Mammalian PERIOD complex regulates repair of DSB in active chromatin through anchoring to the nuclear envelope

ABSTRACT: Repair of DNA Double Strand Breaks produced in transcriptionally active chromatin occurs through a mechanism, Transcription-Coupled DSB repair (TC-DSBR), that is yet poorly characterized. Here, using a screening approach scoring multiple outputs in human cells, we identified the PER complex, a key module ensuring circadian oscillations, as a novel TC-DSBR player, being enriched at DSB occurring in transcribed loci, as compared to DSB induced in un-transcribed loci. We further found that PER2 contributes to target TC-DSBs at the nuclear envelope (NE) and to foster Rad51- mediated repair. PER2 deficiency triggers decreased DSB anchoring to NE, resulting in an increase of DSB clustering, checkpoint activation and translocation frequency. In agreement, we found that the circadian clock also re

INSTRUMENT(S): NextSeq 500, NextSeq 2000

ORGANISM(S): Homo sapiens

SUBMITTER: Vincent ROCHER 

PROVIDER: E-MTAB-12712 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress