Abstract
We show that mutants lacking either the phosphatase activator Rrd1 or the phosphatase Pph3 are resistant to rapamycin and that double mutants exhibit a synergistic response. This phenotype could be related to an inability of the mutants to degrade RNA polymerase II, leading to transcription of critical genes that sustain growth.
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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Blotting, Northern
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Gene Expression Regulation, Fungal / drug effects
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Gene Expression Regulation, Fungal / physiology*
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Intracellular Signaling Peptides and Proteins
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Mutation
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Peptidylprolyl Isomerase
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Phosphoprotein Phosphatases / genetics
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Phosphoprotein Phosphatases / physiology
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Saccharomyces cerevisiae / drug effects
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Saccharomyces cerevisiae / genetics*
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Saccharomyces cerevisiae Proteins / genetics
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Saccharomyces cerevisiae Proteins / physiology*
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Sirolimus / pharmacology*
Substances
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Antifungal Agents
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Intracellular Signaling Peptides and Proteins
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Saccharomyces cerevisiae Proteins
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PPH3 protein, S cerevisiae
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Phosphoprotein Phosphatases
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Peptidylprolyl Isomerase
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RRD1 protein, S cerevisiae
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Sirolimus