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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Autores principales: Marion S Dorer, Jutta Fero, Nina R Salama
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Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2010
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Acceso en línea:https://doaj.org/article/4ca3f9b0907d439e8732375ff79ace8c
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spelling oai:doaj.org-article:4ca3f9b0907d439e8732375ff79ace8c2021-11-18T06:01:47ZDNA damage triggers genetic exchange in Helicobacter pylori.1553-73661553-737410.1371/journal.ppat.1001026https://doaj.org/article/4ca3f9b0907d439e8732375ff79ace8c2010-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20686662/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Many 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.Marion S DorerJutta FeroNina R SalamaPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 6, Iss 7, p e1001026 (2010)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Marion S Dorer
Jutta Fero
Nina R Salama
DNA damage triggers genetic exchange in Helicobacter pylori.
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 article
author Marion S Dorer
Jutta Fero
Nina R Salama
author_facet Marion S Dorer
Jutta Fero
Nina R Salama
author_sort Marion S Dorer
title DNA damage triggers genetic exchange in Helicobacter pylori.
title_short DNA damage triggers genetic exchange in Helicobacter pylori.
title_full DNA damage triggers genetic exchange in Helicobacter pylori.
title_fullStr DNA damage triggers genetic exchange in Helicobacter pylori.
title_full_unstemmed DNA damage triggers genetic exchange in Helicobacter pylori.
title_sort dna damage triggers genetic exchange in helicobacter pylori.
publisher Public Library of Science (PLoS)
publishDate 2010
url https://doaj.org/article/4ca3f9b0907d439e8732375ff79ace8c
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AT juttafero dnadamagetriggersgeneticexchangeinhelicobacterpylori
AT ninarsalama dnadamagetriggersgeneticexchangeinhelicobacterpylori
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