Regulated transcription of Clostridium difficile toxin genes
| Autor: | Abraham L. Sonenshein, Bruno Dupuy |
|---|---|
| Přispěvatelé: | Génétique Moléculaire Bactérienne, Institut Pasteur [Paris] (IP), Department of Molecular Biology and Microbiology [Tufts, Boston], Tufts University School of Medicine [Boston], This work was supported by the Institut Pasteur (Paris) and by the US Public Health Service through a research grant to A.L.S. (GM42219) and through a pilot project funded by a programme project (DK39428) awarded to the Centre for Gastroenterology Research on Absorptive and Secretory Processes., We thank T. D. Wilkins and L. A. Barroso for gifts of toxin proteins and specific antibodies, Meridian Diagnostics for providing anti‐toxin antibodies, M. Popoff for providing C. difficile strains, S. Melville and K. Matsuno for helpful advice and discussions, and B. Belitsky, N. Mani and C. L. Squires for criticism of the manuscript., Institut Pasteur [Paris] |
| Rok vydání: | 1998 |
| Předmět: |
MESH: Transcription
Genetic/physiology MESH: Clostridium perfringens/chemistry Transcription Genetic Clostridium perfringens MESH: Carbohydrate Metabolism [SDV]Life Sciences [q-bio] Catabolite repression MESH: Base Sequence MESH: Recombinant Fusion Proteins/genetics Polymerase Chain Reaction Transcription (biology) MESH: Clostridium difficile/metabolism Cloning Molecular MESH: Endoribonucleases/chemistry Promoter Regions Genetic Glucuronidase 0303 health sciences MESH: Glucose/metabolism MESH: RNA Messenger/chemistry Clostridium difficile MESH: Recombinant Fusion Proteins/biosynthesis 3. Good health RNA Bacterial Electroporation Carbohydrate Metabolism Electrophoresis Polyacrylamide Gel Recombinant Fusion Proteins Bacterial Toxins Blotting Western Molecular Sequence Data Clostridium difficile toxin A Biology Microbiology MESH: Gene Expression Regulation Bacterial/physiology 03 medical and health sciences Endoribonucleases medicine Escherichia coli MESH: Blotting Western MESH: Electroporation MESH: Cloning Molecular [SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology RNA Messenger Colitis Molecular Biology Gene 030304 developmental biology MESH: Molecular Sequence Data MESH: Bacterial Toxins/biosynthesis Base Sequence 030306 microbiology Clostridioides difficile Promoter MESH: Polymerase Chain Reaction Pseudomembranous colitis MESH: Glucuronidase/genetics Gene Expression Regulation Bacterial MESH: RNA Bacterial/chemistry medicine.disease Culture Media Glucose MESH: Glucuronidase/chemistry MESH: Promoter Regions Genetic/genetics MESH: Culture Media MESH: Escherichia coli/chemistry MESH: Clostridium difficile/genetics MESH: Bacterial Toxins/genetics MESH: Electrophoresis Polyacrylamide Gel |
| Zdroj: | Molecular Microbiology Molecular Microbiology, 1998, 27 (1), pp.107-120. ⟨10.1046/j.1365-2958.1998.00663.x⟩ Molecular Microbiology, Wiley, 1998, 27 (1), pp.107-120. ⟨10.1046/j.1365-2958.1998.00663.x⟩ |
| ISSN: | 0950-382X 1365-2958 |
| DOI: | 10.1046/j.1365-2958.1998.00663.x⟩ |
| Popis: | International audience; The Clostridium difficile toxA and toxB genes, encoding cytotoxic and enterotoxic proteins responsible for antibiotic‐associated colitis and pseudomembranous colitis, were shown to be transcribed both from gene‐specific promoters and from promoters of upstream genes. However, the gene‐specific transcripts represented the majority of tox gene mRNAs. The 5′ ends of these mRNAs were shown to correspond to DNA sequences that had promoter activity when fused to the Escherichia coliβ‐glucuronidase (gusA) gene and introduced into C. perfringens. The appearance of tox mRNA in C. difficile was repressed during exponential growth phase but increased substantially as cells entered stationary phase. When glucose or other rapidly metabolizable sugars were present in the medium, the stationary phase‐associated induction was inhibited, indicating that the toxin genes are subject to a form of catabolite repression. This glucose effect was general to many toxinogenic strains having varying levels of toxin production. |
| Databáze: | OpenAIRE |
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