Limits...
Regulatory effects of cAMP receptor protein (CRP) on porin genes and its own gene in Yersinia pestis.

Gao H, Zhang Y, Yang L, Liu X, Guo Z, Tan Y, Han Y, Huang X, Zhou D, Yang R - BMC Microbiol. (2011)

Bottom Line: Y. pestis employs a distinct mechanism indicating that CRP has no regulatory effect on the ompR-envZ operon; however, it stimulates ompC and ompF directly, while repressing ompX.Although the CRP of Y. pestis shows a very high homology to that of E. coli, and the consensus DNA sequence recognized by CRP is shared by the two bacteria, the Y. pestis CRP can recognize the promoters of ompC, F, and X directly rather than that of its own gene, which is different from the relevant regulatory circuit of E. coli.Data presented here indicate a remarkable remodeling of the CRP-mediated regulation of porin genes and of its own one between these two bacteria.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, PR China.

ABSTRACT

Background: The cAMP receptor protein (CRP) is a global bacterial regulator that controls many target genes. The CRP-cAMP complex regulates the ompR-envZ operon in E. coli directly, involving both positive and negative regulations of multiple target promoters; further, it controls the production of porins indirectly through its direct action on ompR-envZ. Auto-regulation of CRP has also been established in E. coli. However, the regulation of porin genes and its own gene by CRP remains unclear in Y. pestis.

Results: Y. pestis employs a distinct mechanism indicating that CRP has no regulatory effect on the ompR-envZ operon; however, it stimulates ompC and ompF directly, while repressing ompX. No transcriptional regulatory association between CRP and its own gene can be detected in Y. pestis, which is also in contrast to the fact that CRP acts as both repressor and activator for its own gene in E. coli. It is likely that Y. pestis OmpR and CRP respectively sense different signals (medium osmolarity, and cellular cAMP levels) to regulate porin genes independently.

Conclusion: Although the CRP of Y. pestis shows a very high homology to that of E. coli, and the consensus DNA sequence recognized by CRP is shared by the two bacteria, the Y. pestis CRP can recognize the promoters of ompC, F, and X directly rather than that of its own gene, which is different from the relevant regulatory circuit of E. coli. Data presented here indicate a remarkable remodeling of the CRP-mediated regulation of porin genes and of its own one between these two bacteria.

Show MeSH
Promoter structure for ompC, F, X and R. The start codon (ATG) of each gene is shown at the 3' terminus. The nucleotide number corresponding to the transcription start site was taken as "+1", from which the promoter -10 and-35 elements were predicted accordingly. Data of OmpR-promoter DNA association came from the previous data [12].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3050693&req=5

Figure 5: Promoter structure for ompC, F, X and R. The start codon (ATG) of each gene is shown at the 3' terminus. The nucleotide number corresponding to the transcription start site was taken as "+1", from which the promoter -10 and-35 elements were predicted accordingly. Data of OmpR-promoter DNA association came from the previous data [12].

Mentions: The footprint regions determined by DNase I footprinting were considered as the binding sites of relevant regulators. The primer extension product could be used to map the 5' terminus of RNA transcript of each gene tested, allowing for the determination of transcriptional start sites and localization of the core promoter region (-10 and -35 elements). Considering the data here and those described previously [12], we depicted OmpR- or CRP-binding sites, transcriptional start sites, and -10/-35 elements within the promoter-proximal regions of ompC, F, X and R (Figure 5), resulting in a map of regulator-promoter DNA association for mediating transcriptional regulation. Since we failed to detect the 5' terminus of the RNA transcript for ompC using primer extension assay, a transcriptional start site was predicted for this gene with the NNPP tool http://searchlauncher.bcm.tmc.edu/seq-search/gene-search.html. The results showed that a single distinct promoter was transcribed for all the four genes, and the detecting promoters for ompC, F, and X were dependent on both OmpR and CRP, while that of ompR was regulated by its own protein product but not by CRP. A single distinct OmpR- or CRP-binding site was respectively detected in ompC, F, and X, all of which were upstream of the promoter -35 elements. The detecting OmpR- and CRP-binding sites contained the corresponding consensus-like sequences as predicted by computational promoter analysis.


Regulatory effects of cAMP receptor protein (CRP) on porin genes and its own gene in Yersinia pestis.

Gao H, Zhang Y, Yang L, Liu X, Guo Z, Tan Y, Han Y, Huang X, Zhou D, Yang R - BMC Microbiol. (2011)

Promoter structure for ompC, F, X and R. The start codon (ATG) of each gene is shown at the 3' terminus. The nucleotide number corresponding to the transcription start site was taken as "+1", from which the promoter -10 and-35 elements were predicted accordingly. Data of OmpR-promoter DNA association came from the previous data [12].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3050693&req=5

Figure 5: Promoter structure for ompC, F, X and R. The start codon (ATG) of each gene is shown at the 3' terminus. The nucleotide number corresponding to the transcription start site was taken as "+1", from which the promoter -10 and-35 elements were predicted accordingly. Data of OmpR-promoter DNA association came from the previous data [12].
Mentions: The footprint regions determined by DNase I footprinting were considered as the binding sites of relevant regulators. The primer extension product could be used to map the 5' terminus of RNA transcript of each gene tested, allowing for the determination of transcriptional start sites and localization of the core promoter region (-10 and -35 elements). Considering the data here and those described previously [12], we depicted OmpR- or CRP-binding sites, transcriptional start sites, and -10/-35 elements within the promoter-proximal regions of ompC, F, X and R (Figure 5), resulting in a map of regulator-promoter DNA association for mediating transcriptional regulation. Since we failed to detect the 5' terminus of the RNA transcript for ompC using primer extension assay, a transcriptional start site was predicted for this gene with the NNPP tool http://searchlauncher.bcm.tmc.edu/seq-search/gene-search.html. The results showed that a single distinct promoter was transcribed for all the four genes, and the detecting promoters for ompC, F, and X were dependent on both OmpR and CRP, while that of ompR was regulated by its own protein product but not by CRP. A single distinct OmpR- or CRP-binding site was respectively detected in ompC, F, and X, all of which were upstream of the promoter -35 elements. The detecting OmpR- and CRP-binding sites contained the corresponding consensus-like sequences as predicted by computational promoter analysis.

Bottom Line: Y. pestis employs a distinct mechanism indicating that CRP has no regulatory effect on the ompR-envZ operon; however, it stimulates ompC and ompF directly, while repressing ompX.Although the CRP of Y. pestis shows a very high homology to that of E. coli, and the consensus DNA sequence recognized by CRP is shared by the two bacteria, the Y. pestis CRP can recognize the promoters of ompC, F, and X directly rather than that of its own gene, which is different from the relevant regulatory circuit of E. coli.Data presented here indicate a remarkable remodeling of the CRP-mediated regulation of porin genes and of its own one between these two bacteria.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, PR China.

ABSTRACT

Background: The cAMP receptor protein (CRP) is a global bacterial regulator that controls many target genes. The CRP-cAMP complex regulates the ompR-envZ operon in E. coli directly, involving both positive and negative regulations of multiple target promoters; further, it controls the production of porins indirectly through its direct action on ompR-envZ. Auto-regulation of CRP has also been established in E. coli. However, the regulation of porin genes and its own gene by CRP remains unclear in Y. pestis.

Results: Y. pestis employs a distinct mechanism indicating that CRP has no regulatory effect on the ompR-envZ operon; however, it stimulates ompC and ompF directly, while repressing ompX. No transcriptional regulatory association between CRP and its own gene can be detected in Y. pestis, which is also in contrast to the fact that CRP acts as both repressor and activator for its own gene in E. coli. It is likely that Y. pestis OmpR and CRP respectively sense different signals (medium osmolarity, and cellular cAMP levels) to regulate porin genes independently.

Conclusion: Although the CRP of Y. pestis shows a very high homology to that of E. coli, and the consensus DNA sequence recognized by CRP is shared by the two bacteria, the Y. pestis CRP can recognize the promoters of ompC, F, and X directly rather than that of its own gene, which is different from the relevant regulatory circuit of E. coli. Data presented here indicate a remarkable remodeling of the CRP-mediated regulation of porin genes and of its own one between these two bacteria.

Show MeSH