EZH2 promotes degradation of stalled replication forks by recruiting MUS81 through histone H3 trimethylation

Rondinelli et al. show that EZH2-mediated H3K27me3 at stalled replication forks recruits MUS81 nuclease to facilitate fork degradation. Loss of EZH2 contributes to PARPi resistance in BRCA2-deficient tumours. The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat...

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Vydáno v:	Nature cell biology Ročník 19; číslo 11; s. 1371 - 1378
Hlavní autoři:	Rondinelli, Beatrice, Gogola, Ewa, Yücel, Hatice, Duarte, Alexandra A., van de Ven, Marieke, van der Sluijs, Roxanne, Konstantinopoulos, Panagiotis A., Jonkers, Jos, Ceccaldi, Raphaël, Rottenberg, Sven, D’Andrea, Alan D.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London Nature Publishing Group UK 01.11.2017 Nature Publishing Group
Témata:	42/89 45/61 631/337/100/2285 631/337/1427 631/67 64/60 82/29 96/1 Adenosine diphosphate Analysis Animals Biomarkers Biomarkers, Tumor - metabolism BRCA mutations BRCA1 protein BRCA1 Protein - metabolism BRCA2 protein BRCA2 Protein - metabolism Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cancer Cancer Research Cell Biology Cell Line Cell Line, Tumor Chemoresistance Chemotherapy Control stability Deoxyribonucleic acid Developmental Biology DNA DNA biosynthesis DNA damage DNA replication DNA Replication - drug effects DNA Replication - genetics DNA-Binding Proteins - metabolism Drug Resistance, Neoplasm - genetics Endonucleases - metabolism Enhancer of Zeste Homolog 2 Protein - metabolism Female Genetic aspects Genomic Instability - drug effects Genomic Instability - genetics Genomics HEK293 Cells HeLa Cells Histone H3 Histones Histones - metabolism Humans letter Life Sciences Methylation Methylation - drug effects Mice Mice, Nude Nuclease Patient outcomes Physiological aspects Poly(ADP-ribose) Polymerase Inhibitors - pharmacology Recruitment Replication Replication forks Ribose Stabilization Stem Cells Tumors United States
ISSN:	1465-7392, 1476-4679, 1476-4679
On-line přístup:	Získat plný text
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Abstract	Rondinelli et al. show that EZH2-mediated H3K27me3 at stalled replication forks recruits MUS81 nuclease to facilitate fork degradation. Loss of EZH2 contributes to PARPi resistance in BRCA2-deficient tumours. The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours 1 . Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers 2 . Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease. Low EZH2 levels reduce H3K27 methylation, prevent MUS81 recruitment at stalled forks and cause fork stabilization. As a consequence, loss of function of the EZH2/MUS81 axis promotes PARPi resistance in BRCA2-deficient cells. Accordingly, low EZH2 or MUS81 expression levels predict chemoresistance and poor outcome in patients with BRCA2-mutated tumours. Moreover, inhibition of Ezh2 in a murine Brca2 −/− breast tumour model is associated with acquired PARPi resistance. Our findings identify EZH2 as a critical regulator of genomic stability at stalled forks that couples histone modifications to nuclease recruitment. Our data identify EZH2 expression as a biomarker of BRCA2-deficient tumour response to chemotherapy.
AbstractList	The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours. Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers. Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease. Low EZH2 levels reduce H3K27 methylation, prevent MUS81 recruitment at stalled forks and cause fork stabilization. As a consequence, loss of function of the EZH2/MUS81 axis promotes PARPi resistance in BRCA2-deficient cells. Accordingly, low EZH2 or MUS81 expression levels predict chemoresistance and poor outcome in patients with BRCA2-mutated tumours. Moreover, inhibition of Ezh2 in a murine Brca2-/- breast tumour model is associated with acquired PARPi resistance. Our findings identify EZH2 as a critical regulator of genomic stability at stalled forks that couples histone modifications to nuclease recruitment. Our data identify EZH2 expression as a biomarker of BRCA2-deficient tumour response to chemotherapy.The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours. Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers. Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease. Low EZH2 levels reduce H3K27 methylation, prevent MUS81 recruitment at stalled forks and cause fork stabilization. As a consequence, loss of function of the EZH2/MUS81 axis promotes PARPi resistance in BRCA2-deficient cells. Accordingly, low EZH2 or MUS81 expression levels predict chemoresistance and poor outcome in patients with BRCA2-mutated tumours. Moreover, inhibition of Ezh2 in a murine Brca2-/- breast tumour model is associated with acquired PARPi resistance. Our findings identify EZH2 as a critical regulator of genomic stability at stalled forks that couples histone modifications to nuclease recruitment. Our data identify EZH2 expression as a biomarker of BRCA2-deficient tumour response to chemotherapy. The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours. Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers. Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease. Low EZH2 levels reduce H3K27 methylation, prevent MUS81 recruitment at stalled forks and cause fork stabilization. As a consequence, loss of function of the EZH2/MUS81 axis promotes PARPi resistance in BRCA2-deficient cells. Accordingly, low EZH2 or MUS81 expression levels predict chemoresistance and poor outcome in patients with BRCA2-mutated tumours. Moreover, inhibition of Ezh2 in a murine Brca2 breast tumour model is associated with acquired PARPi resistance. Our findings identify EZH2 as a critical regulator of genomic stability at stalled forks that couples histone modifications to nuclease recruitment. Our data identify EZH2 expression as a biomarker of BRCA2-deficient tumour response to chemotherapy. Rondinelli et al. show that EZH2-mediated H3K27me3 at stalled replication forks recruits MUS81 nuclease to facilitate fork degradation. Loss of EZH2 contributes to PARPi resistance in BRCA2-deficient tumours. The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours 1 . Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers 2 . Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease. Low EZH2 levels reduce H3K27 methylation, prevent MUS81 recruitment at stalled forks and cause fork stabilization. As a consequence, loss of function of the EZH2/MUS81 axis promotes PARPi resistance in BRCA2-deficient cells. Accordingly, low EZH2 or MUS81 expression levels predict chemoresistance and poor outcome in patients with BRCA2-mutated tumours. Moreover, inhibition of Ezh2 in a murine Brca2 −/− breast tumour model is associated with acquired PARPi resistance. Our findings identify EZH2 as a critical regulator of genomic stability at stalled forks that couples histone modifications to nuclease recruitment. Our data identify EZH2 expression as a biomarker of BRCA2-deficient tumour response to chemotherapy. Rondinelli et al. show that EZH2-mediated H3K27me3 at stalled replication forks recruits MUS81 nuclease to facilitate fork degradation. Loss of EZH2 contributes to PARPi resistance in BRCA2-deficient tumours. The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours.sup.1. Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers.sup.2. Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease. Low EZH2 levels reduce H3K27 methylation, prevent MUS81 recruitment at stalled forks and cause fork stabilization. As a consequence, loss of function of the EZH2/MUS81 axis promotes PARPi resistance in BRCA2-deficient cells. Accordingly, low EZH2 or MUS81 expression levels predict chemoresistance and poor outcome in patients with BRCA2-mutated tumours. Moreover, inhibition of Ezh2 in a murine Brca2.sup.-/- breast tumour model is associated with acquired PARPi resistance. Our findings identify EZH2 as a critical regulator of genomic stability at stalled forks that couples histone modifications to nuclease recruitment. Our data identify EZH2 expression as a biomarker of BRCA2-deficient tumour response to chemotherapy. Rondinelli et al. show that EZH2-mediated H3K27me3 at stalled replication forks recruits MUS81 nuclease to facilitate fork degradation. Loss of EZH2 contributes to PARPi resistance in BRCA2-deficient tumours. The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours. Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers. Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease. Low EZH2 levels reduce H3K27 methylation, prevent MUS81 recruitment at stalled forks and cause fork stabilization. As a consequence, loss of function of the EZH2/MUS81 axis promotes PARPi resistance in BRCA2-deficient cells. Accordingly, low EZH2 or MUS81 expression levels predict chemoresistance and poor outcome in patients with BRCA2-mutated tumours. Moreover, inhibition of Ezh2 in a murine Brca2-/- breast tumour model is associated with acquired PARPi resistance. Our findings identify EZH2 as a critical regulator of genomic stability at stalled forks that couples histone modifications to nuclease recruitment. Our data identify EZH2 expression as a biomarker of BRCA2-deficient tumour response to chemotherapy.
Audience	Academic
Author	Ceccaldi, Raphaël Yücel, Hatice Jonkers, Jos Rottenberg, Sven Gogola, Ewa Konstantinopoulos, Panagiotis A. D’Andrea, Alan D. Duarte, Alexandra A. Rondinelli, Beatrice van der Sluijs, Roxanne van de Ven, Marieke
Author_xml	– sequence: 1 givenname: Beatrice surname: Rondinelli fullname: Rondinelli, Beatrice organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Center for DNA Damage and Repair, Dana-Farber Cancer Institute, Harvard Medical School – sequence: 2 givenname: Ewa surname: Gogola fullname: Gogola, Ewa organization: Division of Molecular Pathology and Cancer Genomics Netherlands, The Netherlands Cancer Institute – sequence: 3 givenname: Hatice surname: Yücel fullname: Yücel, Hatice organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School – sequence: 4 givenname: Alexandra A. surname: Duarte fullname: Duarte, Alexandra A. organization: Division of Molecular Pathology and Cancer Genomics Netherlands, The Netherlands Cancer Institute – sequence: 5 givenname: Marieke surname: van de Ven fullname: van de Ven, Marieke organization: Mouse Clinic for Cancer and Aging (MCCA), Preclinical Intervention Unit, The Netherlands Cancer Institute – sequence: 6 givenname: Roxanne surname: van der Sluijs fullname: van der Sluijs, Roxanne organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, University of Amsterdam – sequence: 7 givenname: Panagiotis A. surname: Konstantinopoulos fullname: Konstantinopoulos, Panagiotis A. organization: Center for DNA Damage and Repair, Dana-Farber Cancer Institute, Harvard Medical School, Department of Medical Oncology, Medical Gynecologic Oncology Program, Dana-Farber Cancer Institute, Harvard Medical School – sequence: 8 givenname: Jos surname: Jonkers fullname: Jonkers, Jos organization: Division of Molecular Pathology and Cancer Genomics Netherlands, The Netherlands Cancer Institute – sequence: 9 givenname: Raphaël surname: Ceccaldi fullname: Ceccaldi, Raphaël organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Center for DNA Damage and Repair, Dana-Farber Cancer Institute, Harvard Medical School – sequence: 10 givenname: Sven surname: Rottenberg fullname: Rottenberg, Sven organization: Division of Molecular Pathology and Cancer Genomics Netherlands, The Netherlands Cancer Institute, Institute of Animal Pathology, Vetsuisse Faculty, University of Bern – sequence: 11 givenname: Alan D. orcidid: 0000-0001-6168-6294 surname: D’Andrea fullname: D’Andrea, Alan D. email: alan_dandrea@dfci.harvard.edu organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Center for DNA Damage and Repair, Dana-Farber Cancer Institute, Harvard Medical School
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29035360$$D View this record in MEDLINE/PubMed
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Snippet	Rondinelli et al. show that EZH2-mediated H3K27me3 at stalled replication forks recruits MUS81 nuclease to facilitate fork degradation. Loss of EZH2... The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours.... Rondinelli et al. show that EZH2-mediated H3K27me3 at stalled replication forks recruits MUS81 nuclease to facilitate fork degradation. Loss of EZH2...
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SubjectTerms	42/89 45/61 631/337/100/2285 631/337/1427 631/67 64/60 82/29 96/1 Adenosine diphosphate Analysis Animals Biomarkers Biomarkers, Tumor - metabolism BRCA mutations BRCA1 protein BRCA1 Protein - metabolism BRCA2 protein BRCA2 Protein - metabolism Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cancer Cancer Research Cell Biology Cell Line Cell Line, Tumor Chemoresistance Chemotherapy Control stability Deoxyribonucleic acid Developmental Biology DNA DNA biosynthesis DNA damage DNA replication DNA Replication - drug effects DNA Replication - genetics DNA-Binding Proteins - metabolism Drug Resistance, Neoplasm - genetics Endonucleases - metabolism Enhancer of Zeste Homolog 2 Protein - metabolism Female Genetic aspects Genomic Instability - drug effects Genomic Instability - genetics Genomics HEK293 Cells HeLa Cells Histone H3 Histones Histones - metabolism Humans letter Life Sciences Methylation Methylation - drug effects Mice Mice, Nude Nuclease Patient outcomes Physiological aspects Poly(ADP-ribose) Polymerase Inhibitors - pharmacology Recruitment Replication Replication forks Ribose Stabilization Stem Cells Tumors
Title	EZH2 promotes degradation of stalled replication forks by recruiting MUS81 through histone H3 trimethylation
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