Xeroderma Pigmentosum Group A Protein Loads as a Separate Factor onto DNA Lesions

摘要: Nucleotide excision repair (NER) is the main DNA pathway in mammals for removal of UV-induced lesions. NER involves concerted action more than 25 polypeptides a coordinated fashion. The xeroderma pigmentosum group A protein (XPA) has been suggested to function as central organizer and damage verifier NER. How XPA reaches lesions how distributed time space living cells are unknown. Here we studied vivo by using cell line stably expressing physiological levels functional fused green fluorescent applying quantitative fluorescence microscopy. majority moves rapidly through nucleoplasm with diffusion rate different from those other factors tested, arguing against preassembled XPA-containing complex. induced transient ( approximately 5-min) immobilization maximally 30% XPA. Immobilization depends on XPC, indicating that not initial lesion recognition vivo. Moreover, loading replication was dependent Thus, participates incorporation free diffusing molecules XPC-dependent NER-DNA complexes. This study supports model rapid consecutive assembly factors, relatively slow simultaneous disassembly, after repair.