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O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B
Acquisition of new prophages that are able to increase the bacterial fitness by the lysogenic conversion is believed to be an important strategy of bacterial adaptation to the changing environment. However, in contrast to the factors determining the range of bacteriophage lytic activity, little is k...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7862636/ https://www.ncbi.nlm.nih.gov/pubmed/33542282 http://dx.doi.org/10.1038/s41598-021-82422-x |
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author | Golomidova, A. K. Efimov, A. D. Kulikov, E. E. Kuznetsov, A. S. Belalov, I. Sh. Letarov, A. V. |
author_facet | Golomidova, A. K. Efimov, A. D. Kulikov, E. E. Kuznetsov, A. S. Belalov, I. Sh. Letarov, A. V. |
author_sort | Golomidova, A. K. |
collection | PubMed |
description | Acquisition of new prophages that are able to increase the bacterial fitness by the lysogenic conversion is believed to be an important strategy of bacterial adaptation to the changing environment. However, in contrast to the factors determining the range of bacteriophage lytic activity, little is known about the factors that define the lysogenization host range. Bacteriophage phi24B is the paradigmal model of Stx-converting phages, encoding the toxins of the Shiga-toxigenic E. coli (STEC). This virus has been shown to lysogenize a wide range of E. coli strains that is much broader than the range of the strains supporting its lytic growth. Therefore, phages produced by the STEC population colonizing the small or large intestine are potentially able to lysogenize symbiotic E. coli in the hindgut, and these secondary lysogens may contribute to the overall patient toxic load and to lead to the emergence of new pathogenic STEC strains. We demonstrate, however, that O antigen effectively limit the lysogenization of the wild E. coli strains by phi24B phage. The lysogens are formed from the spontaneous rough mutants and therefore have increased sensitivity to other bacteriophages and to the bactericidal activity of the serum if compared to their respective parental strains. |
format | Online Article Text |
id | pubmed-7862636 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-78626362021-02-08 O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B Golomidova, A. K. Efimov, A. D. Kulikov, E. E. Kuznetsov, A. S. Belalov, I. Sh. Letarov, A. V. Sci Rep Article Acquisition of new prophages that are able to increase the bacterial fitness by the lysogenic conversion is believed to be an important strategy of bacterial adaptation to the changing environment. However, in contrast to the factors determining the range of bacteriophage lytic activity, little is known about the factors that define the lysogenization host range. Bacteriophage phi24B is the paradigmal model of Stx-converting phages, encoding the toxins of the Shiga-toxigenic E. coli (STEC). This virus has been shown to lysogenize a wide range of E. coli strains that is much broader than the range of the strains supporting its lytic growth. Therefore, phages produced by the STEC population colonizing the small or large intestine are potentially able to lysogenize symbiotic E. coli in the hindgut, and these secondary lysogens may contribute to the overall patient toxic load and to lead to the emergence of new pathogenic STEC strains. We demonstrate, however, that O antigen effectively limit the lysogenization of the wild E. coli strains by phi24B phage. The lysogens are formed from the spontaneous rough mutants and therefore have increased sensitivity to other bacteriophages and to the bactericidal activity of the serum if compared to their respective parental strains. Nature Publishing Group UK 2021-02-04 /pmc/articles/PMC7862636/ /pubmed/33542282 http://dx.doi.org/10.1038/s41598-021-82422-x Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Golomidova, A. K. Efimov, A. D. Kulikov, E. E. Kuznetsov, A. S. Belalov, I. Sh. Letarov, A. V. O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B |
title | O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B |
title_full | O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B |
title_fullStr | O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B |
title_full_unstemmed | O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B |
title_short | O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B |
title_sort | o antigen restricts lysogenization of non-o157 escherichia coli strains by stx-converting bacteriophage phi24b |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7862636/ https://www.ncbi.nlm.nih.gov/pubmed/33542282 http://dx.doi.org/10.1038/s41598-021-82422-x |
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