Dissecting the transcriptional response to DNA damage in Helicobacter pylori.

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.