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DNA Damage Triggers Genetic Exchange in Helicobacter pylori
Many organisms respond to DNA damage by inducing expression of DNA repair genes. We find that the human stomach pathogen Helicobacter pylori instead induces transcription and translation of natural competence genes, thus increasing transformation frequency. Transcription of a lysozyme-like protein t...
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Formato: | Texto |
Lenguaje: | English |
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Public Library of Science
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912397/ https://www.ncbi.nlm.nih.gov/pubmed/20686662 http://dx.doi.org/10.1371/journal.ppat.1001026 |
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author | Dorer, Marion S. Fero, Jutta Salama, Nina R. |
author_facet | Dorer, Marion S. Fero, Jutta Salama, Nina R. |
author_sort | Dorer, Marion S. |
collection | PubMed |
description | Many organisms respond to DNA damage by inducing expression of DNA repair genes. We find that the human stomach pathogen Helicobacter pylori instead induces transcription and translation of natural competence genes, thus increasing transformation frequency. Transcription of a lysozyme-like protein that promotes DNA donation from intact cells is also induced. Exogenous DNA modulates the DNA damage response, as both recA and the ability to take up DNA are required for full induction of the response. This feedback loop is active during stomach colonization, indicating a role in the pathogenesis of the bacterium. As patients can be infected with multiple genetically distinct clones of H. pylori, DNA damage induced genetic exchange may facilitate spread of antibiotic resistance and selection of fitter variants through re-assortment of preexisting alleles in this important human pathogen. |
format | Text |
id | pubmed-2912397 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-29123972010-08-03 DNA Damage Triggers Genetic Exchange in Helicobacter pylori Dorer, Marion S. Fero, Jutta Salama, Nina R. PLoS Pathog Research Article Many organisms respond to DNA damage by inducing expression of DNA repair genes. We find that the human stomach pathogen Helicobacter pylori instead induces transcription and translation of natural competence genes, thus increasing transformation frequency. Transcription of a lysozyme-like protein that promotes DNA donation from intact cells is also induced. Exogenous DNA modulates the DNA damage response, as both recA and the ability to take up DNA are required for full induction of the response. This feedback loop is active during stomach colonization, indicating a role in the pathogenesis of the bacterium. As patients can be infected with multiple genetically distinct clones of H. pylori, DNA damage induced genetic exchange may facilitate spread of antibiotic resistance and selection of fitter variants through re-assortment of preexisting alleles in this important human pathogen. Public Library of Science 2010-07-29 /pmc/articles/PMC2912397/ /pubmed/20686662 http://dx.doi.org/10.1371/journal.ppat.1001026 Text en Dorer et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Dorer, Marion S. Fero, Jutta Salama, Nina R. DNA Damage Triggers Genetic Exchange in Helicobacter pylori |
title | DNA Damage Triggers Genetic Exchange in Helicobacter pylori
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title_full | DNA Damage Triggers Genetic Exchange in Helicobacter pylori
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title_fullStr | DNA Damage Triggers Genetic Exchange in Helicobacter pylori
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title_full_unstemmed | DNA Damage Triggers Genetic Exchange in Helicobacter pylori
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title_short | DNA Damage Triggers Genetic Exchange in Helicobacter pylori
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title_sort | dna damage triggers genetic exchange in helicobacter pylori |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912397/ https://www.ncbi.nlm.nih.gov/pubmed/20686662 http://dx.doi.org/10.1371/journal.ppat.1001026 |
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