ABSTRACT
Staphylococcus utilizes vancomycin-resistance associated sensor/regulator ( VraSR) , a two-component signal transduction system ( TCS) , to sense and respond to cell wall damage and to adapt to environmental changes through regulating transcriptions of downstream genes. It has been indicated that VraSR can regulate the transcription of a series of genes involved in the synthesis of peptidoglycan, drug re-sistance, and virulence in Staphylococcus aureus ( S. aureus) . A similar two-component system, VraSR, is also present in Staphylococcus epidermidis ( S. epidermidis ) , sharing a high homology with the VraSR of S. aureus. Little is known about the functions of VraSR in S. epidermidis and it is not yet clear what the simi-larities and differences in resistance and pathogenicity are. Based on the previous work of our group, a brief review on the regulation mechanism of staphylococcal VraSR was performed.
ABSTRACT
Vibrio vulnificus is an estuarine bacterium that opportunistically infects humans with underlying hepatic diseases, heavy alcohol drinking habits, and other immunocompromised conditions. A locus in the V. vulnificus genome was cloned and sequenced, which showed similarities to the bacterial two-component signal transduction system. The locus encoded a putative sensor kinase, designated vvgS, and a divergently transcribed putative response regulator, designated vvgR. VvgS was predicted to be a protein belonging to the tripartite hybrid sensor kinase subfamily such as ArcB and BvgS. VvgR showed similarities to well known response regulators. An insertional mutation of vvgS in a V. vulnificus strain led to a remarkable decrease of cytotoxicity to HeLa cells, while the production of exotoxins, the hemolysin and the protease, slightly increased by the vvgS mutation. Adhesion to HeLa cells only slightly decreased. However, the vvgS mutation had no effect on the motility of V. vulnificus. The vvgS mutation resulted in a significant decrease of lethality to mice. These results indicate that vvgRS two-component system plays a very important role in regulating novel virulence factor(s) of V. vulnificus associated with cytotoxicity other than hemolysin and protease during the infection process.
Subject(s)
Animals , Humans , Mice , Alcohol Drinking , Clone Cells , Exotoxins , Genome , HeLa Cells , Phosphotransferases , Signal Transduction , Vibrio vulnificus , Vibrio , VirulenceABSTRACT
Vibrio vulnificus is an estuarine bacterium that opportunistically infects humans with underlying hepatic diseases, heavy alcohol drinking habits, and other immunocompromised conditions. A locus in the V. vulnificus genome was cloned and sequenced, which showed similarities to the bacterial two-component signal transduction system. The locus encoded a putative sensor kinase, designated vvgS, and a divergently transcribed putative response regulator, designated vvgR. VvgS was predicted to be a protein belonging to the tripartite hybrid sensor kinase subfamily such as ArcB and BvgS. VvgR showed similarities to well known response regulators. An insertional mutation of vvgS in a V. vulnificus strain led to a remarkable decrease of cytotoxicity to HeLa cells, while the production of exotoxins, the hemolysin and the protease, slightly increased by the vvgS mutation. Adhesion to HeLa cells only slightly decreased. However, the vvgS mutation had no effect on the motility of V. vulnificus. The vvgS mutation resulted in a significant decrease of lethality to mice. These results indicate that vvgRS two-component system plays a very important role in regulating novel virulence factor(s) of V. vulnificus associated with cytotoxicity other than hemolysin and protease during the infection process.
Subject(s)
Animals , Humans , Mice , Alcohol Drinking , Clone Cells , Exotoxins , Genome , HeLa Cells , Phosphotransferases , Signal Transduction , Vibrio vulnificus , Vibrio , VirulenceABSTRACT
To construct gene knock-out mutant of a two-component signal transduction system named 2148hk/rr in Streptococcus suis type 2 virulent strain 05ZYH33.Recombinant gene knock-out vector was constructed consisting of Spc~r cassette with flanking homology regions to the target genes,the isogenic 2148hk/rr-deficient mutant was screened by allelic replacement.PCR analysis and Southern hybridization confirmed that the coding genes of 2148hk/rr were replaced completely by spc~r cassette.Conclusion The mutant of 05ZYH33 2148hk/rr system was successfully constructed,which laid the foundation for farther research on the role of this two-component signal transduction system during infection.