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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Molecular microbiology 40 (2001), S. 0 
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: In the yeast Saccharomyces cerevisiae, the interplay between Gal3p, Gal80p and Gal4p determines the transcriptional status of the genes needed for galactose utilization. The interaction between Gal80p and Gal4p has been studied in great detail; however, our understanding of the mechanism of Gal3p in transducing the signal from galactose to Gal4p has only begun to emerge recently. Historically, Gal3p was believed to be an enzyme (catalytic model) that converts galactose to an inducer or co-inducer, which was thought to interact with GAL80p, the repressor of the system. However, recent genetic analyses indicate an alternative ‘protein–protein interaction model’. According to this model, Gal3p is activated by galactose, which leads to its interaction with Gal80p. Biochemical and genetic experiments that support this model provided new insights into how Gal3p interacts with the Gal80p–Gal4p complex, alleviates the repression of Gal80p and thus allows Gal4p to activate transcription. Recently, a galactose-independent signal was suggested to co-ordinate the induction of GAL genes with the energy status of the cell.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1617-4623
    Keywords: Key wordsGAL regulon ; Transcription ; Saccharomyces cerevisiae ; Galactose suppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract A plasmid clone that suppresses galactose toxicity in a gal7 yeast strain has been isolated from a multicopy genomic DNA library. Molecular analysis revealed that the region responsible for the suppression of galactose toxicity corresponds to the ORF YPR030w, which was named MRG19. A CEN-based plasmid carrying the above ORF was unable to suppress the toxicity. Galactokinase activity was substantially reduced in cell extracts obtained from transformants bearing multiple copies of MRG19. Multiple copies of MRG19 were also able to suppress galactokinase expression driven by the CYC1 promoter but not the TEF1 promoter. Multiple copies of MRG19 could not suppress GAL1-driven galactokinase expression in a gal80 strain. However, MRG19-mediated suppression of CYC1-driven galactokinase expression was independent of GAL80 function. These results imply that multiple copies of MRG19 suppress galactokinase expression probably at the level of transcription. In agreement with this idea, multiple copies of MRG19 also suppress β-galactosidase expression driven by the GAL1 promoter in a GAL80-dependent manner. Disruption of MRG19 leads to an increase in the cell density at stationary phase in synthetic complete medium. MRG19 encodes a previously uncharacterised 124-kDa protein that shows no sequence homology to any known proteins.
    Type of Medium: Electronic Resource
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