Data presented herein, as well as those described previously [12], disclose a regulatory circuit involving CRP-cAMP, EnvZ/OmpR, and a set of porins in Y. pestis (Figure 1). Noticeable remodeling was observed when this regulatory circuit was compared to the counterpart in E. coli (Figure 1). The Y. pestis CRP-cAMP or EnvZ/OmpR has shown a very high homology to the orthologous one in E.

coli (data not shown), and CRP [16] or OmpR [12] from these two bacteria share an identical consensus sequence, indicating that conserved signals recognized by CRP or OmpR are shared by these bacteria. However, the promoter regions of crp and ompR, C, F, and X have undergone genetic variations between E. coli and Y. pestis, thereby promoting selleck chemical relevant target genes to split from or integrate into the CRP or OmpR regulon of Y. pestis relative to that of E. coli. The complex regulatory circuit of porins may contribute Cell Cycle inhibitor to bacterial adaptation to the hosts. Conclusion Y. pestis CRP-cAMP has no regulatory effect on the ompR-envZ operon, although it stimulates ompC and ompF directly, while repressesing ompX at the same time. This is different from the fact that CRP-cAMP regulates ompR-envZ directly in E. coli and further controls the porin production indirectly through its direct action on ompR-envZ. No transcriptional regulatory association between

CRP and its own Idoxuridine gene can be detected in Y. pestis, which is also in contrast to the observation that CRP acts as both repressor and activator for its own gene in E. coli. Acknowledgements Financial support for this work came from the National Natural Science Foundation of China (30930001, 30900823, and 30771179) and the 973 Program (2009CB522600). The English writing of the manuscript was polished by EnPapers. Electronic supplementary material Additional file 1: Oligonucleotide primers used in this study. (DOC 52 KB) Additional file 2: Promoter activity of ompF within WT, Δcrp and C-crp. (DOC 282 KB) References 1. Kawaji H, Mizuno T, Mizushima S: Influence

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