scholarly journals Interaction between the transmembrane domains of Sho1 and Opy2 enhances the signaling efficiency of the Hog1 MAP kinase cascade in Saccharomyces cerevisiae

PLoS ONE ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. e0211380 ◽  
Author(s):  
Tomomi Takayama ◽  
Katsuyoshi Yamamoto ◽  
Haruo Saito ◽  
Kazuo Tatebayashi
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Map Kinase ◽  
Transmembrane Domains ◽  
Map Kinase Cascade ◽  
Kinase Cascade ◽  
Signaling Efficiency

scholarly journals Cyclic AMP-Dependent Protein Kinase Regulates Pseudohyphal Differentiation in Saccharomyces cerevisiae

1999 ◽  
Vol 19 (7) ◽  
pp. 4874-4887 ◽  
Author(s):  
Xuewen Pan ◽  
Joseph Heitman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Map Kinase ◽  
Filamentous Growth ◽  
Dependent Protein Kinase ◽  
Catalytic Subunits ◽  
Map Kinase Cascade ◽  
Kinase Cascade ◽  
Dependent Protein ◽  
Pseudohyphal Differentiation

ABSTRACT In response to nitrogen starvation, diploid cells of the yeastSaccharomyces cerevisiae differentiate to a filamentous growth form known as pseudohyphal differentiation. Filamentous growth is regulated by elements of the pheromone mitogen-activated protein (MAP) kinase cascade and a second signaling cascade involving the receptor Gpr1, the Gα protein Gpa2, Ras2, and cyclic AMP (cAMP). We show here that the Gpr1-Gpa2-cAMP pathway signals via the cAMP-dependent protein kinase, protein kinase A (PKA), to regulate pseudohyphal differentiation. Activation of PKA by mutation of the regulatory subunit Bcy1 enhances filamentous growth. Mutation and overexpression of the PKA catalytic subunits reveal that the Tpk2 catalytic subunit activates filamentous growth, whereas the Tpk1 and Tpk3 catalytic subunits inhibit filamentous growth. The PKA pathway regulates unipolar budding and agar invasion, whereas the MAP kinase cascade regulates cell elongation and invasion. Epistasis analysis supports a model in which PKA functions downstream of the Gpr1 receptor and the Gpa2 and Ras2 G proteins. Activation of filamentous growth by PKA does not require the transcription factors Ste12 and Tec1 of the MAP kinase cascade, Phd1, or the PKA targets Msn2 and Msn4. PKA signals pseudohyphal growth, in part, by regulating Flo8-dependent expression of the cell surface flocculin Flo11. In summary, the cAMP-dependent protein kinase plays an intimate positive and negative role in regulating filamentous growth, and these findings may provide insight into the roles of PKA in mating, morphogenesis, and virulence in other yeasts and pathogenic fungi.

scholarly journals Methylglyoxal Activates the Target of Rapamycin Complex 2-Protein Kinase C Signaling Pathway in Saccharomyces cerevisiae

2015 ◽  
Vol 35 (7) ◽  
pp. 1269-1280 ◽  
Author(s):  
Wataru Nomura ◽  
Yoshiharu Inoue
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Map Kinase ◽  
Target Of Rapamycin ◽  
Dependent Manner ◽  
Content Type ◽  
Protein Levels ◽  
Map Kinase Cascade ◽  
Phosphorylated Akt ◽  
Mitogen Activated Protein ◽  
Kinase Cascade

Methylglyoxal is a typical 2-oxoaldehyde derived from glycolysis. We show here that methylglyoxal activates the Pkc1-Mpk1 mitogen-activated protein (MAP) kinase cascade in a target of rapamycin complex 2 (TORC2)-dependent manner in the budding yeastSaccharomyces cerevisiae. We demonstrate that TORC2 phosphorylates Pkc1 at Thr1125and Ser1143. Methylglyoxal enhanced the phosphorylation of Pkc1 at Ser1143, which transmitted the signal to the downstream Mpk1 MAP kinase cascade. We found that the phosphorylation status of Pkc1T1125affected the phosphorylation of Pkc1 at Ser1143, in addition to its protein levels. Methylglyoxal activated mammalian TORC2 signaling, which, in turn, phosphorylated Akt at Ser473. Our results suggest that methylglyoxal is a conserved initiator of TORC2 signaling among eukaryotes.

scholarly journals A Third Osmosensing Branch in Saccharomyces cerevisiae Requires the Msb2 Protein and Functions in Parallel with the Sho1 Branch

2002 ◽  
Vol 22 (13) ◽  
pp. 4739-4749 ◽  
Author(s):  
Sean M. O'Rourke ◽  
Ira Herskowitz
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Map Kinase ◽  
Cross Talk ◽  
Dna Microarrays ◽  
Hog Pathway ◽  
Gene Sets ◽  
Map Kinase Cascade ◽  
Mitogen Activated Protein ◽  
Kinase Cascade ◽  
Membrane Spanning

ABSTRACT Two Saccharomyces cerevisiae plasma membrane-spanning proteins, Sho1 and Sln1, function during increased osmolarity to activate a mitogen-activated protein (MAP) kinase cascade. One of these proteins, Sho1, utilizes the MAP kinase kinase kinase Ste11 to activate Pbs2. We previously used the FUS1 gene of the pheromone response pathway as a reporter to monitor cross talk in hog1 mutants. Cross talk requires the Sho1-Ste11 branch of the HOG pathway, but some residual signaling, which is STE11 dependent, still occurs in the absence of Sho1. These observations led us to propose the existence of another osmosensor upstream of Ste11. To identify such an osmosensor, we screened for mutants in which the residual signaling in a hog1 sho1 mutant was further reduced. We identified the MSB2 gene, which encodes a protein with a single membrane-spanning domain and a large presumptive extracellular domain. Assay of the FUS1-lacZ reporter (in a hog1 mutant background) showed that sho1 and msb2 mutations both reduced the expression of the reporter partially and that the hog1 sho1 msb2 mutant was severely defective in the expression of the reporter. The use of DNA microarrays to monitor gene expression revealed that Sho1 and Msb2 regulate identical gene sets in hog1 mutants. A role for MSB2 in HOG1 strains was also seen in strains defective in the two known branches that activate Pbs2: an ssk1 sho1 msb2 strain was more osmosensitive than an ssk1 sho1 MSB2 strain. These observations indicate that Msb2 is partially redundant with the Sho1 osmosensing branch for the activation of Ste11.

scholarly journals The G Protein-Coupled Receptor Gpr1 Is a Nutrient Sensor That Regulates Pseudohyphal Differentiation in Saccharomyces cerevisiae

Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 609-622 ◽  
Author(s):  
Michael C Lorenz ◽  
Xuewen Pan ◽  
Toshiaki Harashima ◽  
Maria E Cardenas ◽  
Yong Xue ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Carbon Source ◽  
Map Kinase ◽  
G Protein ◽  
Nitrogen Starvation ◽  
G Protein Coupled Receptor ◽  
Map Kinase Cascade ◽  
Kinase Cascade ◽  
Pseudohyphal Differentiation ◽  
G Protein Coupled

Abstract Pseudohyphal differentiation in the budding yeast Saccharomyces cerevisiae is induced in diploid cells in response to nitrogen starvation and abundant fermentable carbon source. Filamentous growth requires at least two signaling pathways: the pheromone responsive MAP kinase cascade and the Gpa2p-cAMP-PKA signaling pathway. Recent studies have established a physical and functional link between the Gα protein Gpa2 and the G protein-coupled receptor homolog Gpr1. We report here that the Gpr1 receptor is required for filamentous and haploid invasive growth and regulates expression of the cell surface flocculin Flo11. Epistasis analysis supports a model in which the Gpr1 receptor regulates pseudohyphal growth via the Gpa2p-cAMP-PKA pathway and independently of both the MAP kinase cascade and the PKA related kinase Sch9. Genetic and physiological studies indicate that the Gpr1 receptor is activated by glucose and other structurally related sugars. Because expression of the GPR1 gene is known to be induced by nitrogen starvation, the Gpr1 receptor may serve as a dual sensor of abundant carbon source (sugar ligand) and nitrogen starvation. In summary, our studies reveal a novel G protein-coupled receptor senses nutrients and regulates the dimorphic transition to filamentous growth via a Gα protein-cAMP-PKA signal transduction cascade.

scholarly journals Fus3p and Kss1p Control G1 Arrest in Saccharomyces cerevisiae Through a Balance of Distinct Arrest and Proliferative Functions That Operate in Parallel With Far1p

Genetics ◽  
1999 ◽  
Vol 151 (3) ◽  
pp. 989-1004 ◽  
Author(s):  
Vera Cherkasova ◽  
David M Lyons ◽  
Elaine A Elion
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Map Kinase ◽  
Map Kinases ◽  
G1 Arrest ◽  
Multiple Functions ◽  
Map Kinase Cascade ◽  
Kinase Cascade ◽  
Map Kinase Pathway ◽  
Kinase Pathway ◽  
Cyclin Genes

AbstractIn Saccharomyces cerevisiae, mating pheromones activate two MAP kinases (MAPKs), Fus3p and Kss1p, to induce G1 arrest prior to mating. Fus3p is known to promote G1 arrest by activating Far1p, which inhibits three Clnp/Cdc28p kinases. To analyze the contribution of Fus3p and Kss1p to G1 arrest that is independent of Far1p, we constructed far1 CLN strains that undergo G1 arrest from increased activation of the mating MAP kinase pathway. We find that Fus3p and Kss1p both control G1 arrest through multiple functions that operate in parallel with Far1p. Fus3p and Kss1p together promote G1 arrest by repressing transcription of G1/S cyclin genes (CLN1, CLN2, CLB5) by a mechanism that blocks their activation by Cln3p/Cdc28p kinase. In addition, Fus3p and Kss1p counteract G1 arrest through overlapping and distinct functions. Fus3p and Kss1p together increase the expression of CLN3 and PCL2 genes that promote budding, and Kss1p inhibits the MAP kinase cascade. Strikingly, Fus3p promotes proliferation by a novel function that is not linked to reduced Ste12p activity or increased levels of Cln2p/Cdc28p kinase. Genetic analysis suggests that Fus3p promotes proliferation through activation of Mcm1p transcription factor that upregulates numerous genes in G1 phase. Thus, Fus3p and Kss1p control G1 arrest through a balance of arrest functions that inhibit the Cdc28p machinery and proliferative functions that bypass this inhibition.

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