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    Mutation of a phosphorylatable residue in Put3p affects the magnitude of rapamycin-induced PUT1 activation in a Gat1p-dependent manner.

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    Authors
    Leverentz, Michael K
    Campbell, Robert N
    Connolly, Yvonne
    Whetton, Anthony D
    Reece, Richard J
    Affiliation
    Faculty of Life Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, United Kingdom.
    Issue Date
    2009-09-04
    
    Metadata
    Show full item record
    Abstract
    Saccharomyces cerevisiae can utilize high quality (e.g. glutamine and ammonia) as well as low quality (e.g. gamma-amino butyric acid and proline) nitrogen sources. The transcriptional activator Put3p allows yeast cells to utilize proline as a nitrogen source through expression of the PUT1 and PUT2 genes. Put3p activates high level transcription of these genes by binding proline directly. However, Put3p also responds to other lower quality nitrogen sources. As nitrogen quality decreases, Put3p exhibits an increase in phosphorylation concurrent with an increase in PUT gene expression. The proline-independent activation of the PUT genes requires both Put3p and the positively acting GATA factors, Gln3p and Gat1p. Conversely, the phosphorylation of Put3p is not dependent on GATA factor activity. Here, we find that the mutation of Put3p at amino acid Tyr-788 modulates the proline-independent activation of PUT1 through Gat1p. The phosphorylation of Put3p appears to influence the association of Gat1p, but not Gln3p, to the PUT1 promoter. Combined, our findings suggest that this may represent a mechanism through which yeast cells rapidly adapt to use proline as a nitrogen source under nitrogen limiting conditions.
    Citation
    Mutation of a phosphorylatable residue in Put3p affects the magnitude of rapamycin-induced PUT1 activation in a Gat1p-dependent manner. 2009, 284 (36):24115-22 J. Biol. Chem.
    Journal
    The Journal of Biological Chemistry
    URI
    http://hdl.handle.net/10541/87562
    DOI
    10.1074/jbc.M109.030361
    PubMed ID
    19574222
    Type
    Article
    Language
    en
    ISSN
    0021-9258
    ae974a485f413a2113503eed53cd6c53
    10.1074/jbc.M109.030361
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research
    Molecular Biology Core Facility

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