scholarly journals Induction of meiosis in Saccharomyces cerevisiae depends on conversion of the transcriptional represssor Ume6 to a positive regulator by its regulated association with the transcriptional activator Ime1.

1996 ◽  
Vol 16 (5) ◽  
pp. 2518-2526 ◽  
Author(s):  
I Rubin-Bejerano ◽  
S Mandel ◽  
K Robzyk ◽  
Y Kassir
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Dna Binding ◽  
Budding Yeast ◽  
Transcriptional Activator ◽  
Dna Binding Protein ◽  
Activation Domain ◽  
Yeast Saccharomyces Cerevisiae ◽  
Binding Motifs ◽  
Dna Binding Motifs

The transcription of meiosis-specific genes, as well as the initiation of meiosis, in the budding yeast Saccharomyces cerevisiae depends on IME1. IME1 encodes a transcriptional activator which lacks known DNA binding motifs. In this study we have determined the mode by which Ime1 specifically activates the transcription of meiotic genes. We demonstrate that Ime1 is recruited to the promoters of meiotic genes by interacting with a DNA-binding protein, Ume6. This association between Ime1 and Ume6 depends on both starvation and the activity of a protein kinase, encoded by RIM11 In the absence of Ime1, Ume6 represses the transcription of meiotic genes. However, in the presence of Ime1, or when Ume6 is fused in frame to the Gal4 activation domain, Ume6 is converted from a repressor to an activator, resulting in the transcription of meiosis-specific genes and the formation of asci.

scholarly journals Synergistic release from glucose repression by mig1 and ssn mutations in Saccharomyces cerevisiae.

Genetics ◽  
1994 ◽  
Vol 137 (1) ◽  
pp. 49-54 ◽  
Author(s):  
L G Vallier ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Dna Binding ◽  
Glucose Repression ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Yeast Saccharomyces Cerevisiae ◽  
Suc2 Promoter ◽  
Repressor Complex ◽  
Glucose Availability

Abstract In the yeast Saccharomyces cerevisiae, glucose repression of SUC2 transcription requires the SSN6-TUP1 repressor complex. It has been proposed that the DNA-binding protein MIG1 secures SSN6-TUP1 to the SUC2 promoter. Here we show that a mig1 deletion does not cause nearly as dramatic a loss of repression as ssn6: glucose-grown mig1 mutants display 20-fold lower SUC2 expression than ssn6 mutants. Thus, repression by SSN6-TUP1 is not mediated solely by MIG1, but also involves MIG1-independent mechanisms. We report that mig1 partially restores SUC2 expression in mutants lacking the SNF1 protein kinase and show that mig1 is allelic to ssn1, a mutation selected as a suppressor of snf1. Other SSN genes identified in this selection were therefore candidates for a role in repression of SUC2. We show that mig1 acts synergistically with ssn2 through ssn5, ssn7, and ssn8 to relieve glucose repression of SUC2 and to suppress the requirement for SNF1. These findings indicate that the SSN proteins contribute to repression of SUC2, and the pleiotropic phenotypes of the ssn mutants suggest global roles in repression. Finally, the regulated SUC2 expression observed in snf1 mig1 mutants indicates that signals regarding glucose availability can be transmitted independently of the SNF1 protein kinase.

Phosphorylation of Cdc28 and regulation of cell size by the protein kinase CKII in Saccharomyces cerevisiae

2000 ◽  
Vol 351 (1) ◽  
pp. 143-150 ◽  
Author(s):  
Gian Luigi RUSSO ◽  
Christian VAN DEN BOS ◽  
Ann SUTTON ◽  
Paola COCCETTI ◽  
Maurizio D. BARONI ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Division ◽  
Protein Kinase ◽  
Cell Size ◽  
Peptide Mapping ◽  
Budding Yeast ◽  
Cell Division Cycle ◽  
Yeast Saccharomyces Cerevisiae ◽  
Protein Kinase Ckii

The CDK (cyclin-dependent kinase) family of enzymes is required for the G1-to-S-phase and G2-to-M-phase transitions during the cell-division cycle of eukaryotes. We have shown previously that the protein kinase CKII catalyses the phosphorylation of Ser-39 in Cdc2 during the G1 phase of the HeLa cell-division cycle [Russo, Vandenberg, Yu, Bae, Franza and Marshak (1992) J. Biol. Chem. 267, 20317–20325]. To identify a functional role for this phosphorylation, we have studied the homologous enzymes in the budding yeast Saccharomyces cerevisiae. The S. cerevisiae homologue of Cdc2, Cdc28, contains a consensus CKII site (Ser-46), which is homologous with that of human Cdc2. Using in vitro kinase assays, metabolic labelling, peptide mapping and phosphoamino acid analysis, we demonstrate that this site is phosphorylated in Cdc28 in vivo as well in vitro. In addition, S. cerevisiae cells in which Ser-46 has been mutated to alanine show a decrease in both cell volume and protein content of 33%, and this effect is most pronounced in the stationary phase. Because cell size in S. cerevisiae is regulated primarily at the G1 stage, we suggest that CKII contributes to the regulation of the cell cycle in budding yeast by phosphorylation of Cdc28 as a checkpoint for G1 progression.

scholarly journals A mutation in the gene encoding the Saccharomyces cerevisiae single-stranded DNA-binding protein Rfa1 stimulates a RAD52-independent pathway for direct-repeat recombination.

1995 ◽  
Vol 15 (3) ◽  
pp. 1632-1641 ◽  
Author(s):  
J Smith ◽  
R Rothstein
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Binding ◽  
Binding Protein ◽  
Large Subunit ◽  
Direct Repeat ◽  
Fold Increase ◽  
Dna Binding Protein ◽  
Yeast Saccharomyces Cerevisiae ◽  
Single Stranded Dna ◽  
Mutant Strains

In the yeast Saccharomyces cerevisiae, recombination between direct repeats is synergistically reduced in rad1 rad52 double mutants, suggesting that the two genes define alternate recombination pathways. Using a classical genetic approach, we searched for suppressors of the recombination defect in the double mutant. One mutation that restores wild-type levels of recombination was isolated. Cloning by complementation and subsequent physical and genetic analysis revealed that it maps to RAF1. This locus encodes the large subunit of the single-stranded DNA-binding protein complex, RP-A, which is conserved from S. cerevisiae to humans. The rfa1 mutation on its own causes a 15-fold increase in direct-repeat recombination. However, unlike most other hyperrecombination mutations, the elevated levels in rfa1 mutants occur independently of RAD52 function. Additionally, rfa1 mutant strains grow slowly, are UV sensitive, and exhibit decreased levels of heteroallelic recombination. DNA sequence analysis of rfa1 revealed a missense mutation that alters a conserved residue of the protein (aspartic acid 228 to tyrosine [D228Y]). Biochemical analysis suggests that this defect results in decreased levels of RP-A in mutant strains. Overexpression of the mutant subunit completely suppresses the UV sensitivity and partially suppresses the recombination phenotype. We propose that the defective complex fails to interact properly with components of the repair, replication, and recombination machinery. Further, this may permit the bypass of the recombination defect of rad1 rad52 mutants by activating an alternative single-stranded DNA degradation pathway.

G1 cyclins regulate proliferation of the budding yeast Saccharomyces cerevisiae

1992 ◽  
Vol 70 (10-11) ◽  
pp. 946-953
Author(s):  
Adele Rowley ◽  
Gerald C. Johnston ◽  
Richard A. Singer
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Protein Kinase ◽  
Budding Yeast ◽  
Cell Types ◽  
Eukaryotic Cell ◽  
Yeast Saccharomyces Cerevisiae ◽  
Functional Conservation ◽  
Cycle Regulation

The eukaryotic cell cycle is regulated at two points, the G1-S and G2-M boundaries. The molecular basis for these regulatory activities has recently been elucidated, in large part by the use of molecular and genetic analyses using unicellular yeast. The molecular characterization of cell-cycle regulation has revealed striking functional conservation among evolutionarily diverse cell types. For many eukaryotic cells, regulation of cell proliferation occurs primarily in the G1 interval. The G2 regulatory step, termed start, requires the activation of a highly conserved p34 protein kinase by association with a functionally redundant family of proteins, the G1 cyclins. Here we review studies using the genetically tractable budding yeast Saccharomyces cerevisiae, which have provided insight into the role of G1 cyclins in the regulation of start.Key words: cell cycle, cyclin proteins, cdc2 protein kinase, start.

scholarly journals Identification of a Saccharomyces cerevisiae DNA-binding protein involved in transcriptional regulation.

1990 ◽  
Vol 10 (4) ◽  
pp. 1743-1753 ◽  
Author(s):  
H Wang ◽  
P R Nicholson ◽  
D J Stillman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Binding ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Rrna Gene ◽  
Yeast Saccharomyces Cerevisiae ◽  
Yeast Genes

A DNA-binding protein has been identified from extracts of the budding yeast Saccharomyces cerevisiae which binds to sites present in the promoter regions of a number of yeast genes transcribed by RNA polymerase II, including SIN3 (also known as SDI1), SWI5, CDC9, and TOP1. This protein also binds to a site present in the enhancer for the 35S rRNA gene, which is transcribed by RNA polymerase I, and appears to be identical to the previously described REB1 protein (B. E. Morrow, S. P. Johnson, and J. R. Warner, J. Biol. Chem. 264:9061-9068, 1989). When oligonucleotides containing a REB1-binding site are placed between the CYC1 upstream activating sequence and TATA box, transcription by RNA polymerase II in vivo is substantially reduced, suggesting that REB1 acts as a repressor of RNA polymerase II transcription. The in vitro levels of the REB1 DNA-binding activity are reduced in extracts prepared from strains bearing a mutation in the SIN3 gene. A greater reduction in REB1 activity is observed if the sin3 mutant strain is grown in media containing galactose as a carbon source.

Identification of a Saccharomyces cerevisiae DNA-binding protein involved in transcriptional regulation

1990 ◽  
Vol 10 (4) ◽  
pp. 1743-1753
Author(s):  
H Wang ◽  
P R Nicholson ◽  
D J Stillman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Binding ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Rrna Gene ◽  
Yeast Saccharomyces Cerevisiae ◽  
Yeast Genes

A DNA-binding protein has been identified from extracts of the budding yeast Saccharomyces cerevisiae which binds to sites present in the promoter regions of a number of yeast genes transcribed by RNA polymerase II, including SIN3 (also known as SDI1), SWI5, CDC9, and TOP1. This protein also binds to a site present in the enhancer for the 35S rRNA gene, which is transcribed by RNA polymerase I, and appears to be identical to the previously described REB1 protein (B. E. Morrow, S. P. Johnson, and J. R. Warner, J. Biol. Chem. 264:9061-9068, 1989). When oligonucleotides containing a REB1-binding site are placed between the CYC1 upstream activating sequence and TATA box, transcription by RNA polymerase II in vivo is substantially reduced, suggesting that REB1 acts as a repressor of RNA polymerase II transcription. The in vitro levels of the REB1 DNA-binding activity are reduced in extracts prepared from strains bearing a mutation in the SIN3 gene. A greater reduction in REB1 activity is observed if the sin3 mutant strain is grown in media containing galactose as a carbon source.

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