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Intrinsic plasmids influence MicF-mediated translational repression of ompF in Yersinia pestis.

Liu Z, Wang H, Wang H, Wang J, Bi Y, Wang X, Yang R, Han Y - Front Microbiol (2015)

Bottom Line: Unexpectedly, upon MicF overexpression, the slightly upregulated expression of OmpF were found in the wild-type strain, which contradicted the previously established model.Further examination showed that plasmid pPCP1 is likely the main contributor to the abolishment of MicF-mediated translational repression of endogenous or plasmid-borne ompF.It represents that the possible roles of intrinsic plasmids should be considered upon investigating sRNA-mediated gene regulation, at least in Y. pestis, even if the exact mechanism is not fully understood.

View Article: PubMed Central - PubMed

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

ABSTRACT
Yersinia pestis, which is the causative agent of plague, has acquired exceptional pathogenicity potential during its evolution from Y. pseudotuberculosis. Two laterally acquired plasmids, namely, pMT1 and pPCP1, are specific to Y. pestis and are critical for pathogenesis and flea transmission. Small regulatory RNAs (sRNAs) commonly function as regulators of gene expression in bacteria. MicF, is a paradigmatic sRNA that acts as a post-transcriptional repressor through imperfect base pairing with the 5'-UTR of its target mRNA, ompF, in Escherichia coli. The high sequence conservation and minor variation in the RNA duplex of MicF-ompF has been reported in Yersinia. In this study, we utilized super-folder GFP reporter gene fusion to validate the post-transcriptional MicF-mediated regulation of target mRNA ompF in Y. pestis. Unexpectedly, upon MicF overexpression, the slightly upregulated expression of OmpF were found in the wild-type strain, which contradicted the previously established model. Interestingly, the translational repression of ompF target fusions was restored in the intrinsic plasmids-cured Y. pestis strain, suggesting intrinsic plasmids influence the MicF-mediated translational repression of ompF in Y. pestis. Further examination showed that plasmid pPCP1 is likely the main contributor to the abolishment of MicF-mediated translational repression of endogenous or plasmid-borne ompF. It represents that the possible roles of intrinsic plasmids should be considered upon investigating sRNA-mediated gene regulation, at least in Y. pestis, even if the exact mechanism is not fully understood.

No MeSH data available.


Related in: MedlinePlus

Detection of MicF expression in various strains of Y. pestis. MicF expression detected by Northern Blot, in which 5S rRNA images from each tested strain were provided as control.
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Figure 3: Detection of MicF expression in various strains of Y. pestis. MicF expression detected by Northern Blot, in which 5S rRNA images from each tested strain were provided as control.

Mentions: We also monitored MicF in the different bacterial strains under the same conditions as those shown in Figures 1, 2. No MicF were found expressed in the pBAD control of various Y. pestis strains by using Northern Blot, which might be mainly due to huge disparity in copy number of MicF between plasmid pBAD and chromosome and/or low expression levels of endogeneous MicF under our experimental conditions. Additionally, no significant differences in MicF overexpression were found among Y. pestis strains (Figure 3).


Intrinsic plasmids influence MicF-mediated translational repression of ompF in Yersinia pestis.

Liu Z, Wang H, Wang H, Wang J, Bi Y, Wang X, Yang R, Han Y - Front Microbiol (2015)

Detection of MicF expression in various strains of Y. pestis. MicF expression detected by Northern Blot, in which 5S rRNA images from each tested strain were provided as control.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4543863&req=5

Figure 3: Detection of MicF expression in various strains of Y. pestis. MicF expression detected by Northern Blot, in which 5S rRNA images from each tested strain were provided as control.
Mentions: We also monitored MicF in the different bacterial strains under the same conditions as those shown in Figures 1, 2. No MicF were found expressed in the pBAD control of various Y. pestis strains by using Northern Blot, which might be mainly due to huge disparity in copy number of MicF between plasmid pBAD and chromosome and/or low expression levels of endogeneous MicF under our experimental conditions. Additionally, no significant differences in MicF overexpression were found among Y. pestis strains (Figure 3).

Bottom Line: Unexpectedly, upon MicF overexpression, the slightly upregulated expression of OmpF were found in the wild-type strain, which contradicted the previously established model.Further examination showed that plasmid pPCP1 is likely the main contributor to the abolishment of MicF-mediated translational repression of endogenous or plasmid-borne ompF.It represents that the possible roles of intrinsic plasmids should be considered upon investigating sRNA-mediated gene regulation, at least in Y. pestis, even if the exact mechanism is not fully understood.

View Article: PubMed Central - PubMed

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

ABSTRACT
Yersinia pestis, which is the causative agent of plague, has acquired exceptional pathogenicity potential during its evolution from Y. pseudotuberculosis. Two laterally acquired plasmids, namely, pMT1 and pPCP1, are specific to Y. pestis and are critical for pathogenesis and flea transmission. Small regulatory RNAs (sRNAs) commonly function as regulators of gene expression in bacteria. MicF, is a paradigmatic sRNA that acts as a post-transcriptional repressor through imperfect base pairing with the 5'-UTR of its target mRNA, ompF, in Escherichia coli. The high sequence conservation and minor variation in the RNA duplex of MicF-ompF has been reported in Yersinia. In this study, we utilized super-folder GFP reporter gene fusion to validate the post-transcriptional MicF-mediated regulation of target mRNA ompF in Y. pestis. Unexpectedly, upon MicF overexpression, the slightly upregulated expression of OmpF were found in the wild-type strain, which contradicted the previously established model. Interestingly, the translational repression of ompF target fusions was restored in the intrinsic plasmids-cured Y. pestis strain, suggesting intrinsic plasmids influence the MicF-mediated translational repression of ompF in Y. pestis. Further examination showed that plasmid pPCP1 is likely the main contributor to the abolishment of MicF-mediated translational repression of endogenous or plasmid-borne ompF. It represents that the possible roles of intrinsic plasmids should be considered upon investigating sRNA-mediated gene regulation, at least in Y. pestis, even if the exact mechanism is not fully understood.

No MeSH data available.


Related in: MedlinePlus