Kakuda Tsutomu, Hirota Takuya, Takeuchi Tatsuya, Hagiuda Hirofumi, Miyazaki Shiko, Takai Shinji
Laboratory of Animal Hygiene, School of Veterinary Medicine, Kitasato University, Higashi 23-35-1, Towada 034-8628, Aomori, Japan.
BMC Microbiol. 2014 Oct 3;14:243. doi: 10.1186/s12866-014-0243-1.
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.
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.
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.
马红球菌是幼驹和免疫功能低下个体重要的肺部病原体。有毒力的马红球菌菌株携带一个80 - 90 kb的毒力质粒,该质粒表达与毒力相关的蛋白A(VapA)。VapA的表达受温度和pH值调控。LysR型转录调节因子VirR参与vapA基因的调控。为了研究vapA转录调控的潜在机制,我们对一个马红球菌突变体进行了表征,该突变体缺失了毒力质粒上编码的另一个假定转录调节因子VirS。
VirS的缺失将vapA启动子活性降低到不可诱导水平。即使在非诱导条件下(30°C和pH 8.0),在virS缺失突变体中互补表达VirS也能恢复PvapA启动子处的转录。此外,在没有功能性VirR的情况下,VirS的表达增加了PvapA启动子活性。此外,包含virS的icgA操纵子的转录受pH值和温度的调控方式与vapA相同。
本研究表明VirS是VapA表达所必需的,并且通过控制VirS的表达水平可能实现对PvapA启动子活性的调控。