CovS/CovR of group B streptococcus: a two-component global regulatory system involved in virulence

Autor: Marie-Cécile, Lamy, Mohammed, Zouine, Juliette, Fert, Massimo, Vergassola, Elisabeth, Couve, Elisabeth, Pellegrini, Philippe, Glaser, Frank, Kunst, Tarek, Msadek, Patrick, Trieu-Cuot, Claire, Poyart
Přispěvatelé: Biologie des Bactéries Pathogènes à Gram-positif, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique ( CNRS ), Pathogénie des infections systémiques ( UMR_S 570 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Bactériologie, CHU Cochin [AP-HP], Génomique des Microorganismes Pathogènes, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Pathogénie des infections systémiques (UMR_S 570), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This work was supported by research funds from the Institut National de la Santé et de la Recherche Médicale, the European Commission (Grant QLG2‐CT‐1999‐01455), the Centre National de la Recherche Scientifique, the Institut Pasteur (PTR No. 17 and GPH No. 9), and the Universities Paris 5 and Paris 7. M.‐C. Lamy was supported by the Ministère de la Recherche et des Technologies and the Fondation pour la Recherche Médicale., We are grateful to J.L. Berretti for determination of haemolytic activities, D. Euphrasie for help in the construction of the ΔCylE mutant, and S. Dubrac and C. Buchrieser for helpful discussion., Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)
Jazyk: angličtina
Rok vydání: 2004
Předmět:
MESH: Signal Transduction
MESH : Virulence Factors
MESH : Hemolysis
Transcription
Genetic
MESH : Operon
MESH : Streptococcal Infections
MESH : Gene Deletion
MESH: Virulence
[ SDV.MP.BAC ] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology
Bacterial Adhesion
Hemolysin Proteins
MESH: Streptococcal Infections
MESH : Bacterial Proteins
MESH: Animals
Promoter Regions
Genetic
MESH: Bacterial Proteins
MESH: Gene Expression Regulation
Bacterial
Virulence
MESH : Rats
MESH : Genes
Bacterial
MESH : Virulence
MESH : Streptococcus agalactiae
MESH: Hemolysis
MESH : Epithelial Cells
MESH: Promoter Regions (Genetics)
MESH: Hemolysin Proteins
MESH: Repressor Proteins
MESH: Epithelial Cells
MESH: Regulon
MESH: Genes
Bacterial
MESH : Repressor Proteins
Signal Transduction
MESH : Gene Expression Regulation
Bacterial
MESH: Operon
MESH: Rats
Virulence Factors
MESH : Bacterial Adhesion
MESH : Regulon
MESH : Hemolysin Proteins
MESH : Protein Kinases
Hemolysis
Regulon
Streptococcus agalactiae
Lethal Dose 50
MESH: Gene Expression Profiling
Bacterial Proteins
Streptococcal Infections
Operon
Animals
Humans
MESH : Lethal Dose 50
MESH: Bacterial Adhesion
MESH: Protein Kinases
MESH: Virulence Factors
MESH : Signal Transduction
MESH: Humans
Gene Expression Profiling
MESH: Transcription
Genetic
MESH : Gene Expression Profiling
MESH : Humans
MESH : Transcription
Genetic
Epithelial Cells
Gene Expression Regulation
Bacterial
MESH: Streptococcus agalactiae
[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology
MESH : Promoter Regions (Genetics)
MESH : Disease Models
Animal
Rats
Repressor Proteins
Disease Models
Animal
MESH: Lethal Dose 50
Genes
Bacterial
MESH: Gene Deletion
MESH : Animals
MESH: Disease Models
Animal
Protein Kinases
Gene Deletion
Zdroj: Molecular Microbiology
Molecular Microbiology, Wiley, 2004, 54 (5), pp.1250-68. 〈10.1111/j.1365-2958.2004.04365.x〉
Molecular Microbiology, 2004, 54 (5), pp.1250-68. ⟨10.1111/j.1365-2958.2004.04365.x⟩
Molecular Microbiology, Wiley, 2004, 54 (5), pp.1250-68. ⟨10.1111/j.1365-2958.2004.04365.x⟩
ISSN: 0950-382X
1365-2958
Popis: International audience; In this study, we carried out a detailed structural and functional analysis of a Streptococcus agalactiae (GBS) two-component system which is orthologous to the CovS/CovR (CsrS/CsrR) regulatory system of Streptococcus pyogenes. In GBS, covR and covS are part of a seven gene operon transcribed from two promoters that are not regulated by CovR. A DeltacovSR mutant was found to display dramatic phenotypic changes such as increased haemolytic activity and reduced CAMP activity on blood agar. Adherence of the DeltacovSR mutant to epithelial cells was greatly increased and analysis by transmission electron microscopy revealed the presence at its surface of a fibrous extracellular matrix that might be involved in these intercellular interactions. However, the DeltacovSR mutant was unable to initiate growth in RPMI and its viability in human normal serum was greatly impaired. A major finding of this phenotypic analysis was that the CovS/CovR system is important for GBS virulence, as a 3 log increase of the LD(50) of the mutant strain was observed in the neonate rat sepsis model. The pleiotropic phenotype of the DeltacovSR mutant is in full agreement with the large number of genes controlled by CovS/CovR as seen by expression profiling analysis, many of which encode potentially secreted or cell surface-associated proteins: 76 genes are repressed whereas 63 were positively regulated. CovR was shown to bind directly to the regulatory regions of several of these genes and a consensus CovR recognition sequence was proposed using both DNase I footprinting and computational analyses.
Databáze: OpenAIRE
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