Regions in the promoter of the yeast <i>FBP1</i> gene implicated in catabolite repression may bind the product of the regulatory gene <i>MIG1</i>

Mercado, Juan J.; Vincent, Olivier; Gancedo, Juana M.

doi:10.1016/0014-5793(91)81112-l

Cited by 44 publications

(28 citation statements)

References 16 publications

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“…The HXT2-lacZ reporter (see Table 2) was obtained from S. Ö zcan (26); the FBP1-lacZ and PCK1-lacZ reporters were provided by J. M. Gancedo (20). The CYC1-lacZ reporters (see Fig.…”

Section: Methodsmentioning

confidence: 99%

“…By contrast, while Mig1p binds to the SUC2 promoter, disruption of MIG1 only partially relieves glucose repression of SUC2 expression (35). Furthermore, disruption of MIG1 has little or no effect on glucose repression of other genes whose promoters contain Mig1p-binding sites (20,26,28). These observations suggest that there may be other repressors with roles similar to that of Mig1p.…”

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confidence: 90%

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Two Zinc-Finger-Containing Repressors Are Responsible for Glucose Repression of SUC2 Expression

Lutfiyya

Johnston

1996

Molecular and Cellular Biology

149

142

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Expression of the SUC2 gene in Saccharomyces cerevisiae, which encodes invertase, is repressed about 200-fold by high levels of glucose. Mig1p is a Cys 2 His 2 zinc-finger-containing protein required for glucose repression of SUC2 and several other genes. However, SUC2 expression is still about 13-fold repressed by glucose in a mig1 mutant. We have identified a second repressor, Mig2p, containing zinc fingers very similar to those of Mig1p that is responsible for this remaining glucose repression of SUC2 expression. Overexpression of MIG2 represses SUC2 under nonrepressing conditions, and a LexA-Mig2p fusion represses transcription of a lexO-containing promoter in a glucose-dependent manner, supporting the idea that Mig2p is a glucoseactivated repressor. We have shown that Mig2p binds to the Mig1p-binding sites in the SUC2 promoter. Even though Mig1p and Mig2p bind to similar sites and share almost identical zinc fingers, they differ in their relative affinities for various Mig1p-binding sites. This could explain our observation that MIG2 appears to have little role in glucose repression of other promoters with MIG1-binding sites.Transcription of many genes in Saccharomyces cerevisiae is repressed during growth on glucose (for reviews, see references 15, 28, and 34). Glucose-repressed genes are of essentially three types: genes for utilization of carbon sources that are alternatives to glucose (e.g., GAL and SUC), genes encoding proteins of gluconeogenesis (e.g., FBP1 and PCK1), and genes required for oxidation of glucose (e.g., CYC1 and COX6).Mig1p is a DNA-binding repressor responsible for glucose repression of several of these genes (23). In the absence of glucose, Mig1p function is inhibited, directly or indirectly, by the Snf1p protein kinase, leading to derepression of gene expression (3, 4). Mig1p is thought to mediate repression by recruiting Ssn6p and Tup1p, which are general repressors that act through several diverse DNA-binding proteins in the cell (16,33). In the absence of Ssn6p and Tup1p, Mig1p is apparently an activator of transcription (33).Mig1p contains two Cys 2 His 2 zinc fingers related to the mammalian Krox20/Egr and Wilms' tumor proteins and, like these proteins, binds to a GC-rich motif. Unique to the Mig1p-binding site is an AT-rich region preceding the GC-rich sequence that is essential for binding (17). Binding sites for Mig1p have been identified in the promoters of several glucose-repressed genes, including GAL1, GAL4, and SUC2 (11,22,23).Mig1p binds to the GAL1 and GAL4 promoters and is the primary repressor responsible for glucose repression of the GAL genes: disruption of MIG1 relieves nearly all glucose repression of GAL1 and GAL4 expression (9, 11). By contrast, while Mig1p binds to the SUC2 promoter, disruption of MIG1 only partially relieves glucose repression of SUC2 expression (35). Furthermore, disruption of MIG1 has little or no effect on glucose repression of other genes whose promoters contain Mig1p-binding sites (20,26,28). These observations suggest that there may be ...

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“…The HXT2-lacZ reporter (see Table 2) was obtained from S. Ö zcan (26); the FBP1-lacZ and PCK1-lacZ reporters were provided by J. M. Gancedo (20). The CYC1-lacZ reporters (see Fig.…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 90%

Two Zinc-Finger-Containing Repressors Are Responsible for Glucose Repression of SUC2 Expression

Lutfiyya

Johnston

1996

Molecular and Cellular Biology

149

142

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“…3). Both enzymes are subject to catabolite inactivation (Holzer, 1976 (Mercado et al, 1991;Mercado & Gancedo, 1992). The exceptionally high sensitivity of the mRNAs of these genes towards glucose can at least be partly explained by stimulated mRNA degradation, and has been shown to be independent of Migl (Mercado et al, 1994;Yin et al, 1996).…”

Section: Gluconeogenesis and Glyoxylate Shuntmentioning

confidence: 99%

Glucose control in Saccharomyces cerevisiae: the role of MIG1 in metabolic functions

1998

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OverviewIndustrial cultivation media, such as molasses, wort, agricultural waste and lignocellulose hydrolysates, contain a mixture of metabolizable carbohydrates. These carbohydrates are taken up by cells in a certain order with intermittent lag phases due to a set of mechanisms controlled by glucose, referred to hereafter as glucose control. Thus, the presence or uptake of glucose has a negative impact upon the metabolism of other sugars. Glucose repression reduces the transcription rate of repressible genes, and is the most thoroughly investigated mechanism of glucose control (Fig. 1).In this review the different mechanisms of glucose control in Saccharomyces cereuisiae are first discussed, focusing on the mechanism of glucose repression. Next, the function of the regulatory protein Migl in the signalling cascade of glucose repression is explained. The impact of Migl-mediated glucose repression on metabolic functions is then discussed. It will be made clear that glucose repression is not confined to the above-mentioned example of mixed sugar metabolism. The last part of the review summarizes the effects glucose repression has on single metabolic functions. These components are then linked to a holistic view with the aim of understanding the effects of Migl on overall metabolism. Against this background possible physiological impacts of deletion/disruption of the MZGl gene are discussed.Glucose control in 5. cerevisiae

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“…Our second approach involved the analysis of an FBPl : :lacZ gene in which the lacZ sequence was fused after the nineteenth codon of the FBPl gene [17]. The \train CJM88 was transformed with pJJl1 (Table l), subjected to a mild temperature shock using depleted YPP medium, and the response of the FBPI : : lacZ mRNA was compared with the responses of the wild-type FBPI and PCKl mRNAs wder identical conditions (Fig.…”

Section: The Temperature-shock Response Is Mediated Partly At the Levmentioning

confidence: 99%

The Levels of Yeast Gluconeogenic mRNAs Respond to Environmental Factors

Mercado

Smith

Sagliocco

et al. 1994

European Journal of Biochemistry

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The FBPl and PCKl genes encode the gluconeogenic enzymes fructose-l,6-bisphosphatase and phosphoenoZpyruv9te carboxykinase, respectively. In the yeast, Saccharomyces cerevisiae, the corresponding mRNAs are present at low levels during growth on glucose, but are present at elevated levels during growth on gluconeogenic carbon sources. We demonstrate that the levels of the FBPl and PCKl mRNAs are acutely sensitive to the addition of glucose to the medium and that the levels of these mRNAs decrease rapidly when glucose is added to the medium at a concentration of only 0.005%. At this concentration, glucose blocks FBPl and PCKl transcription, but has no effect on iso-1 cytochrome c (CYCI) mRNA levels. Glucose also increases the rate of degradation of the PCKl mRNA approximately twofold, but only has a slight effect upon FBPl mRNA turnover. We show that the levels of the FBPl and PCKl mRNAs are also sensitive to other environmental factors. The levels of these mRNAs decrease transiently in response to a decrease of the pH from pH 7.5 to pH 6.5 in the medium, or to a mild temperature shock (from 24°C to 36°C). The latter response appears to be mediated by accelerated mRNA decay.Glycolysis and gluconeogenesis constitute two antagonistic pathways for the metabolism of different carbon sources. Depending on the resources available to the yeast, one pathway or the other is thought to be operational since their simultaneous function would probably cause futile cycles at the level of the antagonistic enzyme pairs phosphofructokinase/fructose-1,6-bisphosphatase and pyruvate kinaselphosphoenoZpyruvate carboxykinase. Tight regulation of these enzymes might therefore be expected, and in fact the enzymes are subject to multiple mechanisms of control, including allosteric regulation, protein inactivation, and changes in enzyme levels [l]. Glucose increases the levels of phosphofructokinase and pyruvate kinase mRNAs due to changes in the transcription rates of the corresponding genes [2]. Also, glucose-grown yeast has barely detectable levels of the mRNAs corresponding to the gluconeogenic genes FBPl and PCKl ,which encode fructose-l,6-bisphosphatase and phosphoenoZpyruvate carboxykinase, respectively [3 -51. Although it is usually assumed that these low levels are due to repression of transcription caused by glucose, glucose could also affect the stability of the mRNAs. To address this question, we measured the half-lives of the gluconeogenic mRNAs in yeast growing on non-fermentable carbon sources and in yeast shifted to a medium with glucose. In this study, we show that the turnover of the FBPl and PCKl mRNAs is accelerated slightly in the presence of glucose, but that the major response is at the transcriptional level.In the course of the experiments, we observed that the addition of hot fresh medium to yeast strains growing on a non-fermentable carbon source caused the rapid disappearance of the FBPl and PCKl mRNAs. Therefore, we studied the factors which could influence the levels of these gluconeogenic mRNAs in yeast. These...

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Regions in the promoter of the yeast FBP1 gene implicated in catabolite repression may bind the product of the regulatory gene MIG1

Cited by 44 publications

References 16 publications

Two Zinc-Finger-Containing Repressors Are Responsible for Glucose Repression of SUC2 Expression

Two Zinc-Finger-Containing Repressors Are Responsible for Glucose Repression of SUC2 Expression

Glucose control in Saccharomyces cerevisiae: the role of MIG1 in metabolic functions

The Levels of Yeast Gluconeogenic mRNAs Respond to Environmental Factors

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