes of unknown function, had a phenotype, often mild, with 186 showing resistance and 82 hypersensitivity compared to wild type. Only 15 of these genes were previously known to cause a toxin phenotype when mutated. Mutants for 144 genes were analyzed for alkali-soluble beta-glucan levels; 63 showed alterations. Further, mutants for 118 genes with altered toxin sensitivity were screened for SDS, hygromycin B, and calcofluor white sensitivity as indicators of cell surface defects; 88 showed some additional defect. There is a markedly nonrandom functional distribution of the mutants. Many genes affect specific areas of cellular activity, including cell wall glucan and mannoprotein synthesis, secretory pathway trafficking, lipid and sterol biosynthesis, and cell surface signal transduction, and offer new insights into these processes and their integration.
AB - Using the set of Saccharomyces cerevisiae mutants individually deleted for 5718 yeast genes, we screened for altered sensitivity to the antifungal protein, K1 killer toxin, that binds to a cell wall beta-glucan receptor and subsequently forms lethal pores in the plasma membrane. Mutations in 268 genes, including 42 in genes of unknown function, had a phenotype, often mild, with 186 showing resistance and 82 hypersensitivity compared to wild type. Only 15 of these genes were previously known to cause a toxin phenotype when mutated. Mutants for 144 genes were analyzed for alkali-soluble beta-glucan levels; 63 showed alterations. Further, mutants for 118 genes with altered toxin sensitivity were screened for SDS, hygromycin B, and calcofluor white sensitivity as indicators of cell surface defects; 88 showed some additional defect. There is a markedly nonrandom functional distribution of the mutants. Many genes affect specific areas of cellular activity, including cell wall glucan and mannoprotein synthesis, secretory pathway trafficking, lipid and sterol biosynthesis, and cell surface signal transduction, and offer new insights into these processes and their integration.
M3 - Journal article
C2 - 12663529
SN - 0016-6731
VL - 163
SP - 875
EP - 894
JO - Genetics
JF - Genetics
IS - 3
ER -