The tolQRABpal cluster of Escherichia coli K-12 encodes proteins involved in the maintenance of cell-envelope integrity. In addition, tol/pal mutations result in a mucoid colony phenotype at low temperature. The synthesis of capsular polysaccharides by the cps genes is controlled by the positive regulator RcsA and the two-component RcsC/RcsB system. It was shown that the mucoid phenotype of the tol/pal mutants was due to an rcsCB-dependent activation of the cps genes. Furthermore, we have identified a mutation in the rcsC gene that decreased the activity of a tolA-lac operon fusion independently of RcsA and partially independently of RcsB activators. The corresponding rcsC338 mutation resulted in a Glu to Lys substitution at residue 338 of RcsC. This mutation induced mucoidy even at high temperature. We propose that RcsC modulates the phosphorylated forms of RcsB and an uncharacterized regulatory protein involved in the control of the tolQRA genes in an opposite manner. Moreover, our findings strengthen the previous suggestion that RcsC senses some alterations in the cell surface such as those induced by tol, pal or rfa mutations, and activates capsule synthesis to protect the cell against deleterious agents.
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http://dx.doi.org/10.1046/j.1365-2958.1996.343880.x | DOI Listing |
Infect Immun
July 2018
Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
Salmonellae regulate membrane lipids during infection, but the exact proteins and mechanisms that promote their survival during bacteremia remain largely unknown. Mutations in genes encoding the conserved serovar Typhimurium ( Typhimurium) Tol-Pal apparatus caused the outer membrane (OM) sensor lipoprotein, RcsF, to become activated. The capsule activation phenotype for the mutants suggested that Tol-Pal might influence envelope lipid homeostasis.
View Article and Find Full Text PDFMol Microbiol
August 2009
Department of Biological Sciences, Lilly Hall of Life Sciences, Purdue University, West Lafayette, IN 47907, USA.
Only two new genes (fkpA and lepB) have been identified to be required for colicin cytotoxicity in the last 25 years. Genome-wide screening using the 'Keio collection' to test sensitivity to colicins (col) A, B, D, E1, E2, E3, E7 and N from groups A and B, allowed identification of novel genes affecting cytotoxicity and provided new information on mechanisms of action. The requirement of lipopolysaccharide for colN cytotoxicity resides specifically in the lipopolysaccharide inner-core and first glucose.
View Article and Find Full Text PDFMicrobiol Immunol
June 2009
Molecular Microbiology Laboratory, Faculty of Life Sciences, Northwest University, 229 Taibai Road North, Xian, 710069, China.
The tol-pal genes play important roles in maintaining outer membrane integrity, transmembrane transportation, and cell division in Gram-negative bacteria. In Pseudomonas aeruginosa, an important human opportunistic pathogen, the tol-oprL genes are organized uniquely in three operons, orf1-tolQRA, tolB and oprL-orf2, and are regulated by iron availability. Similarity between TolQRA and the iron transport system ExbBD-TonB also exists in P.
View Article and Find Full Text PDFMicrobiology (Reading)
July 2005
Unité de Microbiologie et Génétique, UMR5122 CNRS-INSA-UCBL, Université Claude Bernard Lyon1, bât A. Lwoff, 10, rue Dubois, 69622 Villeurbanne cedex, France.
Curli are necessary for the adherence of Escherichia coli to surfaces, and to each other, during biofilm formation, and the csgBA and csgDEFG operons are both required for their synthesis. A recent survey of gene expression in Pseudomonas aeruginosa biofilms has identified tolA as a gene activated in biofilms. The tol genes play a fundamental role in maintaining the outer-membrane integrity of Gram-negative bacteria.
View Article and Find Full Text PDFJ Bacteriol
February 2003
Division of Geographic Medicine/Infectious Disease, New England Medical Center, 750 Washington Street, Boston, MA 02111, USA.
CTXphi is a filamentous bacteriophage that encodes cholera toxin. CTXphi infection of its host bacterium, Vibrio cholerae, requires the toxin-coregulated pilus (TCP) and the products of the V. cholerae tolQRA genes.
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