UvrD helicase suppresses recombination and DNA damage-induced deletions. Academic Article uri icon

Overview

abstract

  • 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.

publication date

  • August 1, 2006

Research

keywords

  • DNA Damage
  • DNA Helicases
  • DNA, Bacterial
  • Helicobacter pylori
  • Recombination, Genetic

Identity

PubMed Central ID

  • PMC1540021

Scopus Document Identifier

  • 33746602313

Digital Object Identifier (DOI)

  • 10.1128/JB.00275-06

PubMed ID

  • 16855234

Additional Document Info

volume

  • 188

issue

  • 15