title: Recombinational DNA repair is regulated by compartmentalization of DNA lesions at the nuclear pore complex.
abstract: The nuclear pore complex (NPC) is emerging as a center for recruitment of a class of "difficult to repair" lesions such as double-strand breaks without a repair template and eroded telomeres in telomerase-deficient cells. In addition to such pathological situations, a recent study by Su and colleagues shows that also physiological threats to genome integrity such as DNA secondary structure-forming triplet repeat sequences relocalize to the NPC during DNA replication. Mutants that fail to reposition the triplet repeat locus to the NPC cause repeat instability. Here, we review the types of DNA lesions that relocalize to the NPC, the putative mechanisms of relocalization, and the types of recombinational repair that are stimulated by the NPC, and present a model for NPC-facilitated repair.
authors.affiliation: Marseille Cancer Research Center (CRCM), U1068 Inserm, UMR7258 CNRS, Aix Marseille University, Institut Paoli-Calmettes, LNCC (Equipe labellisée), Marseille, France.
authors.forename: Vincent
authors.initials: V
authors.lastname: Géli
authors.affiliation: Department of Biology, University of Copenhagen, Copenhagen, Denmark.
authors.forename: Michael
authors.initials: M
authors.lastname: Lisby
mesh_terms: D004247:DNA / Q000235:genetics*; D004249:DNA Damage / Q000235:genetics; D004261:DNA Replication / Q000235:genetics; D006801:Humans; D022022:Nuclear Pore / Q000235:genetics*; D059767:Recombinational DNA Repair / Q000235:genetics*; D016615:Telomere / Q000235:genetics; D018911:Trinucleotide Repeats / Q000235:genetics
chemical_list: D004247:DNA
keywords: DNA repair; homologous recombination; nuclear organization; nuclear pore complex; sumoylation