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Contributions of chaperone/usher systems to cell binding, biofilm formation and Yersinia pestis virulence

Yersinia pestis genome sequencing projects have revealed six intact uncharacterized chaperone/usher systems with the potential to play roles in plague pathogenesis. We cloned each locus and expressed them in the Δfim Escherichia coli strain AAEC185 to test the assembled Y. pestis surface structures...

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Autores principales: Felek, Suleyman, Jeong, Jenny J., Runco, Lisa M., Murray, Susan, Thanassi, David G., Krukonis, Eric S.
Formato: Texto
Lenguaje:English
Publicado: Microbiology Society 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3081084/
https://www.ncbi.nlm.nih.gov/pubmed/21088108
http://dx.doi.org/10.1099/mic.0.044826-0
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author Felek, Suleyman
Jeong, Jenny J.
Runco, Lisa M.
Murray, Susan
Thanassi, David G.
Krukonis, Eric S.
author_facet Felek, Suleyman
Jeong, Jenny J.
Runco, Lisa M.
Murray, Susan
Thanassi, David G.
Krukonis, Eric S.
author_sort Felek, Suleyman
collection PubMed
description Yersinia pestis genome sequencing projects have revealed six intact uncharacterized chaperone/usher systems with the potential to play roles in plague pathogenesis. We cloned each locus and expressed them in the Δfim Escherichia coli strain AAEC185 to test the assembled Y. pestis surface structures for various activities. Expression of each chaperone/usher locus gave rise to specific novel fibrillar structures on the surface of E. coli. One locus, y0561-0563, was able to mediate attachment to human epithelial cells (HEp-2) and human macrophages (THP-1) but not mouse macrophages (RAW264.7), while several loci were able to facilitate E. coli biofilm formation. When each chaperone/usher locus was deleted in Y. pestis, only deletion of the previously described pH 6 antigen (Psa) chaperone/usher system resulted in decreased adhesion and biofilm formation. Quantitative RT-PCR (qRT-PCR) revealed low expression levels for each novel chaperone/usher system in vitro as well as in mouse tissues following intravenous infection. However, a Y. pestis mutant in the chaperone/usher locus y1858-1862 was attenuated for virulence in mice via the intravenous route of infection, suggesting that expression of this locus is, at some stage, sufficient to affect the outcome of a plague infection. qRT-PCR experiments also indicated that expression of the chaperone/usher-dependent capsule locus, caf1, was influenced by oxygen availability and that the well-described chaperone/usher-dependent pilus, Psa, was strongly induced in minimal medium even at 28 °C rather than 37 °C, a temperature previously believed to be required for Psa expression. These data indicate several potential roles for the novel chaperone/usher systems of Y. pestis in pathogenesis and infection-related functions such as cell adhesion and biofilm formation.
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spelling pubmed-30810842012-03-01 Contributions of chaperone/usher systems to cell binding, biofilm formation and Yersinia pestis virulence Felek, Suleyman Jeong, Jenny J. Runco, Lisa M. Murray, Susan Thanassi, David G. Krukonis, Eric S. Microbiology (Reading) Microbial Pathogenicity Yersinia pestis genome sequencing projects have revealed six intact uncharacterized chaperone/usher systems with the potential to play roles in plague pathogenesis. We cloned each locus and expressed them in the Δfim Escherichia coli strain AAEC185 to test the assembled Y. pestis surface structures for various activities. Expression of each chaperone/usher locus gave rise to specific novel fibrillar structures on the surface of E. coli. One locus, y0561-0563, was able to mediate attachment to human epithelial cells (HEp-2) and human macrophages (THP-1) but not mouse macrophages (RAW264.7), while several loci were able to facilitate E. coli biofilm formation. When each chaperone/usher locus was deleted in Y. pestis, only deletion of the previously described pH 6 antigen (Psa) chaperone/usher system resulted in decreased adhesion and biofilm formation. Quantitative RT-PCR (qRT-PCR) revealed low expression levels for each novel chaperone/usher system in vitro as well as in mouse tissues following intravenous infection. However, a Y. pestis mutant in the chaperone/usher locus y1858-1862 was attenuated for virulence in mice via the intravenous route of infection, suggesting that expression of this locus is, at some stage, sufficient to affect the outcome of a plague infection. qRT-PCR experiments also indicated that expression of the chaperone/usher-dependent capsule locus, caf1, was influenced by oxygen availability and that the well-described chaperone/usher-dependent pilus, Psa, was strongly induced in minimal medium even at 28 °C rather than 37 °C, a temperature previously believed to be required for Psa expression. These data indicate several potential roles for the novel chaperone/usher systems of Y. pestis in pathogenesis and infection-related functions such as cell adhesion and biofilm formation. Microbiology Society 2011-03 /pmc/articles/PMC3081084/ /pubmed/21088108 http://dx.doi.org/10.1099/mic.0.044826-0 Text en Copyright © 2011, SGM
spellingShingle Microbial Pathogenicity
Felek, Suleyman
Jeong, Jenny J.
Runco, Lisa M.
Murray, Susan
Thanassi, David G.
Krukonis, Eric S.
Contributions of chaperone/usher systems to cell binding, biofilm formation and Yersinia pestis virulence
title Contributions of chaperone/usher systems to cell binding, biofilm formation and Yersinia pestis virulence
title_full Contributions of chaperone/usher systems to cell binding, biofilm formation and Yersinia pestis virulence
title_fullStr Contributions of chaperone/usher systems to cell binding, biofilm formation and Yersinia pestis virulence
title_full_unstemmed Contributions of chaperone/usher systems to cell binding, biofilm formation and Yersinia pestis virulence
title_short Contributions of chaperone/usher systems to cell binding, biofilm formation and Yersinia pestis virulence
title_sort contributions of chaperone/usher systems to cell binding, biofilm formation and yersinia pestis virulence
topic Microbial Pathogenicity
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3081084/
https://www.ncbi.nlm.nih.gov/pubmed/21088108
http://dx.doi.org/10.1099/mic.0.044826-0
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