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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MDPI AG
2020-06-01
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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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series | International Journal of Molecular Sciences |
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 |
work_keys_str_mv | AT elisaandreozzi pcheregulationofiescherichiacoliio157h7flagellacontrollingthetransitiontohostcellattachment AT gaylenauhlich pcheregulationofiescherichiacoliio157h7flagellacontrollingthetransitiontohostcellattachment |