PchE Regulation of <i>Escherichia coli</i> O157:H7 Flagella, Controlling the Transition to Host Cell Attachment

Shiga toxins and intimate adhesion controlled by the locus of enterocyte effacement are major enterohemorrhagic <i>Escherichia coli</i> (EHEC) virulence factors. Curli fimbriae also contribute to cell adhesion and are essential biofilm components. The transcriptional regulator PchE repre...

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Main Authors: Elisa Andreozzi, Gaylen A. Uhlich
Format: Article
Language:English
Published: MDPI AG 2020-06-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/21/13/4592
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author Elisa Andreozzi
Gaylen A. Uhlich
author_facet Elisa Andreozzi
Gaylen A. Uhlich
author_sort Elisa Andreozzi
collection DOAJ
description Shiga toxins and intimate adhesion controlled by the locus of enterocyte effacement are major enterohemorrhagic <i>Escherichia coli</i> (EHEC) virulence factors. Curli fimbriae also contribute to cell adhesion and are essential biofilm components. The transcriptional regulator PchE represses the expression of curli and their adhesion to HEp-2 cells. Past studies indicate that <i>pchE</i> also represses additional adhesins that contribute to HEp-2 cell attachment. In this study, we tested for <i>pchE</i> regulation of several tissue adhesins and their regulators. Three adhesin-encoding genes (<i>eae</i>, <i>lpfA1</i>, <i>fliC</i>) and four master regulators (<i>csgD</i>, <i>stpA</i>, <i>ler</i>, <i>flhDC</i>) were controlled by <i>pchE</i>. <i>pchE</i> over-expression strongly up-regulated <i>fliC</i> but the marked flagella induction reduced the attachment of O157:H7 clinical isolate PA20 to HEp-2 cells, indicating that flagella were blocking cell attachments rather than functioning as an adhesin. Chemotaxis, motor, structural, and regulatory genes in the flagellar operons were all increased by <i>pchE</i> expression, as was PA20 motility. This study identifies new members in the <i>pchE</i> regulon and shows that <i>pchE</i> stimulates flagellar motility while repressing cell adhesion, likely to support EHEC movement to the intestinal surface early in infection. However, induced or inappropriate <i>pchE</i>-dependent flagellar expression could block cell attachments later during disease progression.
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spelling doaj.art-a8fda483c52f4b0b8337a31ac7db96ed2023-11-20T05:11:15ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-06-012113459210.3390/ijms21134592PchE Regulation of <i>Escherichia coli</i> O157:H7 Flagella, Controlling the Transition to Host Cell AttachmentElisa Andreozzi0Gaylen A. Uhlich1Molecular Characterization of Foodborne Pathogens Research Unit, Eastern Regional Research Center, Agricultural Research Service, United States Department of Agriculture, Wyndmoor, PA 19038, USAMolecular Characterization of Foodborne Pathogens Research Unit, Eastern Regional Research Center, Agricultural Research Service, United States Department of Agriculture, Wyndmoor, PA 19038, USAShiga toxins and intimate adhesion controlled by the locus of enterocyte effacement are major enterohemorrhagic <i>Escherichia coli</i> (EHEC) virulence factors. Curli fimbriae also contribute to cell adhesion and are essential biofilm components. The transcriptional regulator PchE represses the expression of curli and their adhesion to HEp-2 cells. Past studies indicate that <i>pchE</i> also represses additional adhesins that contribute to HEp-2 cell attachment. In this study, we tested for <i>pchE</i> regulation of several tissue adhesins and their regulators. Three adhesin-encoding genes (<i>eae</i>, <i>lpfA1</i>, <i>fliC</i>) and four master regulators (<i>csgD</i>, <i>stpA</i>, <i>ler</i>, <i>flhDC</i>) were controlled by <i>pchE</i>. <i>pchE</i> over-expression strongly up-regulated <i>fliC</i> but the marked flagella induction reduced the attachment of O157:H7 clinical isolate PA20 to HEp-2 cells, indicating that flagella were blocking cell attachments rather than functioning as an adhesin. Chemotaxis, motor, structural, and regulatory genes in the flagellar operons were all increased by <i>pchE</i> expression, as was PA20 motility. This study identifies new members in the <i>pchE</i> regulon and shows that <i>pchE</i> stimulates flagellar motility while repressing cell adhesion, likely to support EHEC movement to the intestinal surface early in infection. However, induced or inappropriate <i>pchE</i>-dependent flagellar expression could block cell attachments later during disease progression.https://www.mdpi.com/1422-0067/21/13/4592<i>Escherichia coli</i>O157:H7biofilmcell adhesionmotilityflagella
spellingShingle Elisa Andreozzi
Gaylen A. Uhlich
PchE Regulation of <i>Escherichia coli</i> O157:H7 Flagella, Controlling the Transition to Host Cell Attachment
International Journal of Molecular Sciences
<i>Escherichia coli</i>
O157:H7
biofilm
cell adhesion
motility
flagella
title PchE Regulation of <i>Escherichia coli</i> O157:H7 Flagella, Controlling the Transition to Host Cell Attachment
title_full PchE Regulation of <i>Escherichia coli</i> O157:H7 Flagella, Controlling the Transition to Host Cell Attachment
title_fullStr PchE Regulation of <i>Escherichia coli</i> O157:H7 Flagella, Controlling the Transition to Host Cell Attachment
title_full_unstemmed PchE Regulation of <i>Escherichia coli</i> O157:H7 Flagella, Controlling the Transition to Host Cell Attachment
title_short PchE Regulation of <i>Escherichia coli</i> O157:H7 Flagella, Controlling the Transition to Host Cell Attachment
title_sort pche regulation of i escherichia coli i o157 h7 flagella controlling the transition to host cell attachment
topic <i>Escherichia coli</i>
O157:H7
biofilm
cell adhesion
motility
flagella
url https://www.mdpi.com/1422-0067/21/13/4592
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