UvrD helicase suppresses recombination and DNA damage-induced deletions.
UvrD, a highly conserved helicase involved in mismatch repair, nucleotide excision repair (NER), and recombinational repair, plays a critical role in maintaining genomic stability and facilitating DNA lesion repair in many prokaryotic species. In this report, we focus on the UvrD homolog in Helicobacter pylori, a genetically diverse organism that lacks many known DNA repair proteins, including those involved in mismatch repair and recombinational repair, and that is noted for high levels of inter- and intragenomic recombination and mutation. H. pylori contains numerous DNA repeats in its compact genome and inhabits an environment rich in DNA-damaging agents that can lead to increased rearrangements between such repeats. We find that H. pylori UvrD functions to repair DNA damage and limit homologous recombination and DNA damage-induced genomic rearrangements between DNA repeats. Our results suggest that UvrD and other NER pathway proteins play a prominent role in maintaining genome integrity, especially after DNA damage; thus, NER may be especially critical in organisms such as H. pylori that face high-level genotoxic stress in vivo.
Kang
Josephine
J
Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA. kangm01@med.nyu.edu
Blaser
Martin J
MJ
D004249:DNA Damage; D004265:DNA Helicases / Q000235:genetics / Q000502:physiology*; D004260:DNA Repair; D004269:DNA, Bacterial; D015536:Down-Regulation; D016480:Helicobacter pylori / Q000201:enzymology / Q000235:genetics*; D009154:Mutation; D011995:Recombination, Genetic
D004269:DNA, Bacterial; D004265:DNA Helicases