scholarly journals FAR1 is required for posttranscriptional regulation of CLN2 gene expression in response to mating pheromone.

1993 ◽  
Vol 13 (2) ◽  
pp. 1013-1022 ◽  
Author(s):  
M H Valdivieso ◽  
K Sugimoto ◽  
K Y Jahng ◽  
P M Fernandes ◽  
C Wittenberg
Keyword(s):  
Cell Cycle ◽  
Posttranscriptional Regulation ◽  
Signal Transduction Pathway ◽  
Yeast Cells ◽  
Pheromone Response ◽  
Transcript Accumulation ◽  
Mating Pheromone ◽  
Cycle Arrest ◽  
Feedback Pathway ◽  
Posttranscriptional Level

Yeast cells arrest during the G1 interval of the cell cycle in response to peptide mating pheromones. The FAR1 gene is required for cell cycle arrest but not for a number of other aspects of the pheromone response. Genetic evidence suggests that FAR1 is required specifically for inactivation of the G1 cyclin CLN2. From these observations, the FAR1 gene has been proposed to encode an element of the interface between the mating pheromone signal transduction pathway and the cell cycle regulatory apparatus. We show here that FAR1 is necessary for the decrease in CLN1 and CLN2 transcript accumulation observed in response to mating pheromone but is unnecessary for regulation of the same transcripts during vegetative growth. However, the defect in regulation of CLN1 expression is dependent upon CLN2. We show that pheromone regulates the abundance of Cln2 at a posttranscriptional level and that FAR1 is required for that regulation. From these observations, we suggest that FAR1 function is limited to posttranscriptional regulation of CLN2 expression by mating pheromone. The failure of mating pheromone to repress CLN2 transcript levels in far1 mutants can be explained by the stimulatory effect of the persistent Cln2 protein on CLN2 transcription via the CLN/CDC28-dependent feedback pathway.

FAR1 is required for posttranscriptional regulation of CLN2 gene expression in response to mating pheromone

1993 ◽  
Vol 13 (2) ◽  
pp. 1013-1022
Author(s):  
M H Valdivieso ◽  
K Sugimoto ◽  
K Y Jahng ◽  
P M Fernandes ◽  
C Wittenberg
Keyword(s):  
Cell Cycle ◽  
Posttranscriptional Regulation ◽  
Signal Transduction Pathway ◽  
Yeast Cells ◽  
Pheromone Response ◽  
Transcript Accumulation ◽  
Mating Pheromone ◽  
Cycle Arrest ◽  
Feedback Pathway ◽  
Posttranscriptional Level

Yeast cells arrest during the G1 interval of the cell cycle in response to peptide mating pheromones. The FAR1 gene is required for cell cycle arrest but not for a number of other aspects of the pheromone response. Genetic evidence suggests that FAR1 is required specifically for inactivation of the G1 cyclin CLN2. From these observations, the FAR1 gene has been proposed to encode an element of the interface between the mating pheromone signal transduction pathway and the cell cycle regulatory apparatus. We show here that FAR1 is necessary for the decrease in CLN1 and CLN2 transcript accumulation observed in response to mating pheromone but is unnecessary for regulation of the same transcripts during vegetative growth. However, the defect in regulation of CLN1 expression is dependent upon CLN2. We show that pheromone regulates the abundance of Cln2 at a posttranscriptional level and that FAR1 is required for that regulation. From these observations, we suggest that FAR1 function is limited to posttranscriptional regulation of CLN2 expression by mating pheromone. The failure of mating pheromone to repress CLN2 transcript levels in far1 mutants can be explained by the stimulatory effect of the persistent Cln2 protein on CLN2 transcription via the CLN/CDC28-dependent feedback pathway.

Overexpression of the STE4 gene leads to mating response in haploid Saccharomyces cerevisiae

1990 ◽  
Vol 10 (1) ◽  
pp. 217-222
Author(s):  
M Whiteway ◽  
L Hougan ◽  
D Y Thomas
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
G Protein ◽  
Gene Product ◽  
Beta Subunit ◽  
Yeast Cells ◽  
Pheromone Response ◽  
Mating Pheromone ◽  
Cycle Arrest

The STE4 gene of Saccharomyces cerevisiae encodes the beta subunit of the yeast pheromone receptor-coupled G protein. Overexpression of the STE4 protein led to cell cycle arrest of haploid cells. This arrest was like the arrest mediated by mating pheromones in that it led to similar morphological changes in the arrested cells. The arrest occurred in haploid cells of either mating type but not in MATa/MAT alpha diploids, and it was suppressed by defects in genes such as STE12 that are needed for pheromone response. Overexpression of the STE4 gene product also suppressed the sterility of cells defective in the mating pheromone receptors encoded by the STE2 and STE3 genes. Cell cycle arrest mediated by STE4 overexpression was prevented in cells that either were overexpressing the SCG1 gene product (the alpha subunit of the G protein) or lacked the STE18 gene product (the gamma subunit of the G protein). This finding suggests that in yeast cells, the beta subunit is the limiting component of the active beta gamma element and that a proper balance in the levels of the G-protein subunits is critical to a normal mating pheromone response.

scholarly journals Overexpression of the STE4 gene leads to mating response in haploid Saccharomyces cerevisiae.

1990 ◽  
Vol 10 (1) ◽  
pp. 217-222 ◽  
Author(s):  
M Whiteway ◽  
L Hougan ◽  
D Y Thomas
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
G Protein ◽  
Gene Product ◽  
Beta Subunit ◽  
Yeast Cells ◽  
Pheromone Response ◽  
Mating Pheromone ◽  
Cycle Arrest

The STE4 gene of Saccharomyces cerevisiae encodes the beta subunit of the yeast pheromone receptor-coupled G protein. Overexpression of the STE4 protein led to cell cycle arrest of haploid cells. This arrest was like the arrest mediated by mating pheromones in that it led to similar morphological changes in the arrested cells. The arrest occurred in haploid cells of either mating type but not in MATa/MAT alpha diploids, and it was suppressed by defects in genes such as STE12 that are needed for pheromone response. Overexpression of the STE4 gene product also suppressed the sterility of cells defective in the mating pheromone receptors encoded by the STE2 and STE3 genes. Cell cycle arrest mediated by STE4 overexpression was prevented in cells that either were overexpressing the SCG1 gene product (the alpha subunit of the G protein) or lacked the STE18 gene product (the gamma subunit of the G protein). This finding suggests that in yeast cells, the beta subunit is the limiting component of the active beta gamma element and that a proper balance in the levels of the G-protein subunits is critical to a normal mating pheromone response.

scholarly journals CDC36 and CDC39 are negative elements in the signal transduction pathway of yeast.

1990 ◽  
Vol 1 (5) ◽  
pp. 391-401 ◽  
Author(s):  
A M Neiman ◽  
F Chang ◽  
K Komachi ◽  
I Herskowitz
Keyword(s):  
Cell Cycle ◽  
Signal Transduction Pathway ◽  
Yeast Cells ◽  
Control Synthesis ◽  
Temperature Sensitive ◽  
G1 Arrest ◽  
Epistasis Analysis ◽  
Cycle Arrest ◽  
Mating Factor ◽  
Inducible Gene

Mutations in either the CDC36 or CDC39 gene cause yeast cells to arrest in G1 of the cell cycle at the same point as treatment with mating pheromone. We demonstrate here that strains harboring temperature-sensitive mutations in CDC36 or CDC39 activate expression of the pheromone-inducible gene FUS1 when shifted to nonpermissive temperature. We show further that cell-cycle arrest and induction of FUS1 are dependent on known components of the mating factor response pathway, the STE genes. Thus, the G1-arrest phenotype of cdc36 and cdc39 mutants results from activation of the mating factor response pathway. The CDC36 and CDC39 gene products behave formally as negative elements in the response pathway: they are required to block response in the absence of pheromone. Epistasis analysis of mutants defective in CDC36 or CDC39 and different STE genes demonstrates that activation requires the response pathway G protein and suggests that CDC36 and CDC39 products may control synthesis or function of the G alpha subunit.

scholarly journals Antagonistic regulation of Fus2p nuclear localization by pheromone signaling and the cell cycle

2009 ◽  
Vol 184 (3) ◽  
pp. 409-422 ◽  
Author(s):  
Casey A. Ydenberg ◽  
Mark D. Rose
Keyword(s):  
Cell Cycle ◽  
S Phase ◽  
Yeast Cells ◽  
Transcriptional Level ◽  
G1 Arrest ◽  
Cycle Arrest ◽  
Pheromone Signaling ◽  
Dependent Inhibition ◽  
Induced Proteins ◽  
Mating Projection

When yeast cells sense mating pheromone, they undergo a characteristic response involving changes in transcription, cell cycle arrest in early G1, and polarization along the pheromone gradient. Cells in G2/M respond to pheromone at the transcriptional level but do not polarize or mate until G1. Fus2p, a key regulator of cell fusion, localizes to the tip of the mating projection during pheromone-induced G1 arrest. Although Fus2p was expressed in G2/M cells after pheromone induction, it accumulated in the nucleus until after cell division. As cells arrested in G1, Fus2p was exported from the nucleus and localized to the nascent tip. Phosphorylation of Fus2p by Fus3p was required for Fus2p export; cyclin/Cdc28p-dependent inhibition of Fus3p during late G1 through S phase was sufficient to block exit. However, during G2/M, when Fus3p was activated by pheromone signaling, Cdc28p activity again blocked Fus2p export. Our results indicate a novel mechanism by which pheromone-induced proteins are regulated during the transition from mitosis to conjugation.

scholarly journals Temperature-Sensitive Lethal Pseudorevertants of ste Mutations in Saccharomyces cerevisiae

Genetics ◽  
1987 ◽  
Vol 115 (4) ◽  
pp. 627-636
Author(s):  
Margaret E Katz ◽  
Jill Ferguson ◽  
Steven I Reed
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Complementation Group ◽  
Temperature Sensitive ◽  
G1 Arrest ◽  
Pheromone Response ◽  
Cycle Arrest ◽  
Homogeneous Cell ◽  
Complementation Groups ◽  
Mutant Cells

ABSTRACT A procedure was devised to isolate mutations that could restore conjugational competence to temperature sensitive ste mutants and simultaneously confer temperature-sensitive lethal growth phenotypes. Three such mutations, falling into two complementation groups, were identified on the basis of suppression of ste5 alleles. These same mutations were later shown to be capable of suppressing ste4 and ste7 alleles. Five mutations in a single complementation group were isolated as suppressors of ste2 alleles. None of the mutations described in this study conferred a homogeneous cell cycle arrest phenotype, and all were shown to define complementation groups distinct from those previously identified in studies of cell division cycle (cdc) mutations. In no instance did pseudoreversion appear to be achieved by mutational G1 arrest of ste mutant cells. Instead, it is proposed that the mutations restore conjugation by reestablishing the normal pheromone response.

Mutations in cell division cycle genes CDC36 and CDC39 activate the Saccharomyces cerevisiae mating pheromone response pathway

1990 ◽  
Vol 10 (6) ◽  
pp. 2966-2972
Author(s):  
M de Barros Lopes ◽  
J Y Ho ◽  
S I Reed
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
G Protein ◽  
G1 Arrest ◽  
Restrictive Temperature ◽  
Gene Products ◽  
Pheromone Response ◽  
Mating Pheromone ◽  
Pheromone Response Pathway ◽  
Mutational Activation

Conditional mutations in the genes CDC36 and CDC39 cause arrest in the G1 phase of the Saccharomyces cerevisiae cell cycle at the restrictive temperature. We present evidence that this arrest is a consequence of a mutational activation of the mating pheromone response. cdc36 and cdc39 mutants expressed pheromone-inducible genes in the absence of pheromone and conjugated in the absence of a mating pheromone receptor. On the other hand, cells lacking the G beta subunit or overproducing the G alpha subunit of the transducing G protein that couples the receptor to the pheromone response pathway prevented constitutive activation of the pathway in cdc36 and cdc39 mutants. These epistasis relationships imply that the CDC36 and CDC39 gene products act at the level of the transducing G protein. The CDC36 and CDC39 gene products have a role in cellular processes other than the mating pheromone response. A mating-type heterozygous diploid cell, homozygous for either the cdc36 or cdc39 mutation, does not exhibit the G1 arrest phenotype but arrests asynchronously with respect to the cell cycle. A similar asynchronous arrest was observed in cdc36 and cdc39 cells where the pheromone response pathway had been inactivated by mutations in the transducing G protein. Furthermore, cdc36 and cdc39 mutants, when grown on carbon catabolite-derepressing medium, did not arrest in G1 and did not induce pheromone-specific genes at the restrictive temperature.

Saccharomyces cerevisiae mutants lacking a functional vacuole are defective for aspects of the pheromone response

1990 ◽  
Vol 97 (3) ◽  
pp. 517-525 ◽  
Author(s):  
V. Dulic ◽  
H. Riezman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Carbon Sources ◽  
Early Response ◽  
Pheromone Response ◽  
Optimal Response ◽  
Cycle Arrest ◽  
Alpha Factor ◽  
Vacuolar Protein

The end1 mutant belongs to a group of four vacuolar protein sorting mutants (class C vps) that lack a morphologically distinguishable and functional vacuole. These mutants share several other phenotypes, such as the inability to grow at 37 degrees C or on nonfermentable carbon sources. We show that, as in the case of the end1 mutant, vps16, vps18 and vps33 mutants all internalize but do not degrade alpha-factor. In addition, all four mutants are defective for alpha-factor-induced projection formation to the same extent. A more detailed investigation of pheromone response in the end1 mutant reveals that one aspect of the early response (induction of FUS1) is as defective as late responses (cell cycle arrest and projection formation). In contrast, another measure of the early response (induction of STE2) is normal. These data suggest that the biogenesis of a functional vacuole is necessary for optimal response to pheromone.

Characterization of RAD9 of Saccharomyces cerevisiae and evidence that its function acts posttranslationally in cell cycle arrest after DNA damage

1990 ◽  
Vol 10 (12) ◽  
pp. 6554-6564
Author(s):  
T A Weinert ◽  
L H Hartwell
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Dna Sequence ◽  
Negative Regulator ◽  
Yeast Cells ◽  
Protein Synthesis Inhibitor ◽  
Cycle Arrest ◽  
Delta Cells

In eucaryotic cells, incompletely replicated or damaged chromosomes induce cell cycle arrest in G2 before mitosis, and in the yeast Saccharomyces cerevisiae the RAD9 gene is essential for the cell cycle arrest (T.A. Weinert and L. H. Hartwell, Science 241:317-322, 1988). In this report, we extend the analysis of RAD9-dependent cell cycle control. We found that both induction of RAD9-dependent arrest in G2 and recovery from arrest could occur in the presence of the protein synthesis inhibitor cycloheximide, showing that the mechanism of RAD9-dependent control involves a posttranslational mechanism(s). We have isolated and determined the DNA sequence of the RAD9 gene, confirming the DNA sequence reported previously (R. H. Schiestl, P. Reynolds, S. Prakash, and L. Prakash, Mol. Cell. Biol. 9:1882-1886, 1989). The predicted protein sequence for the Rad9 protein bears no similarity to sequences of known proteins. We also found that synthesis of the RAD9 transcript in the cell cycle was constitutive and not induced by X-irradiation. We constructed yeast cells containing a complete deletion of the RAD9 gene; the rad9 null mutants were viable, sensitive to X- and UV irradiation, and defective for cell cycle arrest after DNA damage. Although Rad+ and rad9 delta cells had similar growth rates and cell cycle kinetics in unirradiated cells, the spontaneous rate of chromosome loss (in unirradiated cells) was elevated 7- to 21-fold in rad9 delta cells. These studies show that in the presence of induced or endogenous DNA damage, RAD9 is a negative regulator that inhibits progression from G2 in order to preserve cell viability and to maintain the fidelity of chromosome transmission.

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