Regulation of a Kinase Cascade Involved in Cancer and Normal Cell Growth.

1996 ◽  
Author(s):  
Dennis J. Templeton ◽  
Minhong Yan
Keyword(s):  
Cell Growth ◽  
Normal Cell ◽  
Kinase Cascade

The yeast KRE5 gene encodes a probable endoplasmic reticulum protein required for (1----6)-beta-D-glucan synthesis and normal cell growth

1990 ◽  
Vol 10 (6) ◽  
pp. 3013-3019
Author(s):  
P Meaden ◽  
K Hill ◽  
J Wagner ◽  
D Slipetz ◽  
S S Sommer ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Wall ◽  
Cell Growth ◽  
Normal Cell ◽  
Secretory Pathway ◽  
Endoplasmic Reticulum Retention Signal ◽  
Endoplasmic Reticulum Protein ◽  
Glucan Synthesis ◽  
Retention Signal ◽  
Sequential Assembly

Yeast kre mutants define a pathway of cell wall (1----6)-beta-D-glucan synthesis, and mutants in genes KRE5 and KRE6 appear to interact early in such a pathway. We have cloned KRE5, and the sequence predicts the product to be a large, hydrophilic, secretory glycoprotein which contains the COOH-terminal endoplasmic reticulum retention signal, HDEL. Deletion of the KRE5 gene resulted in cells with aberrant morphology and extremely compromised growth. Suppressors to the KRE5 deletions arose at a frequency of 1 in 10(7) to 1 in 10(8) and permitted an analysis of deletions which were found to contain no alkali-insoluble (1----6)-beta-D-glucan. These results indicate a role for (1----6)-beta-D-glucan in normal cell growth and suggest a model for sequential assembly of (1----6)-beta-D-glucan in the yeast secretory pathway.

scholarly journals Cell Wall Stress Depolarizes Cell Growth via Hyperactivation of Rho1

1999 ◽  
Vol 147 (1) ◽  
pp. 163-174 ◽  
Author(s):  
Pierre-Alain Delley ◽  
Michael N. Hall
Keyword(s):  
Cell Wall ◽  
Cell Growth ◽  
Actin Cytoskeleton ◽  
Mammalian Cells ◽  
Wall Stress ◽  
Mitogen Activated Protein Kinase ◽  
Regulatory Subunit ◽  
Cell Wall Stress ◽  
Mitogen Activated Protein ◽  
Kinase Cascade

Cells sense and physiologically respond to environmental stress via signaling pathways. Saccharomyces cerevisiae cells respond to cell wall stress by transiently depolarizing the actin cytoskeleton. We report that cell wall stress also induces a transient depolarized distribution of the cell wall biosynthetic enzyme glucan synthase FKS1 and its regulatory subunit RHO1, possibly as a mechanism to repair general cell wall damage. The redistribution of FKS1 is dependent on the actin cytoskeleton. Depolarization of the actin cytoskeleton and FKS1 is mediated by the plasma membrane protein WSC1, the RHO1 GTPase switch, PKC1, and a yet-to-be defined PKC1 effector branch. WSC1 behaves like a signal transducer or a stress-specific actin landmark that both controls and responds to the actin cytoskeleton, similar to the bidirectional signaling between integrin receptors and the actin cytoskeleton in mammalian cells. The PKC1-activated mitogen-activated protein kinase cascade is not required for depolarization, but rather for repolarization of the actin cytoskeleton and FKS1. Thus, activated RHO1 can mediate both polarized and depolarized cell growth via the same effector, PKC1, suggesting that RHO1 may function as a rheostat rather than as a simple on-off switch.

scholarly journals Characterization of the Tellurite-Resistance Properties and Identification of the Core Function Genes for Tellurite Resistance in Pseudomonas citronellolis SJTE-3

2022 ◽  
Vol 10 (1) ◽  
pp. 95
Author(s):  
Wanli Peng ◽  
Yanqiu Wang ◽  
Yali Fu ◽  
Zixin Deng ◽  
Shuangjun Lin ◽  
...  
Keyword(s):  
Cell Growth ◽  
Normal Cell ◽  
Pathogenic Bacteria ◽  
Tellurite Resistance ◽  
Bacterial Pathogenicity ◽  
The Core ◽  
Core Function ◽  
High Concentrations ◽  
Tellurite Reduction

Tellurite is highly toxic to bacteria and commonly used in the clinical screening for pathogens; it is speculated that there is a potential relationship between tellurite resistance and bacterial pathogenicity. Until now, the core function genes of tellurite resistance and their characteristics are still obscure. Pseudomonas citronellolis SJTE-3 was found able to resist high concentrations of tellurite (250 μg/mL) and formed vacuole-like tellurium nanostructures. The terZABCDE gene cluster located in the large plasmid pRBL16 endowed strain SJTE-3 with the tellurite resistance of high levels. Although the terC and terD genes were identified as the core function genes for tellurite reduction and resistance, the inhibition of cell growth was observed when they were used solely. Interestingly, co-expression of the terA gene or terZ gene could relieve the burden caused by the expression of the terCD genes and recover normal cell growth. TerC and TerD proteins commonly shared the conserved sequences and are widely distributed in many pathogenic bacteria, highly associated with the pathogenicity factors.

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