The Signal Transduction Pathway Upstream of CDC25 — ras — Adenylate Cyclase in the Yeast Saccharomyces Cerevisiae and its Relationship to Nutrient Control of Cell Cycle Progression

1991 ◽  
pp. 57-66
Author(s):  
Johan M. Thevelein ◽  
Linda Van Aelst ◽  
Peter Durnez ◽  
Stefan Hohmann
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Signal Transduction ◽  
Adenylate Cyclase ◽  
Cell Cycle Progression ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cycle Progression ◽  
Nutrient Control

scholarly journals A Genetic Study of Signaling Processes for Repression of PHO5 Transcription in Saccharomyces cerevisiae

Genetics ◽  
1998 ◽  
Vol 150 (4) ◽  
pp. 1349-1359 ◽  
Author(s):  
W-T Walter Lau ◽  
Ken R Schneider ◽  
Erin K O’Shea
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Signal Transduction ◽  
Constitutive Expression ◽  
Signal Transduction Pathway ◽  
Acid Synthesis ◽  
Phosphate Transport ◽  
Transduction Pathway ◽  
Plasma Membrane Atpase ◽  
Yeast Saccharomyces Cerevisiae

Abstract In the yeast Saccharomyces cerevisiae, transcription of a secreted acid phosphatase, PHO5, is repressed in response to high concentrations of extracellular inorganic phosphate. To investigate the signal transduction pathway leading to transcriptional regulation of PHO5, we carried out a genetic selection for mutants that express PHO5 constitutively. We then screened for mutants whose phenotypes are also dependent on the function of PHO81, which encodes an inhibitor of the Pho80p-Pho85p cyclin/cyclin-dependent kinase complex. These mutations are therefore likely to impair upstream functions in the signaling pathway, and they define five complementation groups. Mutations were found in a gene encoding a plasma membrane ATPase (PMA1), in genes required for the in vivo function of the phosphate transport system (PHO84 and PHO86), in a gene involved in the fatty acid synthesis pathway (ACC1), and in a novel, nonessential gene (PHO23). These mutants can be classified into two groups: pho84, pho86, and pma1 are defective in high-affinity phosphate uptake, whereas acc1 and pho23 are not, indicating that the two groups of mutations cause constitutive expression of PHO5 by distinct mechanisms. Our observations suggest that these gene products affect different aspects of the signal transduction pathway for PHO5 repression.

Glucose as a hormone: receptor-mediated glucose sensing in the yeast Saccharomyces cerevisiae

2005 ◽  
Vol 33 (1) ◽  
pp. 247-252 ◽  
Author(s):  
M. Johnston ◽  
J.-H. Kim
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Signal Transduction ◽  
Signal Transduction Pathway ◽  
Glucose Transporters ◽  
Glucose Sensing ◽  
Yeast Cells ◽  
Transduction Pathway ◽  
Yeast Saccharomyces Cerevisiae ◽  
Expression Of Genes ◽  
Genes Encoding

Because glucose is the principal carbon and energy source for most cells, most organisms have evolved numerous and sophisticated mechanisms for sensing glucose and responding to it appropriately. This is especially apparent in the yeast Saccharomyces cerevisiae, where these regulatory mechanisms determine the distinctive fermentative metabolism of yeast, a lifestyle it shares with many kinds of tumour cells. Because energy generation by fermentation of glucose is inefficient, yeast cells must vigorously metabolize glucose. They do this, in part, by carefully regulating the first, rate-limiting step of glucose utilization: its transport. Yeast cells have learned how to sense the amount of glucose that is available and respond by expressing the most appropriate of its 17 glucose transporters. They do this through a signal transduction pathway that begins at the cell surface with the Snf3 and Rgt2 glucose sensors and ends in the nucleus with the Rgt1 transcription factor that regulates expression of genes encoding glucose transporters. We explain this glucose signal transduction pathway, and describe how it fits into a highly interconnected regulatory network of glucose sensing pathways that probably evolved to ensure rapid and sensitive response of the cell to changing levels of glucose.

scholarly journals Identification of Genes Controlling Growth Polarity in the Budding Yeast Saccharomyces cerevisiae: A Possible Role of N-Glycosylation and Involvement of the Exocyst Complex

Genetics ◽  
1997 ◽  
Vol 147 (2) ◽  
pp. 421-434 ◽  
Author(s):  
G Mondésert ◽  
D J Clarke ◽  
S I Reed
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Surface ◽  
Actin Cytoskeleton ◽  
Cell Cycle Progression ◽  
Cellular Systems ◽  
Surface Growth ◽  
Polarized Growth ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cycle Progression

The regulation of secretion polarity and cell surface growth during the cell cycle is critical for proper morphogenesis and viability of Saccharomyces cerevisiae. A shift from isotropic cell surface growth to polarized growth is necessary for bud emergence and a repolarization of secretion to the bud neck is necessary for cell separation. Although alterations in the actin cytoskeleton have been implicated in these changes in secretion polarity, clearly other cellular systems involved in secretion are likely to be targets of cell cycle regulation. To investigate mechanisms coupling cell cycle progression to changes in secretion polarity in parallel with and downstream of regulation of actin polarization, we implemented a screen for mutants defective specifically in polarized growth but with normal actin cytoskeleton structure. These mutants fell into three classes: those partially defective in N-glycosylation, those linked to specific defects in the exocyst, and a third class neither defective in glycosylation nor linked to the exocyst. These results raise the possibility that changes in N-linked glycosylation may be involved in a signal linking cell cycle progression and secretion polarity and that the exocyst may have regulatory functions in coupling the secretory machinery to the polarized actin cytoskeleton.

scholarly journals A Role for the Replication Proteins PCNA, RF-C, Polymerase ε and Cdc45 in Transcriptional Silencing in Saccharomyces cerevisiae

Genetics ◽  
1999 ◽  
Vol 153 (3) ◽  
pp. 1171-1182
Author(s):  
Ann E Ehrenhofer-Murray ◽  
Rohinton T Kamakaka ◽  
Jasper Rine
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Origin Recognition Complex ◽  
Transcriptional Silencing ◽  
Replication Timing ◽  
Replication Proteins ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cycle Progression

Abstract Transcriptional silencing in the budding yeast Saccharomyces cerevisiae may be linked to DNA replication and cell cycle progression. In this study, we have surveyed the effect of 41 mutations in genes with a role in replication, the cell cycle, and DNA repair on silencing at HMR. Mutations in PCNA (POL30), RF-C (CDC44), polymerase ε (POL2, DPB2, DPB11), and CDC45 were found to restore silencing at a mutant HMR silencer allele that was still a chromosomal origin of replication. Replication timing experiments indicated that the mutant HMR locus was replicated late in S-phase, at the same time as wild-type HMR. Restoration of silencing by PCNA and CDC45 mutations required the origin recognition complex binding site of the HMR-E silencer. Several models for the precise role of these replication proteins in silencing are discussed.

scholarly journals Identification and Characterization of FAR3, a Gene Required for Pheromone-Mediated G1 Arrest in Saccharomyces cerevisiae

Genetics ◽  
1996 ◽  
Vol 144 (3) ◽  
pp. 905-921 ◽  
Author(s):  
Joe Horecka ◽  
George F Sprague
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Signal Transduction ◽  
Signal Transduction Pathway ◽  
Selection Strategy ◽  
G1 Arrest ◽  
Amino Acid Residues ◽  
Transduction Pathway ◽  
G1 Cyclin ◽  
Cyclin Protein

Abstract In haploid Saccharomyces cerevisiae cells, mating pheromones activate a signal transduction pathway that leads to cell cycle arrest in the G1 phase and to transcription induction of genes that promote conjugation. To identify genes that link the signal transduction pathway and the cell cycle machinery, we developed a selection strategy to isolate yeast mutants specifically defective for G1 arrest. Several of these mutants identified previously known genes, including CLN3, FUS3, and FAR1. In addition, a new gene, FAR3, was identified and characterized. FAR3 encodes a novel protein of 204 amino acid residues that is dispensable for viability. Northern blot experiments indicated that FAR3 expression is constitutive with respect to cell type, pheromone treatment, and cell cycle position. As a first step toward elucidating the mechanism by which Far3 promotes pheromone-mediated G1 arrest, we performed genetic and molecular experiments to test the possibility that Far3 participates in one of the heretofore characterized mechanisms, namely Fus3/Farl-mediated inhibition of Cdc28-Cln kinase activity, G1 cyclin gene repression, and G1, cyclin protein turnover. Our data indicate that Far3 effects G1 arrest by a mechanism distinct from those previously known.

Sign in / Sign up

Export Citation Format

Share Document