Abstract
The fungal metabolite Brefeldin A (BFA) disrupts the Golgi apparatus and its incoming protein flux. We developed a genetic approach to identify yeast proteins involved in the protein transport step that BFA blocks. The BFR2 gene (YDR299W) was thus isolated as a high-copy suppressor of the growth defects induced by BFA in a sensitive strain of Saccharomyces cerevisiae. Although BFR2 over-expression did not cause a secretory block or slow-down, it partially suppressed the growth defect of four mutants blocked at the step of budding or docking of small vesicles en route to the Golgi (sec13-1, sec16-2, sec23-1, ypt1-1). The essential BFR2 gene was predicted to encode an extremely hydrophilic product containing two short regions with potential coiled-coils, one of which corresponds to a cluster of acidic residues.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antifungal Agents / pharmacology
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Brefeldin A
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Cyclopentanes / pharmacology*
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Endoplasmic Reticulum / genetics*
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Endoplasmic Reticulum / metabolism
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Gene Expression Regulation, Fungal / drug effects*
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Genes, Fungal / drug effects
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Genes, Suppressor / drug effects*
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Golgi Apparatus / genetics*
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Golgi Apparatus / metabolism
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Mutation
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Nystatin / pharmacology
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Organelles / genetics
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Organelles / metabolism
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Receptors, Fibroblast Growth Factor / biosynthesis
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Receptors, Fibroblast Growth Factor / genetics*
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Saccharomyces cerevisiae / drug effects
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Saccharomyces cerevisiae / genetics*
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Saccharomyces cerevisiae / growth & development*
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Saccharomyces cerevisiae Proteins*
Substances
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Antifungal Agents
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BFR2 protein, S cerevisiae
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Cyclopentanes
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Receptors, Fibroblast Growth Factor
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Saccharomyces cerevisiae Proteins
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Nystatin
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Brefeldin A