scholarly journals Synergistic Operation of the CAR2(Ornithine Transaminase) Promoter Elements in Saccharomyces cerevisiae

1999 ◽  
Vol 181 (22) ◽  
pp. 7052-7064 ◽  
Author(s):  
Heui-Dong Park ◽  
Stephanie Scott ◽  
Rajendra Rai ◽  
Rosemary Dorrington ◽  
Terrance G. Cooper
Keyword(s):  
Gene Expression ◽  
Transcriptional Activation ◽  
Catabolite Repression ◽  
Early Report ◽  
Formal Structure ◽  
Nitrogen Catabolite Repression ◽  
Ornithine Transaminase ◽  
Transcription Activators ◽  
And Control ◽  
Gata Family

ABSTRACT Dal82p binds to the UIS ALL sites of allophanate-induced genes of the allantoin-degradative pathway and functions synergistically with the GATA family Gln3p and Gat1p transcriptional activators that are responsible for nitrogen catabolite repression-sensitive gene expression. CAR2, which encodes the arginine-degradative enzyme ornithine transaminase, is not nitrogen catabolite repression sensitive, but its expression can be modestly induced by the allantoin pathway inducer. The dominant activators ofCAR2 transcription have been thought to be the ArgR and Mcm1 factors, which mediate arginine-dependent induction. These observations prompted us to investigate the structure of theCAR2 promoter with the objectives of determining whether other transcription factors were required for CAR2expression and, if so, of ascertaining their relative contributions toCAR2’s expression and control. We show that Rap1p binds upstream of CAR2 and plays a central role in its induced expression irrespective of whether the inducer is arginine or the allantoin pathway inducer analogue oxalurate (OXLU). Our data also explain the early report that ornithine transaminase production is induced when cells are grown with urea. OXLU induction derives from the Dal82p binding site, which is immediately downstream of the Rap1p site, and Dal82p functions synergistically with Rap1p. This synergism is unlike all other known instances of Dal82p synergism, namely, that with the GATA family transcription activators Gln3p and Gat1p, which occurs only in the presence of an inducer. The observations reported suggest that CAR2 gene expression results from strong constitutive transcriptional activation mediated by Rap1p and Dal82p being balanced by the down regulation of an equally strong transcriptional repressor, Ume6p. This balance is then tipped in the direction of expression by the presence of the inducer. The formal structure of theCAR2 promoter and its operation closely follow the model proposed for CAR1.

scholarly journals The Yeast GATA Factor Gat1 Occupies a Central Position in Nitrogen Catabolite Repression-Sensitive Gene Activation

2009 ◽  
Vol 29 (13) ◽  
pp. 3803-3815 ◽  
Author(s):  
Isabelle Georis ◽  
André Feller ◽  
Fabienne Vierendeels ◽  
Evelyne Dubois
Keyword(s):  
Gene Expression ◽  
Catabolite Repression ◽  
Nitrogen Availability ◽  
Gene Activation ◽  
Nitrogen Sources ◽  
Central Position ◽  
Limiting Factor ◽  
Nitrogen Catabolite Repression ◽  
Gata Factor ◽  
Gata Factors

ABSTRACT Saccharomyces cerevisiae cells are able to adapt their metabolism according to the quality of the nitrogen sources available in the environment. Nitrogen catabolite repression (NCR) restrains the yeast's capacity to use poor nitrogen sources when rich ones are available. NCR-sensitive expression is modulated by the synchronized action of four DNA-binding GATA factors. Although the first identified GATA factor, Gln3, was considered the major activator of NCR-sensitive gene expression, our work positions Gat1 as a key factor for the integrated control of NCR in yeast for the following reasons: (i) Gat1 appeared to be the limiting factor for NCR gene expression, (ii) GAT1 expression was regulated by the four GATA factors in response to nitrogen availability, (iii) the two negative GATA factors Dal80 and Gzf3 interfered with Gat1 binding to DNA, and (iv) Gln3 binding to some NCR promoters required Gat1. Our study also provides mechanistic insights into the mode of action of the two negative GATA factors. Gzf3 interfered with Gat1 by nuclear sequestration and by competition at its own promoter. Dal80-dependent repression of NCR-sensitive gene expression occurred at three possible levels: Dal80 represses GAT1 expression, it competes with Gat1 for binding, and it directly represses NCR gene transcription.

scholarly journals cis-Dominant mutations which dramatically enhance DUR1,2 gene expression without affecting its normal regulation.

1984 ◽  
Vol 4 (5) ◽  
pp. 947-955 ◽  
Author(s):  
G Chisholm ◽  
T Cooper
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Control System ◽  
Normal Control ◽  
Chromatin Structure ◽  
Catabolite Repression ◽  
Mutant Phenotype ◽  
Nitrogen Catabolite Repression ◽  
Upstream Control ◽  
Affect Gene Expression

We have isolated three cis-dominant mutations which dramatically enhance DUR1 ,2 gene expression in Saccharomyces cerevisiae. The mutant phenotype, which is expressed both in haploid and MATa/MAT alpha diploid strains, does not appear to be an alteration of the normal control system for this gene because its expression remained fully inducible and sensitive to nitrogen catabolite repression. Instead, we found much higher levels of DUR1 ,2-specific RNA under both uninduced and induced conditions, i.e., the overproduction trait was superimposed on normal regulation of the gene. The mutations seemed to affect gene expression in a unidirectional manner or to be specific for DUR1 ,2 gene expression, because other genes in proximity to the mutations were not affected. We feel that these mutations may alter the chromatin structure in the vicinity of the DUR1 ,2 upstream control sequences or, alternatively, may be Ty insertions which no longer possess the ROAM characteristics reported by others and ourselves.

scholarly journals The Level of DAL80 Expression Down-Regulates GATA Factor-Mediated Transcription inSaccharomyces cerevisiae

2000 ◽  
Vol 182 (23) ◽  
pp. 6584-6591 ◽  
Author(s):  
Thomas S. Cunningham ◽  
Rajendra Rai ◽  
Terrance G. Cooper
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Binding Sites ◽  
Nitrogen Availability ◽  
Transport Proteins ◽  
Catabolic Gene ◽  
Nitrogen Catabolite Repression ◽  
Gata Factor ◽  
Regulatory Circuit ◽  
Gata Family

ABSTRACT Nitrogen-catabolic gene expression in Saccharomyces cerevisiae is regulated by the action of four GATA family transcription factors: Gln3p and Gat1p/Nil1p are transcriptional activators, and Dal80 and Deh1p/Gzf3p are repressors. In addition to the GATA sequences situated upstream of all nitrogen catabolite repression-sensitive genes that encode enzyme and transport proteins, the promoters of the GAT1, DAL80, andDEH1 genes all contain multiple GATA sequences as well. These GATA sequences are the binding sites of the GATA family transcription factors and are hypothesized to mediate their autogenous and cross regulation. Here we show, using DAL80 fused to the carbon-regulated GAL1,10 or copper-regulated CUP1 promoter, that GAT1expression is inversely regulated by the level of DAL80expression, i.e., as DAL80 expression increases,GAT1 expression decreases. The amount of DAL80expression also dictates the level at which DAL3, a gene activated almost exclusively by Gln3p, is transcribed. Gat1p was found to partially substitute for Gln3p in transcription. These data support the contention that regulation of GATA-factor gene expression is tightly and dynamically coupled. Finally, we suggest that the complicated regulatory circuit in which the GATA family transcription factors participate is probably most beneficial as cells make the transition from excess to limited nitrogen availability.

scholarly journals Gat1p, a GATA family protein whose production is sensitive to nitrogen catabolite repression, participates in transcriptional activation of nitrogen-catabolic genes in Saccharomyces cerevisiae.

1996 ◽  
Vol 16 (3) ◽  
pp. 847-858 ◽  
Author(s):  
J A Coffman ◽  
R Rai ◽  
T Cunningham ◽  
V Svetlov ◽  
T G Cooper
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcriptional Activation ◽  
Catabolite Repression ◽  
Nitrogen Sources ◽  
Nitrogen Catabolite Repression ◽  
Triple Mutant ◽  
Regulatory Circuit ◽  
Catabolic Genes ◽  
Family Protein ◽  
Sequence Elements

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.

RTG-dependent Mitochondria-to-Nucleus Signaling Is Regulated byMKS1and Is Linked to Formation of Yeast Prion [URE3]

2002 ◽  
Vol 13 (3) ◽  
pp. 795-804 ◽  
Author(s):  
Takayuki Sekito ◽  
Zhengchang Liu ◽  
Janet Thornton ◽  
Ronald A. Butow
Keyword(s):  
Gene Expression ◽  
Catabolite Repression ◽  
Target Gene ◽  
Negative Regulator ◽  
Yeast Cells ◽  
Nitrogen Catabolite Repression ◽  
Yeast Prion ◽  
Phosphorylation Pattern ◽  
Bhlh Transcription Factors ◽  
Do So

An important function of the RTG signaling pathway is maintenance of intracellular glutamate supplies in yeast cells with dysfunctional mitochondria. Herein, we report that MKS1is a negative regulator of the RTG pathway, acting between Rtg2p, a proximal sensor of mitochondrial function, and the bHLH transcription factors Rtg1p and Rtg3p. In mks1Δcells, RTG target gene expression is constitutive, bypassing the requirement for Rtg2p, and is no longer repressible by glutamate. We show further that Mks1p is a phosphoprotein whose phosphorylation pattern parallels that of Rtg3p in response to activation of the RTG pathway, and that Mks1p is in a complex with Rtg2p. MKS1 was previously implicated in the formation of [URE3], an inactive prion form of a negative regulator of the nitrogen catabolite repression pathway, Ure2p.rtgΔ mutations induce [URE3] and can do so independently of MKS1. We find that glutamate suppresses [URE3] formation, suggesting that the Mks1p effect on the formation of [URE3] can occur indirectly via regulation of theRTG pathway.

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