English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

In  Klebsiella pneumoniae , we have previously shown that IscR, an Fe–S cluster-containing transcriptional factor, plays a dual role in controlling capsular polysaccharide biosynthesis and iron-acquisition systems by switching between its holo and apo forms. In this study, the effect of IscR on type 3 fimbriae expression and biofilm formation was investigated. We found that production of the major subunit of type 3 fimbriae, MrkA, was increased in the Δ iscR  and  iscR  3CA  strains, a strain expressing a mutant IscR that mimics apo-IscR, at both the translational and transcriptional levels. Based on the fact that type 3 fimbriae expression is the major factor affecting biofilm formation, increased biofilm formation was also found in Δ iscR  or  iscR  3CA , suggesting that holo-IscR represses biofilm formation. However, the repression of type 3 fimbriae expression by IscR is indirect. To further understand the regulatory mechanism of IscR, the effect of IscR on the expression of  mrkHIJ , which encodes cyclic di-GMP (c-di-GMP)-related regulatory proteins that control type 3 fimbriae expression, was studied. We found that holo-IscR could directly repress  mrkHI  transcription, indicating that MrkHI is required for IscR regulation of type 3 fimbriae expression. Finally, deletion of  iscR  attenuated  K. pneumoniae  virulence in a peritonitis model of mouse infection, while the absence of the [2Fe–2S] cluster of IscR had no effect on  K. pneumoniae  virulence during infection. Taken together, our results demonstrate the underlying mechanism of the [2Fe–2S] cluster of IscR in controlling type 3 fimbriae expression and its effect on  K. pneumoniae  pathogenesis.

IscR Regulation of Type 3 Fimbriae Expression in Klebsiella pneumoniae CG43