Perinuclear tethers license telomeric DSBs for a broad kinesin- and NPC-dependent DNA repair process

Daniel K.C. Chung, Janet N.Y. Chan, Jonathan Strecker, Wei Zhang, Sasha Ebrahimi-Ardebili, Thomas Lu, Karan J. Abraham, Daniel Durocher and Karim Mekhail ()
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Daniel K.C. Chung: University of Toronto
Janet N.Y. Chan: University of Toronto
Jonathan Strecker: University of Toronto
Wei Zhang: University of Toronto
Sasha Ebrahimi-Ardebili: University of Toronto
Thomas Lu: University of Toronto
Karan J. Abraham: University of Toronto
Daniel Durocher: University of Toronto
Karim Mekhail: University of Toronto

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract DNA double-strand breaks (DSBs) are often targeted to nuclear pore complexes (NPCs) for repair. How targeting is achieved and the DNA repair pathways involved in this process remain unclear. Here, we show that the kinesin-14 motor protein complex (Cik1–Kar3) cooperates with chromatin remodellers to mediate interactions between subtelomeric DSBs and the Nup84 nuclear pore complex to ensure cell survival via break-induced replication (BIR), an error-prone DNA repair process. Insertion of a DNA zip code near the subtelomeric DSB site artificially targets it to NPCs hyperactivating this repair mechanism. Kinesin-14 and Nup84 mediate BIR-dependent repair at non-telomeric DSBs whereas perinuclear telomere tethers are only required for telomeric BIR. Furthermore, kinesin-14 plays a critical role in telomerase-independent telomere maintenance. Thus, we uncover roles for kinesin and NPCs in DNA repair by BIR and reveal that perinuclear telomere anchors license subtelomeric DSBs for this error-prone DNA repair mechanism.

Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8742

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DOI: 10.1038/ncomms8742

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