title: DNA repair triggered by sensors of helical dynamics.
abstract: Nucleotide excision repair is a constitutive stress response that eliminates DNA lesions induced by multiple genotoxic agents. Unlike the immune system, which generates billions of immunoglobulins and T cell receptors for antigen recognition, the nucleotide excision repair complex uses only a few generic factors to detect an astounding diversity of DNA modifications. New data favor an unexpected strategy whereby damage recognition is initiated by the detection of abnormal oscillations in the undamaged strand opposite to DNA lesions. Another core subunit recognizes the increased susceptibility of DNA to be kinked at injured sites. We suggest that early nucleotide excision repair factors gain substrate versatility by avoiding direct contacts with modified residues and exploiting instead the altered dynamics of damaged DNA duplexes.
authors.affiliation: Institute of Pharmacology and Toxicology, University of Zürich-Vetsuisse, Winterthurerstrasse 260, CH-8057 Zürich, Switzerland.
authors.forename: Olivier
authors.initials: O
authors.lastname: Maillard
authors.forename: Ulrike
authors.initials: U
authors.lastname: Camenisch
authors.forename: Flurina C
authors.initials: FC
authors.lastname: Clement
authors.forename: Krastan B
authors.initials: KB
authors.lastname: Blagoev
authors.forename: Hanspeter
authors.initials: H
authors.lastname: Naegeli
mesh_terms: D004249:DNA Damage; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000737:chemistry / Q000235:genetics
chemical_list: D004268:DNA-Binding Proteins; C086984:XPC protein, human