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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Understanding the mechanism of glucose repression in yeast has proved to be a difficult and challenging problem. A multitude of genes in different pathways are repressed by glucose at the level of transcription. The SUC2 gene, which encodes invertase, is an excellent reporter gene for glucose repression, since its expression is controlled exclusively by this pathway. Genetic analysis has identified numerous regulatory mutations which can either prevent derepression of SUC2 or render its expression insensitive to glucose repression. These mutations allow us to sketch the outlines of a pathway for general glucose repression, which has several key elements: hexokinase PII, encoded by HXK2, which seems to play a role in the sensing of glucose levels; the protein kinase encoded by SNF1, whose activity is required for derepression of many glucose-repressible genes; and the MIG1 repressor protein, which binds to the upstream regions of SUC2 and other glucose-repressible genes. Repression by MIG1 requires the activity of the CYC8 and TUP1 proteins. Glucose repression of other sets of genes seems to be controlled by the general glucose repression pathway acting in concert with other mechanisms. In the cases of the GAL genes and possibly CYC1, regulation is mediated by a cascade in which the general pathway represses expression of a positive transcriptional activator.
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PMID:Glucose repression in the yeast Saccharomyces cerevisiae. 131 Jul 93

We have cloned a yeast gene, SKO1, which in high copy number suppresses lethal overexpression of cAMP-dependent protein kinase. SKO1 encodes a bZIP protein that binds to the CRE motif, TGACGTCA. We found that SKO1 also binds to a CRE-like site in SUC2, a yeast gene encoding invertase which is under positive control by cAMP. A disruption of the SKO1 gene causes a partial derepression of SUC2, indicating that SKO1 is a negative regulator of the SUC2 gene. SKO1 interacts positively with MIG1, a zinc finger protein that mediates glucose repression of SUC2. A kinetic analysis revealed a complex regulation of the SUC2 mRNA in response to glucose. First, MIG1 mediates a rapid and strong repression of SUC2, which is complete within 10 minutes. Second, a MIG1-independent process causes a further slow reduction in the mRNA. Third, in the absence of MIG1, there is also a rapid but transient glucose induction of the SUC2 mRNA. This induction is correlated with a transient loss of SKO1-dependent repression.
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PMID:Yeast SKO1 gene encodes a bZIP protein that binds to the CRE motif and acts as a repressor of transcription. 143 46

For expression of the alpha-galactosidase gene from Cyamopsis tetragonoloba in Kluyveromyces marxianus CBS 6556 we have used the promoter of the homologous inulinase-encoding gene (INU1). The INU1 gene has been cloned and sequenced and the coding region shows an identity of 59% with the Saccharomyces cerevisiae invertase gene (SUC2). In the 5'-flanking region of INU1 we found a sequence (TAAATCCGGGG) that perfectly matches to the MIG1 binding consensus sequence (WWWWTSYGGGG) of the S. cerevisiae GAL1, GAL4 and SUC2 genes. Using the K. marxianus INU1 promoter and prepro-signal sequence, we obtained a high alpha-galactosidase production level (153 mg/l) and a secretion efficiency of 99%. Both the production level and the secretion efficiency were significantly reduced when the INU1 pro-peptide was deleted. With either the S. cerevisiae PGK or GAL7 promoter we could obtain only low alpha-galactosidase production levels (2 mg/l).
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PMID:Expression of an alpha-galactosidase gene under control of the homologous inulinase promoter in Kluyveromyces marxianus. 776 85

The expression of Saccharomyces cerevisiae SUC genes is exclusively regulated by catabolic repression, mediated by glucose. Genes involved in this process have been defined by means of mutants either unable to express invertase or with constitutive phenotype, although none of the genes is specific for invertase regulation. The affected genes in mutants unable to produce invertase are designated SNFX. These genes can be assorted into two groups considering either their function in regulation of gene expression or their epistatic relationships. Mutants with constitutive phenotype have been selected either by resistance to 2-deoxyglucose or by suppression of snf mutations. Among the different genes previously outlined, some of which code for transcription factors, only the MIG1 product, a "zinc finger" protein, shows a clear capacity of binding DNA in vitro. Besides the ON/OFF switch mechanism of the expression of SUC genes, some genes seem to play a role in modulating invertase expression, either hindering or stimulating transcription. A model to define the relationship between the different gene products involved in the regulation of transcription of the SUC genes is proposed.
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PMID:Genes involved in the regulation of invertase production in Saccharomyces cerevisiae. 777 93

Expression of the SUC2 gene in Saccharomyces cerevisiae, which encodes invertase, is repressed about 200-fold by high levels of glucose. Mig1p is a Cys2His2 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 glucose-activated repressor. We have shown that Mig2p binds to the Miglp-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.
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PMID:Two zinc-finger-containing repressors are responsible for glucose repression of SUC2 expression. 875 37

Silencing of MIG1, a transcription factor imposing carbon catabolite repression on invertase, was attempted, either by disrupting the gene or by expressing antisense copies of the gene. The performance of the recombinant strains in bioreactor batch cultivations on sucrose, in the presence of glucose, was compared with that of the wild-type strain under the same conditions. In the delta migI strain, the rate of sucrose utilization was independent (10 mmol/g/h) of the glucose concentration. During the cultivations with the wild-type strain and the antisense strains, two distinct phases were observed. The rates of sucrose hydrolysis were < 1 mmol/g/h and 9 to 10 mmol/g/h in the first and second phases, respectively. Entry into the second cultivation phase was characterized by a decline in glucose concentration below 12 mmol/liter. As expected, disruption of MIG1 resulted in a relief of glucose repression. However, silencing of MIG1 expression was not achieved by expressing antisense MIG1, even though antisense MIG1 RNA was sufficiently stable to be detected. In the wild-type and delta migI strains, the specific growth rate was 0.32 to 0.33 h-1, whereas it was lower in the antisense strains, 0.25 to 0.30 h-1.
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PMID:Silencing MIG1 in Saccharomyces cerevisiae: effects of antisense MIG1 expression and MIG1 gene disruption. 917 57

The PKC1 gene in the yeast Saccharomyces cerevisiae encodes for protein kinase C which is known to control a MAP kinase cascade consisting of different kinases: Bck1, Mkk1 and Mkk2, and Mpk1. This cascade affects the cell wall integrity but the phenotype of pkc1Delta mutants suggests additional targets that have not yet been identified [Heinisch et al., Mol. Microbiol. 32 (1999) 671-680]. The pkc1Delta mutant, as opposed to other mutants in the MAP kinase cascade, displays defects in the control of carbon metabolism. One of them occurs in the derepression of SUC2 gene after exhaustion of glucose from the medium, suggesting an involvement of Pkc1p in the derepression process that is not shared by the downstream MAP kinase cascade. In this work, we demonstrate that Pkc1p is required for the increase of the activity of enzymatic systems during the derepression process. We observed that Pkc1p is involved in the derepression of invertase and alcohol dehydrogenase activities. On the other hand, it seems not to be necessary for the derepression of the enzymes of the GAL system. Our results suggest that Pkc1p is acting through the main glucose repression pathway, since introduction of an additional mutation in the PKC1 gene in yeast strains already presenting mutations in the HXKII or MIG1 genes does not interfere with the typical derepressed phenotype observed in these single mutants. Moreover, our data indicate that Pkc1p participates in this process through the control of the cellular localization of the Mig1 transcriptional factor.
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PMID:Relationship between protein kinase C and derepression of different enzymes. 1248 87