Surprisingly, expression of Lkt was found to be elevated in MhΔNarP7 regardless of the presence or absence of additional NaNO3. This suggests that NarP functions, either directly or indirectly, to repress expression of Lkt. In the parent strain, the presence of NaNO3 relieved this repression and higher expression of Lkt can be achieved. Because the lkt promoter does not contain any NarP-binding sequences, it is likely that the repression of the lkt promoter acts through an intermediate molecule. The initial analysis of protein expression in MhΔNarP7 revealed some unexpected observations
regarding regulation of FbpA and Lkt. Our results suggest the role of NarQ/P TCS in regulating genes that may be important for the pathogenesis of this Gefitinib cost microorganism. Analysis of the expression profile of this system with has been initiated with a proteomic approach using 2D gel electrophoresis, and preliminary data have shown a number of protein levels with significant alterations in response to NaNO3. Further research will shed light on the panel of protein expression regulated by NarP in M. haemolytica A1 as well as in other microorganisms.
This work is funded by a grant from the Natural Science and Engineering Research Tacrolimus research buy Council of Canada. We thank Drs Dyanne Brewer and Armen Charcholyan for their assistance with the MS MALDI-TOF analysis. Fig. S1. (a) Clostridium perfringens alpha toxin Alignment of NarQ proteins. (b) Alignment of NarP proteins. Appendix S1. Construction of narP knock-out mutant. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Streptococcus suis serotype 2 (SS2) is an important zoonotic pathogen that infects pigs and sporadically
causes serious infections in humans. Two recent large-scale outbreaks of human streptococcal toxic-shock-like syndrome with high mortality occurred in China, posing new challenges for global public health. However, the global regulation of the virulence of epidemic SS2 isolates lacks a systematic understanding. In this study, we performed a mutational and functional analysis of an SS2 two-component system that is orthologous to the VirR/VirS regulatory system of Clostridium perfringens. An isogenic knockout mutant of VirR/VirS (ΔvirRS) was found to exhibit marked phenotypic changes, including the formation of shorter chains and thinner capsular walls, more easily cleared in whole blood, and decreased oxidative stress tolerance. Furthermore, the ΔvirRS mutant was greatly attenuated in a mouse model.