Repair of Chromosomal Damage : Transcription-Coupled DNA Repair and Its Disorders(Symposium : Manipulating Chromosomes)(Abstracts of the 52nd Annual Meeting of the Society of Chromosome Research)

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Transcription-coupled DNA repair (TCR) efficiently removes a variety of lesions from the transcribed strand of active genes. By allowing rapid resumption of RNA synthesis, the process is of major importance for cellular resistance to transcription-blocking genotoxic damage. Mutations in the Cockayne syndrome group A or B (CSA or CSB) gene result in defective TCR. However, the exact mechanism of TCR in mammalian cells remains to be elucidated. We found a protein designated XAB2 that mainly consists of 15 tetratricopeptide repeats and interacts with XPA (xeroderma pignentosum group A) and TCR-specific proteins CSA, CSB and RNA polymerase II. Antibodies against XAB2 inhibited both TCR and transcription in vivo when microinjected into living fibroblasts. These results indicate that XAB2 is a component involved in TCR and transcription. We also found that CSA protein was rapidly translocated to the nuclear matrix after UV irradiation. The translocation of CSA required the CSB protein. In UV-irradiated cells, CSA protein co-localized with the hyperphosphorylated form of RNA polymerase II that is engaged in transcription elongation. These findings establish a link between TCR and the nuclear matrix mediated by CSA. We also found that the mice lacking both the XPA and CSB genes displayed marked structural abnormalities in cerebellum, reduced neurogenesis and increased apoptotic cell death in the cerebellar external granular layer. These results suggest that XPA and CSB have additive roles in the developing mouse nervous system.
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Repair of Chromosomal Damage : Transcription-Coupled DNA Repair and Its Disorders(Symposium : Manipulating Chromosomes)(Abstracts of the 52nd Annual Meeting of the Society of Chromosome Research)

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