Figure 1

Comparison of porin regulation by OmpR and CRP in E. coli and Y. pestis. The OmpR-mediated reciprocal regulation of OmpF and OmpC in E. coli was discussed in the text [2, 7, 8]. In addition, CRP controlled the production of porins indirectly through its direct regulation of OmpR/EnvZ in E. coli [8, 15]. As shown in this study, Y. pestis employs a distinct mechanism indicating that CRP has no regulatory effect on the ompR-envZ operon, although it stimulates ompC and ompF directly, while repressing ompX at the same time. It is likely that OmpR and CRP respectively sense different signals, medium osmolarity, and cellular cAMP levels to regulate porin genes independently. As shown previously [12], Y. pestis OmpR simulates ompC, F, X, and R directly by occupying the target promoter regions. Notably, all of ompF, C, X, and R give a persistent and dramatic up-regulation with the increasing medium osmolarity in Y. pestis, which is dependent of OmpR. Upon the shifting of medium osmolarity, porin expression in Y. pestis is contrary to the reciprocal regulation of OmpF and OmpC in E. coli. The F1-F2-F3 and C1-C2-C3 sites are detected for ompF and ompC of Y. pestis, respectively. Remarkably, the F4 site is absent from the upstream region of ompF, which probably destroys the OmpR-mediated blocking mechanism of ompF at high osmolarity. In E. coli, CRP acts as both repressor and activator for its own gene [28, 29]. However, no transcriptional regulatory association between CRP and its own gene was detected in Y. pestis.