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Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype
Tellurite (Tel) resistant enterohaemorrhagic Escherichia coli (EHEC) O157:H7 is a global pathogen. In strain EDL933 Tel resistance (Tel(R)) is encoded by duplicate ter cluster in O islands (OI) 43 and 48, which also harbour iha, encoding the adhesin and siderophore receptor Iha. We identified five E...
Autores principales: | , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Blackwell Publishing Ltd
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3064760/ https://www.ncbi.nlm.nih.gov/pubmed/21299654 http://dx.doi.org/10.1111/j.1365-2958.2010.07499.x |
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author | Bielaszewska, Martina Middendorf, Barbara Tarr, Phillip I Zhang, Wenlan Prager, Rita Aldick, Thomas Dobrindt, Ulrich Karch, Helge Mellmann, Alexander |
author_facet | Bielaszewska, Martina Middendorf, Barbara Tarr, Phillip I Zhang, Wenlan Prager, Rita Aldick, Thomas Dobrindt, Ulrich Karch, Helge Mellmann, Alexander |
author_sort | Bielaszewska, Martina |
collection | PubMed |
description | Tellurite (Tel) resistant enterohaemorrhagic Escherichia coli (EHEC) O157:H7 is a global pathogen. In strain EDL933 Tel resistance (Tel(R)) is encoded by duplicate ter cluster in O islands (OI) 43 and 48, which also harbour iha, encoding the adhesin and siderophore receptor Iha. We identified five EHEC O157:H7 strains that differentiate into large (L) colonies and small (S) colonies with high and low Tel minimal inhibitory concentrations (MICs) respectively. S colonies (Tel-MICs ≤ 4 µg ml(−1)) sustained large internal deletions within the Tel(R) OIs via homologous recombination between IS elements and lost ter and iha. Moreover, complete excision of the islands occurred by site-specific recombination between flanking direct repeats. Complete excision of OI 43 and OI 48 occurred in 1.81 × 10(−3) and 1.97 × 10(−4) cells in culture, respectively; internal deletion of OI 48 was more frequent (9.7 × 10(−1) cells). Under iron limitation that promotes iha transcription, iha-negative derivatives adhered less well to human intestinal epithelial cells and grew slower than did their iha-positive counterparts. Experiments utilizing iha deletion and complementation mutants identified Iha as the major factor responsible for these phenotypic differences. Spontaneous deletions affecting Tel(R) OIs contribute to EHEC O157 genome plasticity and might impair virulence and/or fitness. |
format | Text |
id | pubmed-3064760 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-30647602011-03-30 Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype Bielaszewska, Martina Middendorf, Barbara Tarr, Phillip I Zhang, Wenlan Prager, Rita Aldick, Thomas Dobrindt, Ulrich Karch, Helge Mellmann, Alexander Mol Microbiol Research Articles Tellurite (Tel) resistant enterohaemorrhagic Escherichia coli (EHEC) O157:H7 is a global pathogen. In strain EDL933 Tel resistance (Tel(R)) is encoded by duplicate ter cluster in O islands (OI) 43 and 48, which also harbour iha, encoding the adhesin and siderophore receptor Iha. We identified five EHEC O157:H7 strains that differentiate into large (L) colonies and small (S) colonies with high and low Tel minimal inhibitory concentrations (MICs) respectively. S colonies (Tel-MICs ≤ 4 µg ml(−1)) sustained large internal deletions within the Tel(R) OIs via homologous recombination between IS elements and lost ter and iha. Moreover, complete excision of the islands occurred by site-specific recombination between flanking direct repeats. Complete excision of OI 43 and OI 48 occurred in 1.81 × 10(−3) and 1.97 × 10(−4) cells in culture, respectively; internal deletion of OI 48 was more frequent (9.7 × 10(−1) cells). Under iron limitation that promotes iha transcription, iha-negative derivatives adhered less well to human intestinal epithelial cells and grew slower than did their iha-positive counterparts. Experiments utilizing iha deletion and complementation mutants identified Iha as the major factor responsible for these phenotypic differences. Spontaneous deletions affecting Tel(R) OIs contribute to EHEC O157 genome plasticity and might impair virulence and/or fitness. Blackwell Publishing Ltd 2011-02 2011-01-04 /pmc/articles/PMC3064760/ /pubmed/21299654 http://dx.doi.org/10.1111/j.1365-2958.2010.07499.x Text en Copyright © 2011 Blackwell Publishing Ltd http://creativecommons.org/licenses/by/2.5/ Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation. |
spellingShingle | Research Articles Bielaszewska, Martina Middendorf, Barbara Tarr, Phillip I Zhang, Wenlan Prager, Rita Aldick, Thomas Dobrindt, Ulrich Karch, Helge Mellmann, Alexander Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype |
title | Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype |
title_full | Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype |
title_fullStr | Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype |
title_full_unstemmed | Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype |
title_short | Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype |
title_sort | chromosomal instability in enterohaemorrhagic escherichia coli o157:h7: impact on adherence, tellurite resistance and colony phenotype |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3064760/ https://www.ncbi.nlm.nih.gov/pubmed/21299654 http://dx.doi.org/10.1111/j.1365-2958.2010.07499.x |
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