ArticleJournal of bacteriology1998
Regulation of expression of GLT1, the gene encoding glutamate synthase in Saccharomyces cerevisiae.
Article in Journal of bacteriology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 56 citations in OpenAlex.
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- Effect of 21 different nitrogen sources on global gene expression in the yeast Saccharomyces cerevisiae.Molecular and cellular biology · 2007Article
- Identification of a region of the Arabidopsis AtAOX1a promoter necessary for mitochondrial retrograde regulation of expression.Plant molecular biology · 2005Article
- Transcriptional remodeling in response to iron deprivation in Saccharomyces cerevisiae.Molecular biology of the cell · 2004Article
- Evidence for control of nitrogen metabolism by a START-dependent mechanism in Saccharomyces cerevisiae.Molecular genetics and genomics : MGG · 2004Article
- Transcriptional profiling shows that Gcn4p is a master regulator of gene expression during amino acid starvation in yeast.Molecular and cellular biology · 2001Article
- TOR modulates GCN4-dependent expression of genes turned on by nitrogen limitation.Journal of bacteriology · 2001Article
- Differential contribution of the proline and glutamine pathways to glutamate biosynthesis and nitrogen assimilation in yeast lacking glutamate dehydrogenase.Microbiological researchArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Saccharomyces cerevisiae glutamate synthase (GOGAT) is an oligomeric enzyme composed of three 199-kDa identical subunits encoded by GLT1. In this work, we analyzed GLT1 transcriptional regulation. GLT1-lacZ fusions were prepared and GLT1 expression was determined in a GDH1 wild-type strain and in a gdh1 mutant derivative grown in the presence of various nitrogen sources. Null mutants impaired in GCN4, GLN3, GAT1/NIL1, or UGA43/DAL80 were transformed with a GLT1-lacZ fusion to determine whether the above-mentioned transcriptional factors had a role in GLT1 expression. A collection of increasingly larger 5' deletion derivatives of the GLT1 promoter was constructed to identify DNA sequences that could be involved in GLT1 transcriptional regulation. The effect of the lack of GCN4, GLN3, or GAT1/NIL1 was also tested in the pertinent 5' deletion derivatives. Our results indicate that (i) GLT1 expression is negatively modulated by glutamate-mediated repression and positively regulated by Gln3p- and Gcn4p-dependent transcriptional activation; (ii) two cis-acting elements, a CGGN15CCG palindrome and an imperfect poly(dA-dT), are present and could play a role in GLT1 transcriptional activation; and (iii) GLT1 expression is moderately regulated by GCN4 under amino acid deprivation. Our results suggest that in a wild-type strain grown on ammonium, GOGAT constitutes an ancillary pathway for glutamate biosynthesis.
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