Transcription-coupled repair is inducible in hamster cells

In mammalian cells, the rate of nucleotide excision repair of UV dimers is heterogeneous throughout the genome, with repair occurring more rapidly in the transcribed strand of active genes than in the genome overall. This rep air pathway is termed transcription-coupled repair (TCR) and is thought to permit the rapid resumption of RNA synthesis following UV irradiation. To e valuate the inducibility of the TCR process, we examined the repair of UV-i nduced cyclobutane pyrimidine dimers (CPDs) at the level of the gene follow ing exposure of hamster cells to a sub-lethal UV fluence, 3 h prior to a hi gher dose. Repair was detected by a well-established technique allowing qua ntification of CPDs at the level of a specific strand by Southern blot hybr idization. Here, we show that prior low-dose irradiation clearly enhanced t he early rate of CPD removal in the transcribed strand of the active DHFR g ene. Furthermore, the RNA synthesis recovery following UV exposure was stim ulated by the priming UV dose. Thus, we provide evidence for an inducible T CR response to CPDs in hamster cells. This pathway is independent of the p5 3 activation, since the hamster cell line that we used expresses high level s of mutant p53 protein.