Related Experiment Video
Updated: Jul 12, 2026

Visualization of UV-induced Replication Intermediates in E. coli using Two-dimensional Agarose-gel Analysis
Published on: December 21, 2010
DNA damage triggers genetic exchange in Helicobacter pylori
Marion S Dorer1, Jutta Fero, Nina R Salama
1Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Abstract:
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.
Related Concept Videos
Nucleotide Excision Repair
Homologous Recombination
Nucleotide Excision Repair
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Mismatch Repair
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Homologous Recombination
Gastritis II: Pathophysiology

