Nature Communications (Jan 2019)
ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks
- Gabriel Balmus,
- Domenic Pilger,
- Julia Coates,
- Mukerrem Demir,
- Matylda Sczaniecka-Clift,
- Ana C. Barros,
- Michael Woods,
- Beiyuan Fu,
- Fengtang Yang,
- Elisabeth Chen,
- Matthias Ostermaier,
- Tatjana Stankovic,
- Hannes Ponstingl,
- Mareike Herzog,
- Kosuke Yusa,
- Francisco Munoz Martinez,
- Stephen T. Durant,
- Yaron Galanty,
- Petra Beli,
- David J. Adams,
- Allan Bradley,
- Emmanouil Metzakopian,
- Josep V. Forment,
- Stephen P. Jackson
Affiliations
- Gabriel Balmus
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Domenic Pilger
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Julia Coates
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Mukerrem Demir
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Matylda Sczaniecka-Clift
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Ana C. Barros
- Wellcome Trust Sanger Institute
- Michael Woods
- Wellcome Trust Sanger Institute
- Beiyuan Fu
- Wellcome Trust Sanger Institute
- Fengtang Yang
- Wellcome Trust Sanger Institute
- Elisabeth Chen
- Wellcome Trust Sanger Institute
- Matthias Ostermaier
- Institute of Molecular Biology (IMB)
- Tatjana Stankovic
- Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham
- Hannes Ponstingl
- Wellcome Trust Sanger Institute
- Mareike Herzog
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Kosuke Yusa
- Wellcome Trust Sanger Institute
- Francisco Munoz Martinez
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Stephen T. Durant
- DNA Damage Response Biology, Bioscience Oncology IMED Biotech Unit, AstraZeneca
- Yaron Galanty
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Petra Beli
- Institute of Molecular Biology (IMB)
- David J. Adams
- Wellcome Trust Sanger Institute
- Allan Bradley
- Wellcome Trust Sanger Institute
- Emmanouil Metzakopian
- Wellcome Trust Sanger Institute
- Josep V. Forment
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- Stephen P. Jackson
- The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Biochemistry, University of Cambridge
- DOI
- https://doi.org/10.1038/s41467-018-07729-2
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 18
Abstract
Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent toxic DNA end-joining leading to chromosome fusions and cell death.
