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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Cheung, Jackie K. Wisniewski, Jessica A. Adams, Vicki M. Quinsey, Noelene S. Rood, Julian I. |
| Description | Country affiliation: Australia Author Affiliation: Cheung JK ( Infection and Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia.); Wisniewski JA ( Infection and Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia.); Adams VM ( Infection and Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia.); Quinsey NS ( Protein Production Unit, Monash University, Clayton, Victoria 3800, Australia.); Rood JI ( Infection and Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia. Electronic address: julian.rood@monash.edu.) |
| Abstract | Clostridium perfringens is a Gram-positive, anaerobic, spore-forming bacterium that causes human gas gangrene (clostridial myonecrosis) and food poisoning. Early studies showed that virulence was regulated by the VirSR two-component signal transduction system. However, our identification of the RevR orphan response regulator indicated that more than one system was involved in controlling virulence. To further characterize this virulence-associated regulator, gel mobility shift experiments, coupled with DNase I footprinting, were used to identify the RevR DNA binding sequence. Bioinformatics analysis suggested that an orphan sensor histidine kinase, CPE1757 (renamed RevS), was the cognate sensor of RevR. Interaction between RevS and RevR was demonstrated by use of a bacterial two-hybrid system and validated by protein-protein interaction studies using biolayer interferometry. To assess the involvement of RevS in virulence regulation, the revS gene was inactivated by Targetron insertion. When isogenic wild-type, revS and complemented revS strains were tested in a mouse myonecrosis model, the revS mutant was found to be attenuated in virulence, which was similar to the attenuation observed previously with the revR mutant. However, transcriptional analysis of selected RevR-regulated genes in the revS mutant revealed a different pattern of expression to a revR mutant, suggesting that the RevSR system is more complex than originally thought. Taken together, the results have led to the identification and characterization of the two essential parts of a new regulatory network that is involved in the regulation of virulence in C. perfringens. |
| File Format | HTM / HTML |
| ISSN | 14384221 |
| Issue Number | 6 |
| Journal | International Journal of Medical Microbiology |
| Volume Number | 306 |
| e-ISSN | 16180607 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2016-09-01 |
| Publisher Place | Germany |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Microbiology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Infectious Diseases Microbiology Microbiology (medical) |
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