The two-component response regulator RcsB regulates type 1 piliation in Escherichia coli.
ABSTRACT The ability of Escherichia coli cells to produce type 1 pili depends upon the orientation of the fimA promoter. The orientation depends upon the ratios of the FimB and FimE recombinases. Here, we report that the two-component response regulator RcsB influences the piliation state by controlling fimB and fimE transcription.
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ABSTRACT: Proteus mirabilis is a common human pathogen causing recurrent or persistent urinary tract infections (UTIs). The underlying mechanisms for P. mirabilis to establish UTIs are not fully elucidated. In this study, we showed that loss of the sigma factor E (RpoE), mediating extracytoplasmic stress responses, decreased fimbria expression, survival in macrophages, cell invasion and colonization in mice but increased IL-8 expression of urothelial cells and swarming motility. This is the first study to demonstrate that RpoE modulated expression of MR/P fimbriae by regulating mrpI, a gene encoding a recombinase controlling the orientation of MR/P fimbria promoter. By real-time RT-PCR, we found the IL-8 mRNA amount of urothelial cells was induced significantly by lipopolysaccharides extracted from rpoE mutant but not the wild-type. These RpoE-associated virulence factors should be coordinately expressed to enhance the fitness of P. mirabilis in the host including avoidance of immune attacks. Accordingly, rpoE mutant-infected mice displayed more immune cell infiltration in bladders and kidneys during early stages of infection and rpoE mutant had a dramatically impaired ability of colonization. Moreover, it is noteworthy that urea (the major component in urine) and polymyxin B (a cationic antimicrobial peptide) can induce expression of rpoE by the reporter assay, suggesting that RpoE might be activated in the urinary tract. Altogether, our results indicate that RpoE is important in sensing environmental cues of the urinary tract and subsequently triggering expression of virulence factors, associated with the fitness of P. mirabilis, to build up a UTI. Copyright © 2014, American Society for Microbiology. All Rights Reserved.Infection and Immunity 12/2014; DOI:10.1128/IAI.02232-14 · 4.16 Impact Factor
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ABSTRACT: The phase variation (reversible on-off switching) of the type 1 fimbrial adhesin of E.coli involves a DNA inversion catalyzed by FimB (switching in either direction) or FimE (on-to-off switching). Here we demonstrate that RfaH activates expression of a FimB-LacZ protein fusion, while having a modest inhibitory effect on a comparable fimB-lacZ operon construct and on a FimE-LacZ protein fusion, indicating that RfaH selectively controls fimB expression at the post-transcriptional level. Further work demonstrates that loss of RfaH enables sRNA MicA inhibition of fimB expression even in the absence of exogenious inducing stress. This effect is explained by induction of σ(E), and hence MicA, in the absence of RfaH. Additional work confirms that the procaine-dependent induction of micA requires OmpR as reported previously (Coornaert, A., A. Lu, P. Mandin, M. Springer, S. Gottesman and M. Guillier. Mol. Microbiol. 76:467-479, 2010), but also demonstrates that RfaH inhibition of fimB transcription is enhanced by procaine independently of OmpR. While the effect of procaine on fimB transcription is shown to be independent of RcsB, it was found to require SlyA, another known regulator of fimB transcription. These results demonstrate a complex role for RfaH as a regulator of fimB expression.Journal of bacteriology 10/2013; 196(1). DOI:10.1128/JB.00912-13 · 2.69 Impact Factor
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ABSTRACT: Edwardsiella tarda, a Gram-negative bacterium of the family Enterobacteriaceae, is the causative agent of the systemic disease edwardsiellosis, which is a major problem in aquaculture industry worldwide. Many virulence-related genes in E. tarda have been investigated, but the Rcs phosphorelay, a two-component pathway, which regulates several cell-surface-associated structures related to invasion and survival in host cells, has not yet been thoroughly studied. In the present study, an rcsB in-frame deletion mutant ΔrcsB was constructed through double-crossover allelic exchange. To complement the rcsB mutation, the ΔrcsB (pACYC184K-rcsB) mutant was constructed by transformation of a low-copy plasmid carrying the intact rcsB into the ΔrcsB mutant of E. tarda. Several virulence-associated characters of the mutants and wild-type strain were tested. Compared with wild-type strain EIB202, biofilm formation decreased significantly in ΔrcsB, while ΔrcsB (pACYC184K-rcsB) recovered the phenotype to some extent. In addition, the capacity for autoagglutination, the percentage of adherence and internalization to Epithelioma papulosum cyprini cells and lethality toward zebrafish embryos significantly increased in ΔrcsB. All these phenomena displayed by mutant ΔrcsB showed a certain degree of recovery, though incomplete, in strain ΔrcsB (pACYC184K-rcsB). Present results indicate that rcsB is involved in regulating the gene expression of virulence factors in E. tarda, as shown in other members of Enterobacteriaceae.Research in Microbiology 04/2014; DOI:10.1016/j.resmic.2014.02.006 · 2.83 Impact Factor