Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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Dissecting the transcriptional response to DNA damage in Helicobacter pylori.


ABSTRACT: We have completed transcriptional profiles of H. pylori cells undergoing DNA damage, caused by either failure to repair endogenous damage (addA- cells) or exposure to ciprofloxacin, which binds DNA gyrase, thus inducing double strand breaks. The goals of this study were to elucidate factors required to sustain the transcription response to DNA damage. All mutants are complete deletions of the coding sequence. The recA and comB10 genes are disrupted with the chloramphenical acetyl transferase (CAT) gene, encoding chloramphenicol resistance. The addA gene is disrupted with the aph3 gene, which encodes resistence to kanamycin. All mutant phenotypes can be complemented by expression of the gene at a heterologous locus.

ORGANISM(S): Helicobacter pylori

SUBMITTER: Marion Dorer 

PROVIDER: E-GEOD-19334 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

DNA damage triggers genetic exchange in Helicobacter pylori.

Dorer Marion S MS   Fero Jutta J   Salama Nina R NR  

PLoS pathogens 20100729 7


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 respons  ...[more]

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