FANCD2 limits replication stress and genome instability in cells lacking BRCA2

Probing the synthetic lethal effect of FANCD2 deletion in BRCA2-deficient cells reveals independent roles of FANCD2 and BRCA2 in stabilizing stalled replication forks to maintain genome stability and promote cell survival. The tumor suppressor BRCA2 plays a key role in genome integrity by promoting...

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Published in:	Nature structural & molecular biology Vol. 23; no. 8; pp. 755 - 757
Main Authors:	Michl, Johanna, Zimmer, Jutta, Buffa, Francesca M, McDermott, Ultan, Tarsounas, Madalena
Format:	Journal Article
Language:	English
Published:	New York Nature Publishing Group US 01.08.2016 Nature Publishing Group
Subjects:	13 13/2 631/337/1427 631/67/1244 Antineoplastic Agents - pharmacology Biochemistry Biological Microscopy BRCA2 protein BRCA2 Protein - metabolism Breast cancer brief-communication Cancer Cancer cells Cell Line, Tumor Cell Survival DNA Damage DNA repair DNA Replication Fanconi Anemia Complementation Group D2 Protein - physiology Fanconi syndrome Fanconi's anemia Genetic aspects Genetic research Genome, Human Genomes Genomic Instability HEK293 Cells Homologous recombination Humans Life Sciences Membrane Biology Phthalazines - pharmacology Piperazines - pharmacology Protein Structure Replication Structure Tumor suppressor genes United Kingdom
ISSN:	1545-9993, 1545-9985, 1545-9985
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Abstract	Probing the synthetic lethal effect of FANCD2 deletion in BRCA2-deficient cells reveals independent roles of FANCD2 and BRCA2 in stabilizing stalled replication forks to maintain genome stability and promote cell survival. The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication-fork progression and genomic instability. Our results identify a new role of FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, thereby affecting cell survival and treatment responses.
AbstractList	The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication-fork progression and genomic instability. Our results identify a new role of FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, thereby affecting cell survival and treatment responses.The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication-fork progression and genomic instability. Our results identify a new role of FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, thereby affecting cell survival and treatment responses. Probing the synthetic lethal effect of FANCD2 deletion in BRCA2-deficient cells reveals independent roles of FANCD2 and BRCA2 in stabilizing stalled replication forks to maintain genome stability and promote cell survival. The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication-fork progression and genomic instability. Our results identify a new role of FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, thereby affecting cell survival and treatment responses. Probing the synthetic lethal effect of FANCD2 deletion in BRCA2-deficient cells reveals independent roles of FANCD2 and BRCA2 in stabilizing stalled replication forks to maintain genome stability and promote cell survival. The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication-fork progression and genomic instability. Our results identify a new role of FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, thereby affecting cell survival and treatment responses. The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication fork progression and genomic instability. Our results identify a novel role for FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, which impacts on cell survival and treatment responses. Probing the synthetic lethal effect of FANCD2 deletion in BRCA2-deficient cells reveals independent roles of FANCD2 and BRCA2 in stabilizing stalled replication forks to maintain genome stability and promote cell survival. The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we report that human cancer cells lacking BRCA2 rely on the Fanconi anemia protein FANCD2 to limit replication-fork progression and genomic instability. Our results identify a new role of FANCD2 in limiting constitutive replication stress in BRCA2-deficient cells, thereby affecting cell survival and treatment responses.
Audience	Academic
Author	McDermott, Ultan Tarsounas, Madalena Zimmer, Jutta Michl, Johanna Buffa, Francesca M
AuthorAffiliation	1 The CR-UK/MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Oxford, U.K 2 Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK
AuthorAffiliation_xml	– name: 2 Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK – name: 1 The CR-UK/MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Oxford, U.K
Author_xml	– sequence: 1 givenname: Johanna surname: Michl fullname: Michl, Johanna organization: Department of Oncology, CR-UK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 2 givenname: Jutta surname: Zimmer fullname: Zimmer, Jutta organization: Department of Oncology, CR-UK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 3 givenname: Francesca M surname: Buffa fullname: Buffa, Francesca M organization: Department of Oncology, CR-UK/MRC Oxford Institute for Radiation Oncology, University of Oxford – sequence: 4 givenname: Ultan orcidid: 0000-0001-9032-4700 surname: McDermott fullname: McDermott, Ultan organization: Cancer Genome Project, Wellcome Trust Sanger Institute – sequence: 5 givenname: Madalena surname: Tarsounas fullname: Tarsounas, Madalena email: madalena.tarsounas@oncology.ox.ac.uk organization: Department of Oncology, CR-UK/MRC Oxford Institute for Radiation Oncology, University of Oxford
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Snippet	Probing the synthetic lethal effect of FANCD2 deletion in BRCA2-deficient cells reveals independent roles of FANCD2 and BRCA2 in stabilizing stalled... The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication-fork stability and homologous recombination (HR) DNA repair. Here we... The tumor suppressor BRCA2 plays a key role in genome integrity by promoting replication fork stability and homologous recombination (HR) DNA repair. Here we...
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SubjectTerms	13 13/2 631/337/1427 631/67/1244 Antineoplastic Agents - pharmacology Biochemistry Biological Microscopy BRCA2 protein BRCA2 Protein - metabolism Breast cancer brief-communication Cancer Cancer cells Cell Line, Tumor Cell Survival DNA Damage DNA repair DNA Replication Fanconi Anemia Complementation Group D2 Protein - physiology Fanconi syndrome Fanconi's anemia Genetic aspects Genetic research Genome, Human Genomes Genomic Instability HEK293 Cells Homologous recombination Humans Life Sciences Membrane Biology Phthalazines - pharmacology Piperazines - pharmacology Protein Structure Replication Structure Tumor suppressor genes
Title	FANCD2 limits replication stress and genome instability in cells lacking BRCA2
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