Dysfunctional Telomeres The Role of Double-Strand Break Repair Pathways at Functional and Subject Collection DNA Recombination at Functional and Dysfunctional Telomeres The Role of Double-Strand Break Repair Pathways
نویسندگان
چکیده
Meets DNA Transcription and Recombination: When RNA Andrés Aguilera and Hélène Gaillard Mechanism and Regulation End Resection at Double-Strand Breaks: Lorraine S. Symington Resection in Homologous Recombination Structural Studies of DNA End Detection and Christian Linke-Winnebeck, et al. Christian Bernd Schiller, Florian Ulrich Seifert, The Dissolution of Double Holliday Junctions Anna H. Bizard and Ian D. Hickson
منابع مشابه
The role of double-strand break repair pathways at functional and dysfunctional telomeres.
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 te...
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DNA double strand breaks (DSBs) are abrasions caused in both strands of the DNA duplex following exposure to both exogenous and endogenous conditions. Such abrasions have deleterious effect in cells leading to genome rearrangements and cell death. A number of repair systems including homologous recombination (HR) and non-homologous end-joining (NHEJ) have been evolved to minimize the fatal effe...
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TRF1 protects mammalian telomeres from fusion and fragility. Depletion of TRF1 leads to telomere fusions as well as accumulation of γ-H2AX foci and activation of both the ataxia telangiectasia mutated (ATM)- and the ataxia telangiectasia and Rad3 related (ATR)-mediated deoxyribonucleic acid (DNA) damage response (DDR) pathways. 53BP1, which is also present at dysfunctional telomeres, is a targe...
متن کاملRole of 53BP1 oligomerization in regulating double-strand break repair.
Tumor suppressor p53-binding protein 1 (53BP1) regulates the repair of dysfunctional telomeres lacking the shelterin protein TRF2 by promoting their mobility, their nonhomologous end-joining (NHEJ), and, as we show here, by blocking 5' resection by CtIP. We report that these functions of 53BP1 required its N-terminal ATM/ATR target sites and its association with H4K20diMe, but not the BRCT doma...
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Double strand breaks (DSBs) can be repaired via either Non-Homologous End Joining (NHEJ) or Homology directed Repair (HR). Telomeres, which resemble DSBs, are refractory to repair events in order to prevent chromosome end fusions and genomic instability. In some rare instances telomeres engage in Break-Induced Replication (BIR), a type of HR, in order to maintain telomere length in the absence ...
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