The high-osmolarity glycerol (HOG) and cell wall integrity (CWI) signalling pathways interplay: a yeast dialogue between MAPK routes

Yeast ◽  
2010 ◽  
Vol 27 (8) ◽  
pp. 495-502 ◽  
Author(s):  
Jose Manuel Rodríguez-Peña ◽  
Raúl García ◽  
César Nombela ◽  
Javier Arroyo
Keyword(s):  
Cell Wall ◽  
Cell Wall Integrity ◽  
Signalling Pathways ◽  
High Osmolarity ◽  
High Osmolarity Glycerol

scholarly journals Roles of High Osmolarity Glycerol and Cell Wall Integrity Pathways in Cadmium Toxicity in Saccharomyces cerevisiae

2021 ◽  
Vol 22 (12) ◽  
pp. 6169
Author(s):  
Yunying Zhao ◽  
Shiyun Li ◽  
Jing Wang ◽  
Yingli Liu ◽  
Yu Deng
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Cadmium Toxicity ◽  
Cell Wall Integrity ◽  
Yeast Cells ◽  
Nuclear Accumulation ◽  
Hog Pathway ◽  
High Osmolarity ◽  
High Osmolarity Glycerol ◽  
Upr Pathway

Cadmium is a carcinogen that can induce ER stress, DNA damage, oxidative stress and cell death. The yeast mitogen-activated protein kinase (MAPK) signalling pathways paly crucial roles in response to various stresses. Here, we demonstrate that the unfolded protein response (UPR) pathway, the high osmolarity glycerol (HOG) pathway and the cell wall integrity (CWI) pathway are all essential for yeast cells to defend against the cadmium-induced toxicity, including the elevated ROS and cell death levels induced by cadmium. We show that the UPR pathway is required for the cadmium-induced phosphorylation of HOG_MAPK Hog1 but not for CWI_MAPK Slt2, while Slt2 but not Hog1 is required for the activation of the UPR pathway through the transcription factors of Swi6 and Rlm1. Moreover, deletion of HAC1 and IRE1 could promote the nuclear accumulation of Hog1, and increase the cytosolic and bud neck localisation of Slt2, indicating crucial roles of Hog1 and Slt2 in regulating the cellular process in the absence of UPR pathway. Altogether, our findings highlight the significance of these two MAPK pathways of HOG and CWI and their interrelationship with the UPR pathway in responding to cadmium-induced toxicity in budding yeast.

scholarly journals Yeast osmosensor Sln1 and plant cytokinin receptor Cre1 respond to changes in turgor pressure

2003 ◽  
Vol 161 (6) ◽  
pp. 1035-1040 ◽  
Author(s):  
Vladimír Reiser ◽  
Desmond C. Raitt ◽  
Haruo Saito
Keyword(s):  
Cell Wall ◽  
Stress Responses ◽  
Histidine Kinase ◽  
Turgor Pressure ◽  
Hyperosmotic Stress ◽  
Cytokinin Receptor ◽  
High Osmolarity ◽  
High Osmolarity Glycerol ◽  
High Osmolarity Glycerol Pathway ◽  
Cytokinin Response

Very little is known about how cellular osmosensors monitor changes in osmolarity of the environment. Here, we report that in yeast, Sln1 osmosensor histidine kinase monitors changes in turgor pressures. Reductions in turgor caused by either hyperosmotic stress, nystatin, or removal of cell wall activate MAPK Hog1 specifically through the SLN1 branch, but not through the SHO1 branch of the high osmolarity glycerol pathway. The integrity of the periplasmic region of Sln1 was essential for its sensor function. We found that activity of the plant histidine kinase cytokinin response 1 (Cre1) is also regulated by changes in turgor pressure, in a manner identical to that of Sln1, in the presence of cytokinin. We propose that Sln1 and Cre1 are turgor sensors, and that similar turgor-sensing mechanisms might regulate hyperosmotic stress responses both in yeast and plants.

scholarly journals Calcofluor Antifungal Action Depends on Chitin and a Functional High-Osmolarity Glycerol Response (HOG) Pathway: Evidence for a Physiological Role of the Saccharomyces cerevisiae HOG Pathway under Noninducing Conditions

2000 ◽  
Vol 182 (9) ◽  
pp. 2428-2437 ◽  
Author(s):  
L. J. García-Rodriguez ◽  
A. Durán ◽  
C. Roncero
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Wall ◽  
Protein Kinase ◽  
Salt Tolerance ◽  
Map Kinases ◽  
Physiological Role ◽  
Hog Pathway ◽  
High Osmolarity ◽  
High Osmolarity Glycerol

ABSTRACT We have isolated several Saccharomyces cerevisiaemutants resistant to calcofluor that contain mutations in thePBS2 or HOG1 genes, which encode the mitogen-activated protein kinase (MAPK) and MAP kinases, respectively, of the high-osmolarity glycerol response (HOG) pathway. We report that blockage of either of the two activation branches of the pathway, namely, SHO1 and SLN1, leads to partial resistance to calcofluor, while simultaneous disruption significantly increases resistance. However, chitin biosynthesis is independent of the HOG pathway. Calcofluor treatment also induces an increase in salt tolerance and glycerol accumulation, although no activation of the HOG pathway is detected. Our results indicate that the antifungal effect of calcofluor depends on its binding to cell wall chitin but also on the presence of a functional HOG pathway. Characterization of one of the mutants isolated, pbs2-14, revealed that resistance to calcofluor and HOG-dependent osmoadaptation are two different physiological processes. Sensitivity to calcofluor depends on the constitutive functionality of the HOG pathway; when this is altered, the cells become calcofluor resistant but also show very low levels of basal salt tolerance. Characterization of some multicopy suppressors of the calcofluor resistance phenotype indicated that constitutive HOG functionality participates in the maintenance of cell wall architecture, a conclusion supported by the antagonism observed between the protein kinase and HOG signal transduction pathways.

scholarly journals Protein Kinase A and High-Osmolarity Glycerol Response Pathways Cooperatively Control Cell Wall Carbohydrate Mobilization inAspergillus fumigatus

mBio ◽  
2018 ◽  
Vol 9 (6) ◽  
Author(s):  
Leandro José de Assis ◽  
Adriana Manfiolli ◽  
Eliciane Mattos ◽  
João H. T. Marilhano Fabri ◽  
Iran Malavazi ◽  
...  
Keyword(s):  
Cell Wall ◽  
Protein Kinase ◽  
Glycogen Synthesis ◽  
Fungal Cell Wall ◽  
Cell Wall Biosynthesis ◽  
Fungal Cell ◽  
Content Type ◽  
High Osmolarity ◽  
High Osmolarity Glycerol ◽  
Kinase A

ABSTRACTAspergillus fumigatusmitogen-activated protein kinases (MAPKs) are involved in maintaining the normal morphology of the cell wall and providing resistance against cell wall-damaging agents. Upon cell wall stress, cell wall-related sugars need to be synthesized from carbohydrate storage compounds. Here we show that this process is dependent on cAMP-dependent protein kinase A (PKA) activity and regulated by the high-osmolarity glycerol response (HOG) MAPKs SakA and MpkC. These protein kinases are necessary for normal accumulation/degradation of trehalose and glycogen, and the lack of these genes reduces glucose uptake and glycogen synthesis. Alterations in glycogen synthesis were observed for thesakAandmpkCdeletion mutants, which also displayed alterations in carbohydrate exposure on the cell wall. Carbohydrate mobilization is controlled by SakA interaction with PkaC1 and PkaR, suggesting a putative mechanism where the PkaR regulatory subunit leaves the complex and releases the SakA-PkaC1 complex for activation of enzymes involved in carbohydrate mobilization. This work reveals the communication between the HOG and PKA pathways for carbohydrate mobilization for cell wall construction.IMPORTANCEAspergillus fumigatusis an opportunistic human pathogen causing allergic reactions or systemic infections such as invasive pulmonary aspergillosis, especially in immunocompromised patients. The fungal cell wall is the main component responsible for recognition by the immune system, due to the specific composition of polysaccharide carbohydrates exposed on the surface of the fungal cell wall called pathogen-associated molecular patterns (PAMPs). Key enzymes in the fungal cell wall biosynthesis are a good target for fungal drug development. This report elucidates the cooperation between the HOG and PKA pathways in the mobilization of carbohydrates for fungal cell wall biosynthesis. We suggest that the reduced mobilization of simple sugars causes defects in the structure of the fungal cell wall. In summary, we propose that SakA is important for PKA activity, therefore regulating the availability and mobilization of monosaccharides for fungal cell wall biosynthesis during cell wall damage and the osmotic stress response.

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