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)

We have cloned and sequenced the GAM1 gene which is required for transcription of the STA1 gene encoding an extracellular glucoamylase in Saccharomyces cerevisiae var. diastaticus. Complementation tests indicated that GAM1 is the same gene as SNF2 which is required for derepression of the SUC2 gene encoding invertase. Accumulation of SNF2 RNA was not regulated by the GAM2 and GAM3 genes which are also required for STA1 expression. The SNF2 gene was predicted to encode a 194 kDa highly charged protein with a glutamine-rich tract. A bifunctional SNF2-lacZ fusion protein was shown by immunofluorescence microscopy to be localized to the nucleus, suggesting that the SNF2 protein is located in the nucleus.
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PMID:The GAM1/SNF2 gene of Saccharomyces cerevisiae encodes a highly charged nuclear protein required for transcription of the STA1 gene. 188 12

Glucose represses PRB1 expression at the level of transcription. However, release from glucose repression initially does not result in accumulation of protease B (PrB) activity despite transcriptional derepression. PrB activity accumulates only upon a second transcriptional derepression as the cells approach stationary phase. Increasing the PRB1 gene dosage on 2 mu-based plasmids does not overcome glucose repression. Glucose-mediated repression of PRB1 is not subject to the same genetic controls as SUC2. Mutation of the HXK2 gene, which confers glucose-insensitive expression of secreted invertase, had no effect on PRB1 expression at the level of PrB activity. Strains bearing a mutation in any of the SNF1-SNF6 genes cannot derepress secreted invertase synthesis, but did derepress PrB synthesis when grown in the absence of glucose. Mutation of the SNF2 or SNF5 gene led to accumulation of PrB activity to levels ten times that of wild type. Polymorphism for a suppressor gene was observed: in snf5-bearing strains, one allele of this suppressor gene resulted in elevated levels of PrB and the other allele resulted in wild-type levels of PrB; neither allele suppressed the Suc- phenotype of the snf5 mutant. Re-examination of published data on SUC2 expression in snf2 and snf5 mutants and examination of PRB1 expression in these mutants paradoxically suggest that the SNF2 and SNF5 gene products might act as negative regulators of gene expression.
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PMID:Consequences of growth media, gene copy number, and regulatory mutations on the expression of the PRB1 gene of Saccharomyces cerevisiae. 240 4

Mutations in the SNF2 gene of Saccharomyces cerevisiae prevent derepression of the SUC2 (invertase) gene, and other glucose-repressible genes, in response to glucose deprivation. We have isolated 25 partial phenotypic revertants of a snf2 mutant that are able to derepress secreted invertase. These revertants all carried suppressor mutations at a single locus, designated SSN20 (suppressor of snf2). Alleles with dominant, partially dominant and recessive suppressor phenotypes were recovered, but all were only partial suppressors of snf2, reversing the defect in invertase synthesis but not other defects. All alleles also caused recessive, temperature-sensitive lethality and a recessive defect in galactose utilization, regardless of the SNF2 genotype. No significant effect on SUC2 expression was detected in a wild-type (SNF2) genetic background. The ssn20 mutations also suppressed the defects in invertase derepression caused by snf5 and snf6 mutations, and selection for invertase-producing revertants of snf5 mutants yielded only additional ssn20 alleles. These findings suggest that the roles of the SNF2, SNF5 and SNF6 genes in regulation of SUC2 are functionally related and that SSN20 plays a role in expression of a variety of yeast genes.
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PMID:Suppressors of SNF2 mutations restore invertase derepression and cause temperature-sensitive lethality in yeast. 351 73

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

Dominant and recessive mutations at the SSN20 locus were previously isolated as extragenic suppressors of mutations in three genes (SNF2, SNF5, and SNF6) that are required in trans to derepress invertase expression. All ssn20 alleles cause recessive, temperature-sensitive lethality. In this study we cloned the SSN20 gene, identified a 4.6-kilobase poly(A)-containing RNA, and showed that disruption of the gene is lethal in a haploid cell. Genetic mapping of SSN20 to a locus on chromosome VII 10 centimorgans distal to cly8 led to the finding that SSN20 is the same gene as SPT6, which affects expression of delta insertions in the 5' noncoding region of HIS4 (F. Winston, D. T. Chaleff, B. Valent, and G. R. Fink, Genetics 107:179-197, 1984). We also showed that an ssn20 mutation restored expression of secreted invertase from deletions of the SUC2 upstream regulatory region; ssn20 restored derepression of SUC2 mRNA in strains with a SUC2 upstream region deletion or a snf2 mutation. Increased or decreased gene dosage of SSN20 also suppressed defects that are suppressed by ssn20 missense mutations. These findings suggest that SSN20 plays a role in general transcriptional processes.
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PMID:SSN20 is an essential gene with mutant alleles that suppress defects in SUC2 transcription in Saccharomyces cerevisiae. 354 80

Mutations in the SNF8 gene impair derepression of the SUC2 gene, encoding invertase, in response to glucose limitation of Saccharomyces cerevisiae. We report here the cloning of the SNF8 gene by complementation. Sequence analysis predicts a 26,936-dalton product. Disruption of the chromosomal locus caused a five-fold decrease in invertase derepression, defective growth on raffinose, and a sporulation defect in homozygous diploids. Genetic analysis of the interactions of the snf8 null mutation with spt6/ssn20 and ssn6 suppressors distinguished SNF8 from the groups, SNF1, SNF4 and SNF2, SNF5, SNF6. Notably, the snf8 ssn6 double mutants were extremely sick. Mutations of SNF8 and SNF7 showed similar phenotypes and genetic interactions, and the double mutant combination caused no additional phenotypic impairment. These findings suggest that SNF7 and SNF8 are functionally related.
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PMID:Molecular analysis of the SNF8 gene of Saccharomyces cerevisiae. 778 22

Mutations in the SNF7 gene of Saccharomyces cerevisiae prevent full derepression of the SUC2 (invertase) gene in response to glucose limitation. We report the molecular cloning of the SNF7 gene by complementation. Sequence analysis predicts that the gene product is a 27-kDa acidic protein. Disruption of the chromosomal locus causes a fewfold decrease in invertase derepression, a growth defect on raffinose, temperature-sensitive growth on glucose, and a sporulation defect in homozygous diploids. Genetic analysis of the interactions of the snf7 null mutation with ssn6 and spt6/ssn20 suppressor mutations distinguished SNF7 from the SNF2, SNF5 and SNF6 genes. The snf7 mutation also behaved differently from mutations in SNF1 and SNF4 in that snf7 ssn6 double mutants displayed a synthetic phenotype of severe temperature sensitivity for growth. We also mapped SNF7 to the right arm of chromosome XII near the centromere.
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PMID:Molecular and genetic analysis of the SNF7 gene in Saccharomyces cerevisiae. 822 17

A diastatic strain of Saccharomyces cerevisiae producing the STA2-encoded extracellular glucoamylase (GA) in a pronounced glucose-repressible fashion was used as a parent for generating mutants with reduced GA activity under normal conditions of derepression. In addition to mutations in STA2, five other recessive mutations were identified which fell into four complementation groups designated haf1 through haf4. RNA blot analysis suggested that the haf mutations confer defects in STA2 transcription. The haf mutants were pleiotropically defective in utilization of alternative carbon sources and resembled the snf (sucrose non-fermenting) mutants identified previously as unable to derepress the expression of the SUC2 gene encoding invertase. We present evidence strongly suggesting that haf1 = snf2, haf3 = snf1 and haf4 = snf5. By phenotypic criteria, the postulated HAF2 gene (which is none of the SNF genes tested) appears to be similar to SNF2, SNF5 and SNF6, and is possibly a non-redundant extension of this group of functionally related SNF genes.
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PMID:Genes required for derepression of an extracellular glucoamylase gene, STA2, in the yeast Saccharomyces. 832 16