Gene/Protein Disease Symptom Drug Enzyme Compound
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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)

When S. cerevisiae growing in the presence of glucose (repressive condition) was shifted to higher temperatures, invertase was secreted. This secretion required protein synthesis, but was independent of RNA formation (Mormeneo & Sentandreu 1982). In addition accumulation of invertasespecific messenger RNA occurred in the absence of protein synthesis but was expressed only after synthesis of protein. Invertase mRNA was continuously synthesized under repressive conditions and the levels of this mRNA were regulated by the presence of glucose. The hexose regulated the concentration of this mRNA at the level of transcription and/or by sensitization of this messenger RNA. The expression of the invertase mRNA present in the cells under repressive conditions was also regulated by glucose at the level of translation and/or secretion. As a result of these processes, under repressive conditions invertase is eliminated before secretion takes place.
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PMID:Molecular events associated with glucose repression of invertase in Saccharomyces cerevisiae. 352 42

The SNF2 and SNF5 genes are required for derepression of SUC2 and other glucose-repressible genes of Saccharomyces cerevisiae in response to glucose deprivation. Previous genetic evidence suggested that SNF2 and SNF5 have functionally related roles. We cloned both genes by complementation and showed that the cloned DNA was tightly linked to the corresponding chromosomal locus. Both genes in multiple copy complemented only the cognate snf mutation. The SNF2 gene encodes a 5.7-kilobase RNA, and the SNF5 gene encodes a 3-kilobase RNA. Both RNAs contained poly(A) and were present in low abundance. Neither was regulated by glucose repression, and the level of SNF2 RNA was not dependent on SNF5 function or vice versa. Disruption of either gene at its chromosomal locus still allowed low-level derepression of secreted invertase activity, suggesting that these genes are required for high-level expression but are not directly involved in regulation. Further evidence was the finding that snf2 and snf5 mutants failed to derepress acid phosphatase, which is not regulated by glucose repression. The SNF2 and SNF5 functions were required for derepression of SUC2 mRNA.
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PMID:Molecular analysis of SNF2 and SNF5, genes required for expression of glucose-repressible genes in Saccharomyces cerevisiae. 354 May 98

The SUC2 gene produces two differently regulated mRNAs that encode two forms of invertase. The 1.9-kilobase mRNA encoding secreted invertase is regulated by glucose (carbon catabolite) repression, and the 1.8-kilobase mRNA encoding intracellular invertase is synthesized constitutively. Previous work has shown that the 5' noncoding region between -650 and -418 is required for derepression of secreted invertase in response to glucose deprivation. We show here that this upstream region can confer glucose-repressible expression to a heterologous gene, a LEU2-lacZ gene fusion, that is not normally regulated by glucose repression. This expression was found to respond appropriately to mutations in trans-acting genes that affect regulation of SUC2 expression. Mutations in the SNF1 through SNF6 loci reduced derepression of beta-galactosidase, and a mutation at the SSN6 locus caused constitutive expression. These findings indicate that the SUC2 upstream region mediates the regulatory effects of these genes and suggest that regulation occurs at the level of transcription. In addition, the upstream region was partially active in the inverted orientation.
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PMID:Upstream region of the SUC2 gene confers regulated expression to a heterologous gene in Saccharomyces cerevisiae. 393 53

A functional SNF1 gene product is required to derepress expression of many glucose-repressible genes in Saccharomyces cerevisiae. Strains carrying a snf1 mutation are unable to grow on sucrose, galactose, maltose, melibiose, or nonfermentable carbon sources; utilization of these carbon sources is regulated by glucose repression. The inability of snf1 mutants to utilize sucrose results from failure to derepress expression of the structural gene for invertase at the RNA level. We isolated recombinant plasmids carrying the SNF1 gene by complementation of the snf1 defect in S. cerevisiae. A 3.5-kilobase region is common to the DNA segments cloned in five different plasmids. Transformation of S. cerevisiae with an integrating vector carrying a segment of the cloned DNA resulted in integration of the plasmid at the SNF1 locus. This result indicates that the cloned DNA is homologous to sequences at the SNF1 locus. By mapping a plasmid marker linked to SNF1 in this transformant, we showed that the SNF1 gene is located on chromosome IV. We then mapped snf1 to a position 5.6 centimorgans distal to rna3 on the right arm; snf1 is not extremely closely linked to any previously mapped mutation.
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PMID:Cloning and genetic mapping of SNF1, a gene required for expression of glucose-repressible genes in Saccharomyces cerevisiae. 636 12

The SNF1 gene of Saccharomyces cerevisiae is essential for normal regulation of gene expression by glucose repression. A functional SNF1 gene product is required to derepress many glucose-repressible genes in response to conditions of low external glucose. In the case of the SUC2 structural gene for invertase, SNF1 acts at the RNA level. We have reported the isolation of a cloned gene that complements the snf1 defect in S. cerevisiae and that is homologous to DNA at the SNF1 locus (J. L. Celenza and M. Carlson, Mol. Cell. Biol. 4:49-53, 1984). In this work we identified a 2.4-kilobase polyadenylate-containing RNA encoded by the SNF1 gene and showed that its level is neither regulated by glucose repression nor dependent on a functional SNF1 product. The position of the SNF1 RNA relative to the cloned DNA was mapped, and the direction of transcription was determined. The cloned DNA was used to disrupt the SNF1 gene at its chromosomal locus. Gene disruption resulted in A Snf1- phenotype, thereby proving that the cloned gene is the SNF1 gene and showing that the phenotype of a true null mutation is indistinguishable from that of previously isolated snf1 mutations.
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PMID:Structure and expression of the SNF1 gene of Saccharomyces cerevisiae. 636 13

Mutants of Saccharomyces cerevisiae with defects in sucrose or raffinose fermentation were isolated. In addition to mutations in the SUC2 structural gene for invertase, we recovered 18 recessive mutations that affected the regulation of invertase synthesis by glucose repression. These mutations included five new snf1 (sucrose nonfermenting) alleles and also defined five new complementation groups, designated snf2, snf3, snf4, snf5, and snf6. The snf2, snf4, and snf5 mutants produced little or no secreted invertase under derepressing conditions and were pleiotropically defective in galactose and glycerol utilization, which are both regulated by glucose repression. The snf6 mutant produced low levels of secreted invertase under derepressing conditions, and no pleiotropy was detected. The snf3 mutants derepressed secreted invertase to 10-35% the wild-type level but grew less well on sucrose than expected from their invertase activity; in addition, snf3 mutants synthesized some invertase under glucose-repressing conditions.--We examined the interactions between the different snf mutations and ssn6, a mutation causing constitutive (glucose-insensitive) high-level invertase synthesis that was previously isolated as a suppressor of snf1. The ssn6 mutation completely suppressed the defects in derepression of invertase conferred by snf1, snf3, snf4 and snf6, and each double mutant showed the constitutivity for invertase typical of ssn6 single mutants. In contrast, snf2 ssn6 and snf5 ssn6 strains produced only moderate levels of invertase under derepressing conditions and very low levels under repressing conditions. These findings suggest roles for the SNF1 through SNF6 and SSN6 genes in the regulation of SUC2 gene expression by glucose repression.
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PMID:Genes affecting the regulation of SUC2 gene expression by glucose repression in Saccharomyces cerevisiae. 639 17

The SUC2 gene produces two mRNAs with different 5' ends that encode two forms of invertase. The 1.9-kilobase mRNA encoding secreted invertase is regulated by glucose repression (carbon catabolite repression), and the 1.8-kilobase mRNA encoding intracellular invertase is produced constitutively at low levels. To identify 5' noncoding sequences essential for regulated expression of SUC2, we constructed in vitro a series of deletions and inserted them into the yeast genome at the chromosomal SUC2 locus. Analysis of the effects of each deletion on SUC2 gene expression identified an upstream region required for derepression of secreted invertase synthesis. The 3' boundary of this region is near -418. The 5' boundary does not appear to be sharply defined, but lies ca. 100 base pairs upstream. A deletion extending from -418 to -140 allowed high-level derepression, indicating that no essential sequences lie between the upstream region and the TATA box at -133 and that the upstream region can be moved 279 base pairs closer to the transcriptional start site. Interactions between the deletions and several unlinked mutations affecting the regulation of SUC2 gene expression were examined. Sequences between -1,900 and -86 are dispensable for expression of the 1.8-kilobase mRNA.
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PMID:Upstream region required for regulated expression of the glucose-repressible SUC2 gene of Saccharomyces cerevisiae. 639 5

The SUC2 gene of yeast (Saccharomyces) encodes two forms of invertase: a secreted, glycosylated form, the synthesis of which is regulated by glucose repression, and an intracellular, nonglycosylated enzyme that is produced constitutively. The SUC2 gene has been cloned and shown to encode two RNAs (1.8 and 1.9 kb) that differ at their 5' ends. The stable level of the larger RNA is regulated by glucose; the level of the smaller RNA is not. A correspondence between the presence of the 1.9 kb RNA and the secreted invertase, and between the 1.8 kb RNA and the intracellular invertase, was observed in glucose-repressed and -derepressed wild-type cells. In addition, cells carrying a mutation at the SNF1 locus fail to derepress synthesis of the secreted invertase and also fail to produce stable 1.9 kb RNA during growth in low glucose. Glucose regulation of invertase synthesis thus is exerted, at least in part, at the RNA level. A naturally silent allele (suc2 degrees) of the SUC2 locus that does not direct the synthesis of active invertase was found to produce both the 1.8 and 1.9 kb RNAs under normal regulation by glucose. A model is proposed to account for the synthesis and regulation of the two forms of invertase: the larger, regulated mRNA contains the initiation codon for the signal sequence required for synthesis of the secreted, glycosylated form of invertase; the smaller, constitutively transcribed mRNA begins within the coding region of the signal sequence, resulting in synthesis of the intracellular enzyme.
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PMID:Two differentially regulated mRNAs with different 5' ends encode secreted with intracellular forms of yeast invertase. 703 47

Utilization of sucrose as a source of carbon and energy in yeast (Saccharomyces) is controlled by the classical SUC genes, which confer the ability to produce the sucrose-degrading enzyme invertase (Mortimer and Hawthorne 1969). Mutants of S. cerevisiae strain S288C (SUC2+) unable to grow anaerobically on sucrose, but still able to use glucose, were isolated. Two major complementation groups were identified: twenty-four recessive mutations at the SUC2 locus (suc2-); and five recessive mutations defining a new locus, SNF1 (for sucrose nonfermenting), essential for sucrose utilization. Two minor complementation groups, each comprising a single member with a leaky sucrose-nonfermenting phenotype, were also identified. The Suc2 mutations isolated include four suppressible amber mutations and five mutations apparently exhibiting intragenic complementation; complementation analysis and mitotic mapping studies indicated that all of the suc2 mutations are alleles of a single gene. These results suggest that SUC2 encodes a protein, probably a dimer or multimer. No invertase activity was detected in suc2 probably a dimer or multimer. No invertase activity was detected in suc2 mutants,--The SNF1 locus is not tightly linked to SUC2. The snf1 mutations were found to be pleiotropic, preventing sucrose utilization by SUC2+ and SUC7+ strains, and also preventing utilization of galactose, maltose and several nonfermentable carbon sources. Although snf1 mutants thus display a petite phenotype, classic petite mutations do not interfere with utilization of sucrose, galactose or maltose. A common feature of all the carbon utilization systems affected by SNF1 is that all are regulated by glucose repression. The snf1 mutants were found to produce the constitutive nonglycosylated form of invertase, but failed to produce the glucose-repressible, glycosylated, secreted invertase. This failure cannot be attributed to a general defect in production of glycosylated and secreted proteins because synthesis of acid phosphatase, a glycosylated secreted protein not subject to glucose repression, was not affected by snf1 mutations. These findings suggest that the SNF1 locus is involved in the regulation of gene expression by glucose repression.
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PMID:Mutants of yeast defective in sucrose utilization. 704 Jan 63

Non-coding nucleotide sequences located 5' upstream of the transcriptional start site play an essential role in gene expression as they contain binding sites for transcription and regulatory factors. The yeast SUC gene family is a useful model to study the influence that nucleotide exchanges within the promoter regions have on their expression, since (i) these genes, regulated by glucose repression, are differentially transcribed (invertase activity produced by distinct SUC genes may show variations of about 10-fold); and (ii) promoter sequences of SUC3, SUC4, SUC5 and SUC7 are more than 99% homologous, showing only six base exchanges among all of them. Comparison of these nucleotide exchanges with the expression of each SUC gene (located either on chromosomes or on multicopy and centromeric plasmids) points out that naturally occurring base exchanges as few as one nucleotide modification (G to A transition at position -497 relative to the translational start site, C to T transition at position -460 and insertion/deletion of a T at positions -590, -586 and -435) may have a strong effect on gene expression.
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PMID:Differential expression of SUC genes: a question of bases. 794 63


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