RESUMO
A virulence plasmid of Rhodococcus equi harbors the vap mutigene family. Here it is shown that transcription of vap gene family members other than vapA (vapD, vapE and vapG) is regulated by temperature and pH and abolished when either virS or virR is deleted. Expression of VirS in the absence of functional VirR was found to increase the transcription of vap genes to the amount expressed in the presence of VirR. These findings suggest that transcription of vap genes is regulated by VirS and that VirR is involved in the mechanism of transcriptional responses to temperature and pH.
Assuntos
Regulação Bacteriana da Expressão Gênica , Genes Reguladores , Família Multigênica , Rhodococcus equi/genética , Ativação Transcricional/efeitos dos fármacos , Ativação Transcricional/efeitos da radiação , Fatores de Virulência/biossíntese , Concentração de Íons de Hidrogênio , Plasmídeos , Rhodococcus equi/efeitos dos fármacos , Rhodococcus equi/efeitos da radiação , Temperatura , Transcrição Gênica , VirulênciaRESUMO
BACKGROUND: Rhodococcus equi is an important pulmonary pathogen in foals and in immunocompromised individuals. Virulent R. equi strains carry an 80-90 kb virulence plasmid that expresses the virulence-associated protein A (VapA). VapA expression is regulated by temperature and pH. The LysR-type transcriptional regulator, VirR, is involved in the regulation of the vapA gene. To examine the mechanism underlying transcriptional regulation of vapA, we characterized an R. equi mutant in which another putative transcriptional regulator encoded on the virulence plasmid, VirS, was deleted. RESULTS: Deletion of virS reduced vapA promoter activity to non-inducible levels. Complementary expression of VirS in the virS deletion mutant restored transcription at the PvapA promoter, even under non-inducing conditions (30°C and pH 8.0). In addition, VirS expression increased PvapA promoter activity in the absence of functional VirR. Further, transcription of the icgA operon containing virS was regulated by pH and temperature in the same manner as vapA. CONCLUSIONS: This study suggests that VirS is required for VapA expression and that regulation of PvapA-promoter activity may be achieved by controlling VirS expression levels.