dc.contributor.author | Kakarougkas, A | |
dc.contributor.author | Ismail, A | |
dc.contributor.author | Chambers, AL | |
dc.contributor.author | Riballo, E | |
dc.contributor.author | Herbert, AD | |
dc.contributor.author | Künzel, J | |
dc.contributor.author | Löbrich, M | |
dc.contributor.author | Jeggo, PA | |
dc.contributor.author | Downs, JA | |
dc.date.accessioned | 2020-08-13T11:44:55Z | |
dc.date.issued | 2014-09-04 | |
dc.identifier.citation | Molecular cell, 2014, 55 (5), pp. 723 - 732 | |
dc.identifier.issn | 1097-2765 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/3951 | |
dc.identifier.eissn | 1097-4164 | |
dc.identifier.doi | 10.1016/j.molcel.2014.06.028 | |
dc.description.abstract | Actively transcribed regions of the genome are vulnerable to genomic instability. Recently, it was discovered that transcription is repressed in response to neighboring DNA double-strand breaks (DSBs). It is not known whether a failure to silence transcription flanking DSBs has any impact on DNA repair efficiency or whether chromatin remodelers contribute to the process. Here, we show that the PBAF remodeling complex is important for DSB-induced transcriptional silencing and promotes repair of a subset of DNA DSBs at early time points, which can be rescued by inhibiting transcription globally. An ATM phosphorylation site on BAF180, a PBAF subunit, is required for both processes. Furthermore, we find that subunits of the PRC1 and PRC2 polycomb group complexes are similarly required for DSB-induced silencing and promoting repair. Cancer-associated BAF180 mutants are unable to restore these functions, suggesting PBAF's role in repressing transcription near DSBs may contribute to its tumor suppressor activity. | |
dc.format | Print-Electronic | |
dc.format.extent | 723 - 732 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | CELL PRESS | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | |
dc.subject | Cell Line, Tumor | |
dc.subject | Hela Cells | |
dc.subject | Humans | |
dc.subject | Nuclear Proteins | |
dc.subject | Chromosomal Proteins, Non-Histone | |
dc.subject | Histones | |
dc.subject | Transcription Factors | |
dc.subject | DNA Repair | |
dc.subject | Gene Expression Regulation | |
dc.subject | Binding Sites | |
dc.subject | Phosphorylation | |
dc.subject | DNA Breaks | |
dc.subject | Ubiquitination | |
dc.subject | DNA End-Joining Repair | |
dc.title | Requirement for PBAF in transcriptional repression and repair at DNA breaks in actively transcribed regions of chromatin. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2014-06-19 | |
rioxxterms.versionofrecord | 10.1016/j.molcel.2014.06.028 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by/4.0 | |
rioxxterms.licenseref.startdate | 2014-09 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Molecular cell | |
pubs.issue | 5 | |
pubs.notes | Not known | |
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/Cancer Biology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Biology/Epigenetics and Genome Stability | |
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/Cancer Biology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Biology/Epigenetics and Genome Stability | |
pubs.publication-status | Published | |
pubs.volume | 55 | |
pubs.embargo.terms | Not known | |
icr.researchteam | Epigenetics and Genome Stability | |
dc.contributor.icrauthor | Downs, Jessica | |