ArticleMolecular and cellular biology1994
Multiple mechanisms provide rapid and stringent glucose repression of GAL gene expression in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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104 citing papers in PubMed, 248 citations in OpenAlex.
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- Endosomal cargo recycling mediated by Gpa1 and phosphatidylinositol 3-kinase is inhibited by glucose starvation.Molecular biology of the cell · 2022Article
- Transcriptional repressor Gal80 recruits corepressor complex Cyc8-Tup1 to structural genes of the Saccharomyces cerevisiae GAL regulon.Current genetics · 2022Article
- A synthetic promoter system for well-controlled protein expression with different carbon sources in Saccharomyces cerevisiae.Microbial cell factories · 2021Article
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- Decoupling transcription factor expression and activity enables dimmer switch gene regulation.Science (New York, N.Y.) · 2021Article
- Mapping Synthetic Dosage Lethal Genetic Interactions in Saccharomyces cerevisiae.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Computational study on ratio-sensing in yeast galactose utilization pathway.PLoS computational biology · 2020Article
- Evolutionary repair: Changes in multiple functional modules allow meiotic cohesin to support mitosis.PLoS biology · 2020Article
44 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
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Abstract
Expression of the GAL genes of Saccharomyces cerevisiae is induced during growth on galactose by a well-characterized regulatory mechanism that relieves Gal80p inhibition of the Gal4p transcriptional activator. Growth on glucose overrides induction by galactose. Glucose repression acts at three levels to reduce GAL1 expression: (i) it reduces the level of functional inducer in the cell; (ii) it lowers cellular levels of Gal4p by repressing GAL4 transcription; and (iii) it inhibits Gal4p function through a repression element in the GAL1 promoter. We quantified the amount of repression provided by each mechanism by assaying strains with none, one, two, or all three of the repression mechanisms intact. In a strain lacking all three repression mechanisms, there was almost no glucose repression of GAL1 expression, suggesting that these are the major, possibly the only, mechanisms of glucose repression acting upon the GAL genes. The mechanism of repression that acts to reduce Gal4p levels in the cell is established slowly (hours after glucose addition), probably because Gal4p is stable. By contrast, the repression acting through the upstream repression sequence element in the GAL1 promoter is established rapidly (within minutes of glucose addition). Thus, these three mechanisms of repression collaborate to repress GAL1 expression rapidly and stringently. The Mig1p repressor is responsible for most (possibly all) of these repression mechanisms. We show that for GAL1 expression, mig1 mutations are epistatic to snf1 mutations, indicating that Mig1p acts after the Snf1p protein kinase in the glucose repression pathway, which suggests that Snf1p is an inhibitor of Mig1p.
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