title: The role of double-strand break repair pathways at functional and dysfunctional telomeres.
abstract: Telomeres have evolved to protect the ends of linear chromosomes from the myriad of threats posed by the cellular DNA damage signaling and repair pathways. Mammalian telomeres have to block nonhomologous end joining (NHEJ), thus preventing chromosome fusions; they need to control homologous recombination (HR), which could change telomere lengths; they have to avoid activating the ATM (ataxia telangiectasia mutated) and ATR (ATM- and RAD3-related) kinase pathways, which could induce cell cycle arrest; and they have to protect chromosome ends from hyperresection. Recent studies of telomeres have provided insights into the mechanisms of NHEJ and HR, how these double-strand break (DSB) repair pathways can be thwarted, and how telomeres have co-opted DNA repair factors to help in the protection of chromosome ends. These aspects of telomere biology are reviewed here with particular emphasis on recombination, the main focus of this collection.
authors.affiliation: Laboratory for Cell Biology and Genetics, Rockefeller University, New York, New York 10065.
authors.forename: Ylli
authors.initials: Y
authors.lastname: Doksani
authors.affiliation: Laboratory for Cell Biology and Genetics, Rockefeller University, New York, New York 10065.
authors.forename: Titia
authors.initials: T
authors.lastname: de Lange
mesh_terms: D000818:Animals; D053903:DNA Breaks, Double-Stranded; D059766:DNA End-Joining Repair / Q000502:physiology; D004260:DNA Repair / Q000502:physiology*; D019143:Evolution, Molecular; D059765:Homologous Recombination / Q000502:physiology*; D006801:Humans; D008957:Models, Genetic; D000089804:Shelterin Complex; D016615:Telomere / Q000502:physiology*; D034501:Telomere-Binding Proteins / Q000378:metabolism
chemical_list: D000089804:Shelterin Complex; D034501:Telomere-Binding Proteins