TRIP13 regulates DNA repair pathway choice through REV7 conformational change
DNA double-strand breaks (DSBs) are repaired through homology-directed repair (HDR) or non-homologous end joining (NHEJ). BRCA1/2-deficient cancer cells cannot perform HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi). However, concomitant loss of the pro-NHEJ factors 53B...
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| Vydáno v: | Nature cell biology Ročník 22; číslo 1; s. 87 - 96 |
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| Hlavní autoři: | , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Nature Publishing Group
01.01.2020
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| ISSN: | 1465-7392, 1476-4679, 1476-4679 |
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| Abstract | DNA double-strand breaks (DSBs) are repaired through homology-directed repair (HDR) or non-homologous end joining (NHEJ). BRCA1/2-deficient cancer cells cannot perform HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi). However, concomitant loss of the pro-NHEJ factors 53BP1, RIF1, REV7-Shieldin (SHLD1-3) or CST-DNA polymerase alpha (Pol-α) in BRCA1-deficient cells restores HDR and PARPi resistance. Here, we identify the TRIP13 ATPase as a negative regulator of REV7. We show that REV7 exists in active 'closed' and inactive 'open' conformations, and TRIP13 catalyses the inactivating conformational change, thereby dissociating REV7-Shieldin to promote HDR. TRIP13 similarly disassembles the REV7-REV3 translesion synthesis (TLS) complex, a component of the Fanconi anaemia pathway, inhibiting error-prone replicative lesion bypass and interstrand crosslink repair. Importantly, TRIP13 overexpression is common in BRCA1-deficient cancers, confers PARPi resistance and correlates with poor prognosis. Thus, TRIP13 emerges as an important regulator of DNA repair pathway choice-promoting HDR, while suppressing NHEJ and TLS. |
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| AbstractList | DNA double-strand breaks (DSBs) are repaired through homology-directed repair (HDR) or non-homologous end joining (NHEJ). BRCA1/2-deficient cancer cells cannot perform HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi). However, concomitant loss of the pro-NHEJ factors 53BP1, RIF1, REV7-Shieldin (SHLD1-3) or CST-DNA polymerase alpha (Pol-α) in BRCA1-deficient cells restores HDR and PARPi resistance. Here, we identify the TRIP13 ATPase as a negative regulator of REV7. We show that REV7 exists in active 'closed' and inactive 'open' conformations, and TRIP13 catalyses the inactivating conformational change, thereby dissociating REV7-Shieldin to promote HDR. TRIP13 similarly disassembles the REV7-REV3 translesion synthesis (TLS) complex, a component of the Fanconi anaemia pathway, inhibiting error-prone replicative lesion bypass and interstrand crosslink repair. Importantly, TRIP13 overexpression is common in BRCA1-deficient cancers, confers PARPi resistance and correlates with poor prognosis. Thus, TRIP13 emerges as an important regulator of DNA repair pathway choice-promoting HDR, while suppressing NHEJ and TLS.DNA double-strand breaks (DSBs) are repaired through homology-directed repair (HDR) or non-homologous end joining (NHEJ). BRCA1/2-deficient cancer cells cannot perform HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi). However, concomitant loss of the pro-NHEJ factors 53BP1, RIF1, REV7-Shieldin (SHLD1-3) or CST-DNA polymerase alpha (Pol-α) in BRCA1-deficient cells restores HDR and PARPi resistance. Here, we identify the TRIP13 ATPase as a negative regulator of REV7. We show that REV7 exists in active 'closed' and inactive 'open' conformations, and TRIP13 catalyses the inactivating conformational change, thereby dissociating REV7-Shieldin to promote HDR. TRIP13 similarly disassembles the REV7-REV3 translesion synthesis (TLS) complex, a component of the Fanconi anaemia pathway, inhibiting error-prone replicative lesion bypass and interstrand crosslink repair. Importantly, TRIP13 overexpression is common in BRCA1-deficient cancers, confers PARPi resistance and correlates with poor prognosis. Thus, TRIP13 emerges as an important regulator of DNA repair pathway choice-promoting HDR, while suppressing NHEJ and TLS. DNA double-strand breaks (DSBs) are repaired through homology-directed repair (HDR) or non-homologous end joining (NHEJ). BRCA1/2-deficient cancer cells cannot perform HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi). However, concomitant loss of the pro-NHEJ factors 53BP1, RIF1, REV7-Shieldin (SHLD1-3) or CST-DNA polymerase alpha (Pol-α) in BRCA1-deficient cells restores HDR and PARPi resistance. Here, we identify the TRIP13 ATPase as a negative regulator of REV7. We show that REV7 exists in active 'closed' and inactive 'open' conformations, and TRIP13 catalyses the inactivating conformational change, thereby dissociating REV7-Shieldin to promote HDR. TRIP13 similarly disassembles the REV7-REV3 translesion synthesis (TLS) complex, a component of the Fanconi anaemia pathway, inhibiting error-prone replicative lesion bypass and interstrand crosslink repair. Importantly, TRIP13 overexpression is common in BRCA1-deficient cancers, confers PARPi resistance and correlates with poor prognosis. Thus, TRIP13 emerges as an important regulator of DNA repair pathway choice-promoting HDR, while suppressing NHEJ and TLS. DNA double-strand breaks (DSBs) are repaired through homology-directed repair (HDR) or non-homologous end joining (NHEJ). BRCA1/2-deficient cancer cells cannot perform HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi). However, concomitant loss of the pro-NHEJ factors 53BP1, RIF1, REV7–Shieldin (SHLD1–3) or CST–DNA polymerase alpha (Pol-α) in BRCA1-deficient cells restores HDR and PARPi resistance. Here, we identify the TRIP13 ATPase as a negative regulator of REV7. We show that REV7 exists in active ‘closed’ and inactive ‘open’ conformations, and TRIP13 catalyses the inactivating conformational change, thereby dissociating REV7–Shieldin to promote HDR. TRIP13 similarly disassembles the REV7–REV3 translesion synthesis (TLS) complex, a component of the Fanconi anaemia pathway, inhibiting error-prone replicative lesion bypass and interstrand crosslink repair. Importantly, TRIP13 overexpression is common in BRCA1-deficient cancers, confers PARPi resistance and correlates with poor prognosis. Thus, TRIP13 emerges as an important regulator of DNA repair pathway choice—promoting HDR, while suppressing NHEJ and TLS.Clairmont et al. find that the TRIP13 ATPase regulates REV7–Shieldin dissociation to promote homology-directed repair and suppress non-homologous end joining, and show the importance of PARPi resistance in BRCA1-deficient cancers. |
| Author | Galli, Lucas D Chowdhury, Dipanjan Csete, Isabelle Adelmant, Guillaume Marto, Jarrod A Sarangi, Prabha D'Andrea, Alan D Clairmont, Connor S Ponnienselvan, Karthikeyan Moreau, Lisa |
| Author_xml | – sequence: 1 givenname: Connor S surname: Clairmont fullname: Clairmont, Connor S organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA – sequence: 2 givenname: Prabha surname: Sarangi fullname: Sarangi, Prabha organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA – sequence: 3 givenname: Karthikeyan surname: Ponnienselvan fullname: Ponnienselvan, Karthikeyan organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA – sequence: 4 givenname: Lucas D surname: Galli fullname: Galli, Lucas D organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA – sequence: 5 givenname: Isabelle surname: Csete fullname: Csete, Isabelle organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA – sequence: 6 givenname: Lisa surname: Moreau fullname: Moreau, Lisa organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA – sequence: 7 givenname: Guillaume orcidid: 0000-0003-4075-5486 surname: Adelmant fullname: Adelmant, Guillaume organization: Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA – sequence: 8 givenname: Dipanjan orcidid: 0000-0001-5645-3752 surname: Chowdhury fullname: Chowdhury, Dipanjan organization: Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA, USA – sequence: 9 givenname: Jarrod A orcidid: 0000-0003-2086-1134 surname: Marto fullname: Marto, Jarrod A organization: Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA – sequence: 10 givenname: Alan D orcidid: 0000-0001-6168-6294 surname: D'Andrea fullname: D'Andrea, Alan D email: Alan_Dandrea@dfci.harvard.edu, Alan_Dandrea@dfci.harvard.edu organization: Center for DNA Damage and Repair, Dana-Farber Cancer Institute, Boston, MA, USA. Alan_Dandrea@dfci.harvard.edu |
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| SubjectTerms | Adenosine diphosphate Adenosine triphosphatase Anemia ATPases Associated with Diverse Cellular Activities - drug effects ATPases Associated with Diverse Cellular Activities - genetics BRCA1 protein BRCA1 Protein - deficiency Breast cancer Cell Cycle Proteins - drug effects Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Crosslinking Deoxyribonucleic acid Dismantling DNA DNA damage DNA Damage - drug effects DNA End-Joining Repair - genetics DNA polymerase DNA repair DNA Repair - drug effects DNA Repair - genetics DNA Replication - drug effects DNA Replication - genetics DNA-directed DNA polymerase Homology Humans Mad2 Proteins - genetics Non-homologous end joining Poly(ADP-ribose) Poly(ADP-ribose) polymerase Poly(ADP-ribose) Polymerase Inhibitors - pharmacology Recombinational DNA Repair - genetics Repair Ribose Telomere-Binding Proteins - drug effects Telomere-Binding Proteins - genetics |
| Title | TRIP13 regulates DNA repair pathway choice through REV7 conformational change |
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