H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours
Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes phosphorylated on serine residue 139 (known as γH2AX), resulting in the recruitment of the DNA repair effectors 53BP1 and BRCA1. Here, by stud...
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| Vydané v: | Nature communications Ročník 15; číslo 1; s. 4430 - 14 |
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| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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London
Nature Publishing Group UK
24.05.2024
Nature Publishing Group Nature Portfolio |
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| ISSN: | 2041-1723, 2041-1723 |
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| Abstract | Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes phosphorylated on serine residue 139 (known as γH2AX), resulting in the recruitment of the DNA repair effectors 53BP1 and BRCA1. Here, by studying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors in BRCA1/2-deficient mammary tumours, we identify a function for γH2AX in orchestrating drug-induced replication fork degradation. Mechanistically, γH2AX-driven replication fork degradation is elicited by suppressing CtIP-mediated fork protection. As a result, H2AX loss restores replication fork stability and increases chemoresistance in BRCA1/2-deficient tumour cells without restoring homology-directed DNA repair, as highlighted by the lack of DNA damage-induced RAD51 foci. Furthermore, in the attempt to discover acquired genetic vulnerabilities, we find that ATM but not ATR inhibition overcomes PARP inhibitor (PARPi) resistance in H2AX-deficient tumours by interfering with CtIP-mediated fork protection. In summary, our results demonstrate a role for H2AX in replication fork biology in BRCA-deficient tumours and establish a function of H2AX separable from its classical role in DNA damage signalling and DSB repair.
Histone H2AX has a known role in DNA damage repair but interestingly, its loss is associated with resistance to poly(ADP-ribose) polymerase (PARP) inhibition in BRCA-deficient tumours. Here, the authors identify a role of γH2AX in the degradation of replication forks and demonstrate that H2AX loss drives PARP inhibitor resistance via increased stressed fork stability in BRCA-deficient tumours. |
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| AbstractList | Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes phosphorylated on serine residue 139 (known as γH2AX), resulting in the recruitment of the DNA repair effectors 53BP1 and BRCA1. Here, by studying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors in BRCA1/2-deficient mammary tumours, we identify a function for γH2AX in orchestrating drug-induced replication fork degradation. Mechanistically, γH2AX-driven replication fork degradation is elicited by suppressing CtIP-mediated fork protection. As a result, H2AX loss restores replication fork stability and increases chemoresistance in BRCA1/2-deficient tumour cells without restoring homology-directed DNA repair, as highlighted by the lack of DNA damage-induced RAD51 foci. Furthermore, in the attempt to discover acquired genetic vulnerabilities, we find that ATM but not ATR inhibition overcomes PARP inhibitor (PARPi) resistance in H2AX-deficient tumours by interfering with CtIP-mediated fork protection. In summary, our results demonstrate a role for H2AX in replication fork biology in BRCA-deficient tumours and establish a function of H2AX separable from its classical role in DNA damage signalling and DSB repair.Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes phosphorylated on serine residue 139 (known as γH2AX), resulting in the recruitment of the DNA repair effectors 53BP1 and BRCA1. Here, by studying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors in BRCA1/2-deficient mammary tumours, we identify a function for γH2AX in orchestrating drug-induced replication fork degradation. Mechanistically, γH2AX-driven replication fork degradation is elicited by suppressing CtIP-mediated fork protection. As a result, H2AX loss restores replication fork stability and increases chemoresistance in BRCA1/2-deficient tumour cells without restoring homology-directed DNA repair, as highlighted by the lack of DNA damage-induced RAD51 foci. Furthermore, in the attempt to discover acquired genetic vulnerabilities, we find that ATM but not ATR inhibition overcomes PARP inhibitor (PARPi) resistance in H2AX-deficient tumours by interfering with CtIP-mediated fork protection. In summary, our results demonstrate a role for H2AX in replication fork biology in BRCA-deficient tumours and establish a function of H2AX separable from its classical role in DNA damage signalling and DSB repair. Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes phosphorylated on serine residue 139 (known as γH2AX), resulting in the recruitment of the DNA repair effectors 53BP1 and BRCA1. Here, by studying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors in BRCA1/2-deficient mammary tumours, we identify a function for γH2AX in orchestrating drug-induced replication fork degradation. Mechanistically, γH2AX-driven replication fork degradation is elicited by suppressing CtIP-mediated fork protection. As a result, H2AX loss restores replication fork stability and increases chemoresistance in BRCA1/2-deficient tumour cells without restoring homology-directed DNA repair, as highlighted by the lack of DNA damage-induced RAD51 foci. Furthermore, in the attempt to discover acquired genetic vulnerabilities, we find that ATM but not ATR inhibition overcomes PARP inhibitor (PARPi) resistance in H2AX-deficient tumours by interfering with CtIP-mediated fork protection. In summary, our results demonstrate a role for H2AX in replication fork biology in BRCA-deficient tumours and establish a function of H2AX separable from its classical role in DNA damage signalling and DSB repair. Histone H2AX has a known role in DNA damage repair but interestingly, its loss is associated with resistance to poly(ADP-ribose) polymerase (PARP) inhibition in BRCA-deficient tumours. Here, the authors identify a role of γH2AX in the degradation of replication forks and demonstrate that H2AX loss drives PARP inhibitor resistance via increased stressed fork stability in BRCA-deficient tumours. Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes phosphorylated on serine residue 139 (known as γH2AX), resulting in the recruitment of the DNA repair effectors 53BP1 and BRCA1. Here, by studying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors in BRCA1/2-deficient mammary tumours, we identify a function for γH2AX in orchestrating drug-induced replication fork degradation. Mechanistically, γH2AX-driven replication fork degradation is elicited by suppressing CtIP-mediated fork protection. As a result, H2AX loss restores replication fork stability and increases chemoresistance in BRCA1/2-deficient tumour cells without restoring homology-directed DNA repair, as highlighted by the lack of DNA damage-induced RAD51 foci. Furthermore, in the attempt to discover acquired genetic vulnerabilities, we find that ATM but not ATR inhibition overcomes PARP inhibitor (PARPi) resistance in H2AX-deficient tumours by interfering with CtIP-mediated fork protection. In summary, our results demonstrate a role for H2AX in replication fork biology in BRCA-deficient tumours and establish a function of H2AX separable from its classical role in DNA damage signalling and DSB repair.Histone H2AX has a known role in DNA damage repair but interestingly, its loss is associated with resistance to poly(ADP-ribose) polymerase (PARP) inhibition in BRCA-deficient tumours. Here, the authors identify a role of γH2AX in the degradation of replication forks and demonstrate that H2AX loss drives PARP inhibitor resistance via increased stressed fork stability in BRCA-deficient tumours. Abstract Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes phosphorylated on serine residue 139 (known as γH2AX), resulting in the recruitment of the DNA repair effectors 53BP1 and BRCA1. Here, by studying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors in BRCA1/2-deficient mammary tumours, we identify a function for γH2AX in orchestrating drug-induced replication fork degradation. Mechanistically, γH2AX-driven replication fork degradation is elicited by suppressing CtIP-mediated fork protection. As a result, H2AX loss restores replication fork stability and increases chemoresistance in BRCA1/2-deficient tumour cells without restoring homology-directed DNA repair, as highlighted by the lack of DNA damage-induced RAD51 foci. Furthermore, in the attempt to discover acquired genetic vulnerabilities, we find that ATM but not ATR inhibition overcomes PARP inhibitor (PARPi) resistance in H2AX-deficient tumours by interfering with CtIP-mediated fork protection. In summary, our results demonstrate a role for H2AX in replication fork biology in BRCA-deficient tumours and establish a function of H2AX separable from its classical role in DNA damage signalling and DSB repair. Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes phosphorylated on serine residue 139 (known as γH2AX), resulting in the recruitment of the DNA repair effectors 53BP1 and BRCA1. Here, by studying resistance to poly(ADP-ribose) polymerase (PARP) inhibitors in BRCA1/2-deficient mammary tumours, we identify a function for γH2AX in orchestrating drug-induced replication fork degradation. Mechanistically, γH2AX-driven replication fork degradation is elicited by suppressing CtIP-mediated fork protection. As a result, H2AX loss restores replication fork stability and increases chemoresistance in BRCA1/2-deficient tumour cells without restoring homology-directed DNA repair, as highlighted by the lack of DNA damage-induced RAD51 foci. Furthermore, in the attempt to discover acquired genetic vulnerabilities, we find that ATM but not ATR inhibition overcomes PARP inhibitor (PARPi) resistance in H2AX-deficient tumours by interfering with CtIP-mediated fork protection. In summary, our results demonstrate a role for H2AX in replication fork biology in BRCA-deficient tumours and establish a function of H2AX separable from its classical role in DNA damage signalling and DSB repair. |
| ArticleNumber | 4430 |
| Author | Sartori, Alessandro A. Rottenberg, Sven Gogola, Ewa Dibitetto, Diego González Fernández, Martín Duarte, Alexandra Dettwiler, Martina Dogan, Hülya Klebic, Ismar Sørensen, Claus S. Siffert, Myriam Tille, Jean-Christophe Lopes, Massimo Francica, Paola Vivalda, Francesca de Bruijn, Roebi Undurraga, Manuela Kousholt, Arne N. Labidi-Galy, Intidhar Marti, Nicole A. Schmid, Jonas A. Przetocka, Sara Durant, Stephen T. Liptay, Martin Forment, Josep V. Decollogny, Morgane Jonkers, Jos |
| Author_xml | – sequence: 1 givenname: Diego orcidid: 0000-0002-9549-5258 surname: Dibitetto fullname: Dibitetto, Diego email: diego.dibitetto@marionegri.it organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Cancer Therapy Resistance Cluster and Bern Center for Precision Medicine, Department for Biomedical Research, University of Bern, Department of Experimental Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS – sequence: 2 givenname: Martin surname: Liptay fullname: Liptay, Martin organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Cancer Therapy Resistance Cluster and Bern Center for Precision Medicine, Department for Biomedical Research, University of Bern – sequence: 3 givenname: Francesca orcidid: 0009-0008-5300-1505 surname: Vivalda fullname: Vivalda, Francesca organization: Institute of Molecular Cancer Research, University of Zürich – sequence: 4 givenname: Hülya surname: Dogan fullname: Dogan, Hülya organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Cancer Therapy Resistance Cluster and Bern Center for Precision Medicine, Department for Biomedical Research, University of Bern – sequence: 5 givenname: Ewa surname: Gogola fullname: Gogola, Ewa organization: Division of Molecular Pathology, The Netherlands Cancer Institute, Oncode Institute – sequence: 6 givenname: Martín orcidid: 0009-0006-8308-5493 surname: González Fernández fullname: González Fernández, Martín organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Cancer Therapy Resistance Cluster and Bern Center for Precision Medicine, Department for Biomedical Research, University of Bern – sequence: 7 givenname: Alexandra surname: Duarte fullname: Duarte, Alexandra organization: Division of Molecular Pathology, The Netherlands Cancer Institute, Oncode Institute – sequence: 8 givenname: Jonas A. orcidid: 0000-0003-1791-1874 surname: Schmid fullname: Schmid, 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sequence: 13 givenname: Josep V. surname: Forment fullname: Forment, Josep V. organization: DDR Biology, Bioscience, Oncology R&D, AstraZeneca – sequence: 14 givenname: Ismar surname: Klebic fullname: Klebic, Ismar organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern – sequence: 15 givenname: Myriam surname: Siffert fullname: Siffert, Myriam organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern – sequence: 16 givenname: Roebi surname: de Bruijn fullname: de Bruijn, Roebi organization: Division of Molecular Pathology, The Netherlands Cancer Institute, Oncode Institute – sequence: 17 givenname: Arne N. orcidid: 0000-0002-3972-1740 surname: Kousholt fullname: Kousholt, Arne N. organization: Oncode Institute, Biotech Research and Innovation Centre, University of Copenhagen – sequence: 18 givenname: Nicole A. surname: Marti fullname: Marti, Nicole A. organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Cancer Therapy Resistance Cluster and Bern Center for Precision Medicine, Department for Biomedical Research, University of Bern – sequence: 19 givenname: Martina surname: Dettwiler fullname: Dettwiler, Martina organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern – sequence: 20 givenname: Claus S. orcidid: 0000-0001-6022-9710 surname: Sørensen fullname: Sørensen, Claus S. organization: Biotech Research and Innovation Centre, University of Copenhagen – sequence: 21 givenname: Jean-Christophe surname: Tille fullname: Tille, Jean-Christophe organization: Division of Clinical Pathology, Department of Diagnostics, Hôpitaux Universitaires de Genève – sequence: 22 givenname: Manuela surname: Undurraga fullname: Undurraga, Manuela organization: Division of Gynecology, Department of Pediatrics and Gynecology, Hôpitaux Universitaires de Genève – sequence: 23 givenname: Intidhar orcidid: 0000-0002-0824-3475 surname: Labidi-Galy fullname: Labidi-Galy, Intidhar organization: Faculty of Medicine, Department of Medicine and Center of Translational Research in Onco-Hematology, University of Geneva, Swiss Cancer Center Leman, Department of Oncology, Hôpitaux Universitaires de Genève, 4, Rue Gabrielle Perret-Gentil – sequence: 24 givenname: Massimo orcidid: 0000-0003-3847-8133 surname: Lopes fullname: Lopes, Massimo organization: Institute of Molecular Cancer Research, University of Zürich – sequence: 25 givenname: Alessandro A. orcidid: 0000-0003-2770-0333 surname: Sartori fullname: Sartori, Alessandro A. organization: Institute of Molecular Cancer Research, University of Zürich – sequence: 26 givenname: Jos orcidid: 0000-0002-9264-9792 surname: Jonkers fullname: Jonkers, Jos email: j.jonkers@nki.nl organization: Division of Molecular Pathology, The Netherlands Cancer Institute, Oncode Institute – sequence: 27 givenname: Sven orcidid: 0000-0003-2044-9844 surname: Rottenberg fullname: Rottenberg, Sven email: sven.rottenberg@unibe.ch organization: Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, Cancer Therapy Resistance Cluster and Bern Center for Precision Medicine, Department for Biomedical Research, University of Bern, Division of Molecular Pathology, The Netherlands Cancer Institute |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38789420$$D View this record in MEDLINE/PubMed |
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| Snippet | Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX becomes... Abstract Histone H2AX plays a key role in DNA damage signalling in the surrounding regions of DNA double-strand breaks (DSBs). In response to DNA damage, H2AX... |
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| Title | H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours |
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