dc.contributor.author | Zelceski, A | |
dc.contributor.author | Francica, P | |
dc.contributor.author | Lingg, L | |
dc.contributor.author | Mutlu, M | |
dc.contributor.author | Stok, C | |
dc.contributor.author | Liptay, M | |
dc.contributor.author | Alexander, J | |
dc.contributor.author | Baxter, JS | |
dc.contributor.author | Brough, R | |
dc.contributor.author | Gulati, A | |
dc.contributor.author | Haider, S | |
dc.contributor.author | Raghunandan, M | |
dc.contributor.author | Song, F | |
dc.contributor.author | Sridhar, S | |
dc.contributor.author | Forment, JV | |
dc.contributor.author | O'Connor, MJ | |
dc.contributor.author | Davies, BR | |
dc.contributor.author | van Vugt, MATM | |
dc.contributor.author | Krastev, DB | |
dc.contributor.author | Pettitt, SJ | |
dc.contributor.author | Tutt, ANJ | |
dc.contributor.author | Rottenberg, S | |
dc.contributor.author | Lord, CJ | |
dc.coverage.spatial | United States | |
dc.date.accessioned | 2023-08-01T15:00:08Z | |
dc.date.available | 2023-08-01T15:00:08Z | |
dc.date.issued | 2023-05-30 | |
dc.identifier | ARTN 112484 | |
dc.identifier | S2211-1247(23)00495-3 | |
dc.identifier.citation | Cell Reports, 2023, 42 (5), pp. 112484 - | |
dc.identifier.issn | 2211-1247 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/5918 | |
dc.identifier.eissn | 2211-1247 | |
dc.identifier.eissn | 2211-1247 | |
dc.identifier.eissn | 2211-1247 | |
dc.identifier.eissn | 2211-1247 | |
dc.identifier.doi | 10.1016/j.celrep.2023.112484 | |
dc.description.abstract | The PSMC3IP-MND1 heterodimer promotes meiotic D loop formation before DNA strand exchange. In genome-scale CRISPR-Cas9 mutagenesis and interference screens in mitotic cells, depletion of PSMC3IP or MND1 causes sensitivity to poly (ADP-Ribose) polymerase inhibitors (PARPi) used in cancer treatment. PSMC3IP or MND1 depletion also causes ionizing radiation sensitivity. These effects are independent of PSMC3IP/MND1's role in mitotic alternative lengthening of telomeres. PSMC3IP- or MND1-depleted cells accumulate toxic RAD51 foci in response to DNA damage, show impaired homology-directed DNA repair, and become PARPi sensitive, even in cells lacking both BRCA1 and TP53BP1. Epistasis between PSMC3IP-MND1 and BRCA1/BRCA2 defects suggest that abrogated D loop formation is the cause of PARPi sensitivity. Wild-type PSMC3IP reverses PARPi sensitivity, whereas a PSMC3IP p.Glu201del mutant associated with D loop defects and ovarian dysgenesis does not. These observations suggest that meiotic proteins such as MND1 and PSMC3IP have a greater role in mitotic DNA repair. | |
dc.format | Print-Electronic | |
dc.format.extent | 112484 - | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | CELL PRESS | |
dc.relation.ispartof | Cell Reports | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.subject | CP: Molecular biology | |
dc.subject | DNA repair | |
dc.subject | MND1 | |
dc.subject | PARP inhibitor | |
dc.subject | PSMC3IP | |
dc.subject | PSMC3IP and PARPi sensitivity | |
dc.subject | Poly(ADP-ribose) Polymerase Inhibitors | |
dc.subject | Antineoplastic Agents | |
dc.subject | DNA Repair | |
dc.subject | DNA Damage | |
dc.subject | BRCA1 Protein | |
dc.subject | Recombinational DNA Repair | |
dc.subject | Cell Line, Tumor | |
dc.title | MND1 and PSMC3IP control PARP inhibitor sensitivity in mitotic cells. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2023-04-24 | |
dc.date.updated | 2023-08-01T14:59:24Z | |
rioxxterms.version | VoR | |
rioxxterms.versionofrecord | 10.1016/j.celrep.2023.112484 | |
rioxxterms.licenseref.startdate | 2023-05-30 | |
rioxxterms.type | Journal Article/Review | |
pubs.author-url | https://www.ncbi.nlm.nih.gov/pubmed/37163373 | |
pubs.issue | 5 | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research/Gene Function | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Gene Function | |
pubs.publication-status | Published | |
pubs.publisher-url | http://dx.doi.org/10.1016/j.celrep.2023.112484 | |
pubs.volume | 42 | |
icr.researchteam | Gene Function | |
dc.contributor.icrauthor | Haider, Syed | |
dc.contributor.icrauthor | Song, Feifei | |
dc.contributor.icrauthor | Pettitt, Stephen | |
dc.contributor.icrauthor | Tutt, Andrew | |
dc.contributor.icrauthor | Lord, Christopher | |
icr.provenance | Deposited by Mr Arek Surman (impersonating Prof Richard Houlston) on 2023-08-01. Deposit type is initial. No. of files: 1. Files: 1-s2.0-S2211124723004953-main.pdf | |