Reference: Crespo JL, et al. (2004)
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Abstract
The GATA transcription factors GLN3 and GAT1 activate nitrogen-regulated genes in Saccharomyces cerevisiae. NPR1 is a protein kinase that controls post-Golgi sorting of amino acid permeases. In the presence of a good nitrogen source, TOR (target of rapamycin) maintains GLN3 and NPR1 phosphorylated and inactive by inhibiting the type 2A-related phosphatase SIT4. We identified NPR1 as a regulator of GLN3. Specifically, loss of NPR1 causes nuclear translocation and activation of GLN3, but not GAT1, in nitrogen-rich conditions. NPR1-mediated inhibition of GLN3 is independent of the phosphatase SIT4. We also demonstrate that the E3/E4 ubiquitin-protein ligase proteins RSP5 and BUL1/2 are required for GLN3 activation under poor nitrogen conditions. Thus, NPR1 and BUL1/2 antagonistically control GLN3-dependent transcription, suggesting a role for regulated ubiquitination in the control of nutrient-responsive transcription.
- Reference Type
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Journal Article |
Research Support, Non-U.S. Gov't
- Authors
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Crespo JL,
Helliwell SB,
Wiederkehr C,
Demougin P,
Fowler B,
Primig M,
Hall MN
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- GAT1 | GLN3 | SIT4 | BUL1 | BUL2 | RSP5 | NPR1 | MEP2
- URE2
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