Author Correction: A shape-shifting redox foldase contributes to Proteus mirabilis copper resistance.
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ABSTRACT:
SUBMITTER: Furlong EJ
PROVIDER: S-EPMC6397206 | biostudies-literature | 2019 Mar
REPOSITORIES: biostudies-literature
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Author Correction: A shape-shifting redox foldase contributes to Proteus mirabilis copper resistance.
Furlong Emily J EJ Lo Alvin W AW Kurth Fabian F Premkumar Lakshmanane L Totsika Makrina M Achard Maud E S MES Halili Maria A MA Heras Begoña B Whitten Andrew E AE Choudhury Hassanul G HG Schembri Mark A MA Martin Jennifer L JL
Nature communications 20190301 1
This Article contains errors in Fig. 1, Table 1 and the Methods section. In panel c, the labels for PmScsC and EcDsbC in the upper two curves are interchanged. In Table 1 and the Methods section entitled 'Extended structure', the space group of the extended PmScsC structure is incorrectly referred to as H3<sub>2</sub> and should read H32. Correct versions of Fig. 1 and Table 1 are presented below; the errors have not been corrected in the Article. ...[more]
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Project description:This series of microarrays compares gene expression by the bacterial pathogen Proteus mirabilis when the transcriptional regulator mrpJ is deleted or induced to levels found during experimental urinary tract infection. The enteric bacterium Proteus mirabilis is associated with a significant number of catheter-associated urinary tract infections. Strict regulation of the antagonistic processes of adhesion and motility, mediated by fimbriae and flagella, respectively, is essential for successful disease progression. Previously, the transcriptional regulator MrpJ, which is encoded by the mrp fimbrial operon, has been shown to repress both swimming and swarming motility. Here we show that MrpJ affects a wide array of cellular processes beyond adherence and motility. Microarray analysis found that expression of mrpJ mimicking expression levels that occur during UTI leads to differential expression of 217 genes related to, among others, bacterial virulence, type VI secretion and metabolism. We probed the molecular mechanism of transcriptional regulation through MrpJ using reporter assays and chromatin immunoprecipitation (ChIP). Two virulence-associated target genes, the flagellar master regulator flhDC and mrp itself, appear to be regulated through a binding site proximal to the transcriptional start, complemented by a more distantly situated enhancer site. Furthermore, an mrpJ deletion mutant colonized the bladders of mice at significantly lower levels in a transurethral model of infection. Additionally, we observe that mrpJ is widely conserved in a collection of recent clinical isolates, leading us to conclude that our results elucidate an unanticipated role of MrpJ as a global regulator of P. mirabilis virulence.
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Project description:This SuperSeries is composed of the SubSeries listed below.
2010-06-07 | GSE17957 | GEO
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