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A Saccharomyces cerevisiae genome-wide mutant screen for altered sensitivity to K1 killer toxin

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Standard

A Saccharomyces cerevisiae genome-wide mutant screen for altered sensitivity to K1 killer toxin. / Pagé, Nicolas; Gérard-Vincent, Manon; Ménard, Patrice; Beaulieu, Maude; Azuma, Masayuki; Dijkgraaf, Gerrit J P; Li, Huijuan; Marcoux, José; Nguyen, Thuy; Dowse, Tim; Sdicu, Anne-Marie; Bussey, Howard.

I: Genetics, Bind 163, Nr. 3, 2003, s. 875-94.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Pagé, N, Gérard-Vincent, M, Ménard, P, Beaulieu, M, Azuma, M, Dijkgraaf, GJP, Li, H, Marcoux, J, Nguyen, T, Dowse, T, Sdicu, A-M & Bussey, H 2003, 'A Saccharomyces cerevisiae genome-wide mutant screen for altered sensitivity to K1 killer toxin', Genetics, bind 163, nr. 3, s. 875-94.

APA

Pagé, N., Gérard-Vincent, M., Ménard, P., Beaulieu, M., Azuma, M., Dijkgraaf, G. J. P., ... Bussey, H. (2003). A Saccharomyces cerevisiae genome-wide mutant screen for altered sensitivity to K1 killer toxin. Genetics, 163(3), 875-94.

Vancouver

Pagé N, Gérard-Vincent M, Ménard P, Beaulieu M, Azuma M, Dijkgraaf GJP o.a. A Saccharomyces cerevisiae genome-wide mutant screen for altered sensitivity to K1 killer toxin. Genetics. 2003;163(3):875-94.

Author

Pagé, Nicolas ; Gérard-Vincent, Manon ; Ménard, Patrice ; Beaulieu, Maude ; Azuma, Masayuki ; Dijkgraaf, Gerrit J P ; Li, Huijuan ; Marcoux, José ; Nguyen, Thuy ; Dowse, Tim ; Sdicu, Anne-Marie ; Bussey, Howard. / A Saccharomyces cerevisiae genome-wide mutant screen for altered sensitivity to K1 killer toxin. I: Genetics. 2003 ; Bind 163, Nr. 3. s. 875-94.

Bibtex

@article{195238505da511df928f000ea68e967b,
title = "A Saccharomyces cerevisiae genome-wide mutant screen for altered sensitivity to K1 killer toxin",
abstract = "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.",
author = "Nicolas Pag{\'e} and Manon G{\'e}rard-Vincent and Patrice M{\'e}nard and Maude Beaulieu and Masayuki Azuma and Dijkgraaf, {Gerrit J P} and Huijuan Li and Jos{\'e} Marcoux and Thuy Nguyen and Tim Dowse and Anne-Marie Sdicu and Howard Bussey",
note = "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",
year = "2003",
language = "English",
volume = "163",
pages = "875--94",
journal = "Genetics",
issn = "1943-2631",
publisher = "The Genetics Society of America (GSA)",
number = "3",

}

RIS

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

VL - 163

SP - 875

EP - 894

JO - Genetics

JF - Genetics

SN - 1943-2631

IS - 3

ER -

ID: 19709962