The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity

Jordan R. Becker; Raquel Cuella-Martin; Marco Barazas; Rui Liu; Catarina Oliveira; Antony W. Oliver; Kirstin Bilham; Abbey B. Holt; Andrew N. Blackford; Jörg Heierhorst; Jos Jonkers; Sven Rottenberg; J. Ross Chapman

doi:10.1038/s41467-018-07855-x

Nature Communications (Dec 2018)

The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity

Jordan R. Becker,
Raquel Cuella-Martin,
Marco Barazas,
Rui Liu,
Catarina Oliveira,
Antony W. Oliver,
Kirstin Bilham,
Abbey B. Holt,
Andrew N. Blackford,
Jörg Heierhorst,
Jos Jonkers,
Sven Rottenberg,
J. Ross Chapman

Affiliations

Jordan R. Becker: Genome Integrity Laboratory, Wellcome Centre for Human Genetics, University of Oxford
Raquel Cuella-Martin: Genome Integrity Laboratory, Wellcome Centre for Human Genetics, University of Oxford
Marco Barazas: Division of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute
Rui Liu: St. Vincent’s Institute of Medical Research
Catarina Oliveira: Genome Integrity Laboratory, Wellcome Centre for Human Genetics, University of Oxford
Antony W. Oliver: Genome Damage and Stability Centre, School of Life Sciences, University of Sussex
Kirstin Bilham: Genome Integrity Laboratory, Wellcome Centre for Human Genetics, University of Oxford
Abbey B. Holt: MRC Brain Network Dynamics Unit, Department of Pharmacology, University of Oxford
Andrew N. Blackford: Department of Oncology, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital
Jörg Heierhorst: St. Vincent’s Institute of Medical Research
Jos Jonkers: Division of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute
Sven Rottenberg: Division of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute
J. Ross Chapman: Genome Integrity Laboratory, Wellcome Centre for Human Genetics, University of Oxford

DOI: https://doi.org/10.1038/s41467-018-07855-x
Journal volume & issue: Vol. 9, no. 1
pp. 1 – 12

Abstract

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53BP1 is a key player in non-homologous end joining (NHEJ). Here the authors reveal an important role for the multifunctional homodimeric protein hub dynein light chain 1 (DYNLL1) in increasing the efficacy of 53BP1-mediated repair of DNA double-strand breaks (DSBs) by NHEJ.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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