title: The luxS gene is involved in cell-cell signalling for toxin production in Clostridium perfringens.
abstract: A Gram-positive anaerobic pathogen, Clostridium perfringens, causes clostridial myonecrosis or gas gangrene in humans by producing numerous extracellular toxins and enzymes that act in concert to degrade host tissues. C. perfringens possesses a homologue of the luxS gene that is reported to be responsible for the production of autoinducer 2 (AI-2), which participates in quorum sensing in bacteria. The luxS mutant was constructed using C. perfringens strain 13, and the role of the luxS gene in toxin production was examined. The cell-free culture supernatant from wild-type strain 13 greatly stimulated the luminescence of Vibrio harveyi BB170, whereas that from the luxS mutant caused no significant stimulation, indicating that the luxS gene is necessary for AI-2 production in C. perfringens. The luxS mutant showed a reduced level of production of alpha-, kappa- and theta-toxins. In the luxS mutant, the transcription of the theta-toxin gene (pfoA) was lower at mid-exponential growth phase, whereas alpha- and kappa-toxin gene transcription was not significantly affected. The production of toxins in the luxS mutant was stimulated by the addition of the culture supernatant from the wild-type cells, possibly because of the presence of AI-2. Moreover, the expression of the pfoA gene in the luxS mutant was apparently activated when the mutant cells were cultured in the presence of culture supernatants from the wild-type C. perfringens, Escherichia coli DH5alpha carrying the luxS gene of C. perfringens. A deletion analysis of the luxS operon showed that the luxS gene alone is responsible for cell-cell signalling, and that the metB or cysK genes located upstream of luxS are not involved in regulating toxin production. Our results indicate that cell-cell signalling by AI-2 plays an important role in the regulation of toxin production in C. perfringens.
authors.affiliation: Department of Infection Biology, Institute of Basic Medical Sciences, University of Tsukuba, 1-1-1 Tenohdai, Tsukuba, Ibaraki 305-8575, Japan.
authors.forename: Kaori
authors.initials: K
authors.lastname: Ohtani
authors.forename: Hideo
authors.initials: H
authors.lastname: Hayashi
authors.forename: Tohru
authors.initials: T
authors.lastname: Shimizu
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics*; D001427:Bacterial Toxins / Q000235:genetics* / Q000302:isolation & purification / Q000633:toxicity; D001681:Biological Assay; D002135:Calcium-Binding Proteins; D013437:Carbon-Sulfur Lyases; D003016:Clostridium perfringens / Q000235:genetics* / Q000472:pathogenicity; D006460:Hemolysin Proteins; D009876:Operon; D017384:Sequence Deletion; D015398:Signal Transduction / Q000235:genetics; D010738:Type C Phospholipases / Q000235:genetics* / Q000302:isolation & purification / Q000633:toxicity; D014733:Vibrio / Q000187:drug effects
chemical_list: D001426:Bacterial Proteins; D001427:Bacterial Toxins; C031884:CPB protein, Clostridium perfringens; D002135:Calcium-Binding Proteins; D006460:Hemolysin Proteins; C020452:Clostridium perfringens theta-toxin; D010738:Type C Phospholipases; C040649:alpha toxin, Clostridium perfringens; D013437:Carbon-Sulfur Lyases; C117753:LuxS protein, Bacteria