scholarly journals Structure and expression of the SNF1 gene of Saccharomyces cerevisiae.

1984 ◽  
Vol 4 (1) ◽  
pp. 54-60 ◽  
Author(s):  
J L Celenza ◽  
M Carlson
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Gene Product ◽  
Gene Disruption ◽  
Glucose Repression ◽  
Regulation Of Gene Expression ◽  
Null Mutation ◽  
Chromosomal Locus ◽  
Cloned Gene ◽  
External Glucose

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.

Structure and expression of the SNF1 gene of Saccharomyces cerevisiae

1984 ◽  
Vol 4 (1) ◽  
pp. 54-60
Author(s):  
J L Celenza ◽  
M Carlson
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Gene Product ◽  
Gene Disruption ◽  
Glucose Repression ◽  
Regulation Of Gene Expression ◽  
Null Mutation ◽  
Chromosomal Locus ◽  
Cloned Gene ◽  
External Glucose

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.

Null mutations in the SNF3 gene of Saccharomyces cerevisiae cause a different phenotype than do previously isolated missense mutations

1986 ◽  
Vol 6 (11) ◽  
pp. 3569-3574
Author(s):  
L Neigeborn ◽  
P Schwartzberg ◽  
R Reid ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Glucose Uptake ◽  
Gene Disruption ◽  
Glucose Repression ◽  
Gene Products ◽  
Missense Mutations ◽  
Chromosomal Locus ◽  
Growth Properties ◽  
Invertase Gene ◽  
Regulatory Functions

Missense mutations in the SNF3 gene of Saccharomyces cerevisiae were previously found to cause defects in both glucose repression and derepression of the SUC2 (invertase) gene. In addition, the growth properties of snf3 mutants suggested that they were defective in uptake of glucose and fructose. We have cloned the SNF3 gene by complementation and demonstrated linkage of the cloned DNA to the chromosomal SNF3 locus. The gene encodes a 3-kilobase poly(A)-containing RNA, which was fivefold more abundant in cells deprived of glucose. The SNF3 gene was disrupted at its chromosomal locus by several methods to create null mutations. Disruption resulted in growth phenotypes consistent with a defect in glucose uptake. Surprisingly, gene disruption did not cause aberrant regulation of SUC2 expression. We discuss possible mechanisms by which abnormal SNF3 gene products encoded by missense alleles could perturb regulatory functions.

scholarly journals Null mutations in the SNF3 gene of Saccharomyces cerevisiae cause a different phenotype than do previously isolated missense mutations.

1986 ◽  
Vol 6 (11) ◽  
pp. 3569-3574 ◽  
Author(s):  
L Neigeborn ◽  
P Schwartzberg ◽  
R Reid ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Glucose Uptake ◽  
Gene Disruption ◽  
Glucose Repression ◽  
Gene Products ◽  
Missense Mutations ◽  
Chromosomal Locus ◽  
Growth Properties ◽  
Invertase Gene ◽  
Regulatory Functions

Missense mutations in the SNF3 gene of Saccharomyces cerevisiae were previously found to cause defects in both glucose repression and derepression of the SUC2 (invertase) gene. In addition, the growth properties of snf3 mutants suggested that they were defective in uptake of glucose and fructose. We have cloned the SNF3 gene by complementation and demonstrated linkage of the cloned DNA to the chromosomal SNF3 locus. The gene encodes a 3-kilobase poly(A)-containing RNA, which was fivefold more abundant in cells deprived of glucose. The SNF3 gene was disrupted at its chromosomal locus by several methods to create null mutations. Disruption resulted in growth phenotypes consistent with a defect in glucose uptake. Surprisingly, gene disruption did not cause aberrant regulation of SUC2 expression. We discuss possible mechanisms by which abnormal SNF3 gene products encoded by missense alleles could perturb regulatory functions.

scholarly journals Genetic and molecular characterization of GAL83: its interaction and similarities with other genes involved in glucose repression in Saccharomyces cerevisiae.

Genetics ◽  
1993 ◽  
Vol 135 (3) ◽  
pp. 655-664 ◽  
Author(s):  
J R Erickson ◽  
M Johnston
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Molecular Characterization ◽  
Gene Product ◽  
Regulatory Mechanism ◽  
Glucose Repression ◽  
Null Mutation ◽  
Gene Products ◽  
Gal Genes

Abstract Expression of the GAL genes of Saccharomyces cerevisiae is subject to glucose repression, a global regulatory mechanism that requires several gene products. We have isolated GAL83, one of these genes required for glucose repression. The sequence of the predicted Gal83 protein is homologous to two other yeast proteins, Sip1p and Sip2p, which are known to interact with the SNF1 gene product, a protein kinase required for expression of the GAL genes. High-copy clones of SIP1 and SIP2 cross-complement the GAL83-2000 mutation (as well as GAL82-1, a mutation in another gene involved in glucose repression), suggesting that these four genes may perform similar functions in glucose repression. Consistent with this hypothesis, a gal83 null mutation does not affect glucose repression, and only dominant or partially dominant mutations exist in GAL83 (and GAL82). Two other observations were made that suggests that GAL83 functions interdependently with GAL82 and REG1 (another gene involved in glucose repression) to effect glucose repression: 1) REG1 on a low-copy plasmid cross-complements GAL82-1 and GAL83-2000 mutations, and 2) all pairwise combinations of reg1, GAL82-1 and GAL83-2000 fail to complement one another. Such unlinked noncomplementation suggests that Gal83p, Gal82p and Reg1p may interact with one another. Possible roles for GAL83, GAL82 and REG1 are discussed in relation to SNF1, SIP1 and SIP2.

Higher Ploidy in Saccharomyces cerevisiae Supports Enhanced Hepatitis B Virus S Cloned Gene Expression at the Pilot Scale

1996 ◽  
Vol 12 (1) ◽  
pp. 145-148 ◽  
Author(s):  
J. Fu ◽  
C.B. Parker ◽  
P. Burke ◽  
L.D. Schultz ◽  
D.L. Montgomery ◽  
...  
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Pilot Scale ◽  
B Virus ◽  
Cloned Gene

Cloning and genetic mapping of SNF1, a gene required for expression of glucose-repressible genes in Saccharomyces cerevisiae

1984 ◽  
Vol 4 (1) ◽  
pp. 49-53
Author(s):  
J L Celenza ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Genetic Mapping ◽  
Gene Product ◽  
Structural Gene ◽  
Glucose Repression ◽  
Carbon Sources ◽  
Recombinant Plasmids ◽  
The Right ◽  
Integrating Vector

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.

scholarly journals Structure and molecular analysis of RGR1, a gene required for glucose repression of Saccharomyces cerevisiae.

1990 ◽  
Vol 10 (8) ◽  
pp. 4130-4138 ◽  
Author(s):  
A Sakai ◽  
Y Shimizu ◽  
S Kondou ◽  
T Chibazakura ◽  
F Hishinuma
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Gel Electrophoresis ◽  
Daughter Cell ◽  
Glucose Repression ◽  
Pulsed Field Gel Electrophoresis ◽  
Null Mutation ◽  
Electron Microscopic ◽  
Transmission Electron ◽  
Transmission Electron Microscopic ◽  
Carboxy Terminal

An RGR1 gene product is required to repress expression of glucose-regulated genes in Saccharomyces cerevisiae. The abnormal morphology of rgr1 cells was studied. Scanning and transmission electron microscopic observations revealed that the cell wall of the daughter cell remained attached to that of mother cell. We cloned the RGR1 gene by complementation and showed that the cloned DNA was tightly linked to the chromosomal RGR1 locus. The cloned RGR1 gene suppressed all of the phenotypes caused by the mutation and encoded a 3.6-kilobase poly(A)+ RNA. The RGR1 gene is located on chromosome XII, as determined by pulsed-field gel electrophoresis, and we mapped rgr1 between gal2 and pep3 by genetic analysis. rgr1 was shown to be a new locus. We also determined the nucleotide sequence of RGR1, which was predicted to encode a 123-kilodalton protein. The null mutation resulted in lethality, indicating that the RGR1 gene is essential for growth. On the other hand, a carboxy-terminal deletion of the gene caused phenotypes similar to but more severe than those caused by the original mutation. The amount of reserve carbohydrates was reduced in rgr1 cells. Possible functions of the RGR1 product are discussed.

scholarly journals Divergent MLS1 promoters lie on a fitness plateau for gene expression

2015 ◽  
Author(s):  
Andrew C Bergen ◽  
Gerilyn M Olsen ◽  
Justin C Fay
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Dynamic Response ◽  
Yeast Species ◽  
Glucose Repression ◽  
Gene Activation ◽  
Malate Synthase ◽  
Expression Divergence ◽  
Fitness Effects ◽  
Single Promoter

Qualitative patterns of gene activation and repression are often conserved despite an abundance of quantitative variation in expression levels within and between species. A major challenge to interpreting patterns of expression divergence is knowing which changes in gene expression affect fitness. To characterize the fitness effects of gene expression divergence we placed orthologous promoters from eight yeast species upstream of malate synthase (MLS1) in Saccharomyces cerevisiae. As expected, we found these promoters varied in their expression level under activated and repressed conditions as well as in their dynamic response following loss of glucose repression. Despite these differences, only a single promoter driving near basal levels of expression caused a detectable loss of fitness. We conclude that the MLS1 promoter lies on a fitness plateau whereby even large changes in gene expression can be tolerated without a substantial loss of fitness.

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