Transcription Dependence and the Roles of Two Excision Repair Pathways for UV Damage in Fission Yeast Schizosaccharomyces pombe

Abstract

Fission yeasts Schizosaccharomyces pombe possess two types of excision repair systems for UV-induced DNA damage, nucleotide excision repair (NER) and UV-damaged DNA endonuclease (UVDE)-dependent excision repair (UVER). Despite its high efficiency in damage removal, UVER defects have less effect on UV survival than NER defects. To understand the differential roles of two pathways, we examined strand-specific damage removal at the myo2 and rpb2 loci. Although NER removes cyclobutane pyrimidine dimers from the transcribed strand more rapidly than from the nontranscribed strand, UVER repairs cyclobutane pyrimidine dimers equally on both strands and at a much higher rate than NER. The low rate of damage removal from the nontranscribed strand in the absence of UVER indicates inefficient global genome repair (GGR) in this organism and a possible function of UVER as an alternative to GGR. Disruption of rhp26, the S. pombe homolog of CSB/RAD26, eliminated the strand bias of NER almost completely and resulted in a significant increase of UV sensitivity of cells in a uvdeDelta background. We suggest that the combination of transcription-coupled repair of NER and rapid UVER contributes to UV survival in growing S. pombe cells, which is accomplished by transcription-coupled repair and GGR in other organisms.