Stb3 plays a role in the glucose-induced transition from quiescence to growth in Saccharomyces cerevisiae
Addition of glucose to quiescent Saccharomyces cerevisiae cells causes the immediate induction of approximately 1000 genes. These genes include ribosomal proteins (RP) and non-RP genes needed for ribosome production and other growth processes. RRPE sequence elements are commonly found 5' of non...
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Published in | Genetics (Austin) Vol. 185; no. 3; pp. 797 - 810 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Genetics Society of America
01.07.2010
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Subjects | |
Online Access | Get full text |
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Summary: | Addition of glucose to quiescent Saccharomyces cerevisiae cells causes the immediate induction of approximately 1000 genes. These genes include ribosomal proteins (RP) and non-RP genes needed for ribosome production and other growth processes. RRPE sequence elements are commonly found 5' of non-RP growth gene ORFs, and Stb3 has recently been identified as an RRPE binding protein. Stb3 overexpression (Stb3OE) produces a slow growth phenotype that is associated with reduced expression of non-RP genes and a drop in the rate of amino acid incorporation. Genes affected by Stb3 are associated with a TGAAAAA motif. Stb3 is restricted to the nucleus in quiescent cells and is immediately released into the cytoplasm after glucose repletion. The Stb3OE slow growth phenotype is reversed by loss of Hos2 histone deactylase activity, consistent with the idea that repression involves histone deacetylation. SCH9 overexpression or PPH22 deletion, mutations that activate target of rapamycin (Tor) nutrient sensing pathways, also reverse the Stb3OE phenotype. Inhibition of Tor signaling makes the phenotype more severe and restricts Stb3 to the nucleus. The results support a model in which Stb3 is one of the components that repress a large set of growth genes as nutrients are depleted. This repression is ended by glucose. |
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Bibliography: | USDOE Office of Science (SC), Biological and Environmental Research (BER) These authors contributed equally to this work. Supporting information is available online at http://www.genetics.org/cgi/content/full/genetics.110.116665/DC1. Communicating editor: F. Winston |
ISSN: | 1943-2631 0016-6731 1943-2631 |
DOI: | 10.1534/genetics.110.116665 |