TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A.

ABSTRACT: Transcription-blocking DNA lesions are removed by transcription-coupled nucleotide excision repair (TC-NER) to preserve cell viability. TC-NER is triggered by the stalling of RNA polymerase II at DNA lesions, leading to the recruitment of TC-NER-specific factors such as the CSA-DDB1-CUL4A-RBX1 cullin-RING ubiquitin ligase complex (CRL^CSA). Despite its vital role in TC-NER, little is known about the regulation of the CRL^CSA complex during TC-NER. Using conventional and cross-linking immunoprecipitations coupled to mass spectrometry, we uncover a stable interaction between CSA and the TRiC chaperonin. TRiC's binding to CSA ensures its stability and DDB1-dependent assembly into the CRL^CSA complex. Consequently, loss of TRiC leads to mislocalization and depleti

SUBMITTER: Pines A 

PROVIDER: S-EPMC5847541 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature