XPC-RAD23B enhances UV-DDB binding to DNA to facilitate lesion search in nucleotide excision repair.

ABSTRACT: Ultraviolet-induced DNA lesions are removed by the nucleotide excision repair (NER) pathway. In global-genome NER (GG-NER), XPC-RAD23B recognizes the lesions and initiates NER. However, cyclobutane pyrimidine dimers (CPDs), which do not significantly destabilize the DNA duplex, are not bound by XPC-RAD23B with high selectivity. Instead, CPD is preferentially sensed by UV-DDB, which is believed to hand over the lesion to XPC-RAD23B via ubiquitination of both proteins. Here, by combining biochemical and single-molecule DNA curtain assays, we investigate the interactions between UV-DDB and XPC-RAD23B on DNA. Surprisingly, we discover that XPC-RAD23B enhances the binding of UV-DDB to DNA. We demonstrate that this enhancement can be attributed to the complex formation of UV-DDB and XPC-RAD23B (

SUBMITTER: An S 

PROVIDER: S-EPMC12203913 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature