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Gat1p, a GATA Family Protein Whose Production Is Sensitive to Nitrogen Catabolite Repression, Participates in Transcriptional Activation of Nitrogen-Catabolic Genes in Saccharomyces cerevisiae
Author(s) -
Jonathan Coffman,
Rajendra Rai,
Thomas S. Cunningham,
Vladimir Svetlov,
Terrance Cooper
Publication year - 1996
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.16.3.847
Subject(s) - catabolite repression , biology , saccharomyces cerevisiae , psychological repression , gene , transcription (linguistics) , transcription factor , transcriptional regulation , regulation of gene expression , reporter gene , mutant , regulator , catabolism , biochemistry , gene expression , microbiology and biotechnology , genetics , enzyme , linguistics , philosophy
Saccharomyces cerevisiae cells selectively use nitrogen sources in their environment. Nitrogen catabolite repression (NCR) is the basis of this selectivity. Until recently NCR was thought to be accomplished exclusively through the negative regulation of Gln3p function by Ure2p. The demonstration that NCR-sensitive expression of multiple nitrogen-catabolic genes occurs in a gln3 delta ure2 delta dal80::hisG triple mutant indicated that the prevailing view of the nitrogen regulatory circuit was in need of revision; additional components clearly existed. Here we demonstrate that another positive regulator, designated Gat1p, participates in the transcription of NCR-sensitive genes and is able to weakly activate transcription when tethered upstream of a reporter gene devoid of upstream activation sequence elements. Expression of GAT1 is shown to be NCR sensitive, partially Gln3p dependent, and Dal80p regulated. In agreement with this pattern of regulation, we also demonstrate the existence of Gln3p and Dal80p binding sites upstream of GAT1.

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