Removal of cyclobutane pyrimidine dimers by the UV damage repair and nucleotide excision repair pathways of Schizosaccharomyces pombe at nucleotide resolution

In Schizosaccharomyces pombe two different repair mechanisms remove UV-indu ced lesions from DNA, i.e. nucleotide excision repair (NER) and UV damage r epair (UVDR), Here, the kinetics of removal of cyclobutane pyrimidine dimer s (CPDs) by both pathways is determined at base resolution in the transcrib ed strand (TS) and the non-transcribed strand (NTS) of the sprpb2(+) gene. UVDR does not remove lesions in a strand-specific manner, indicating that U VDR is neither stimulated nor inhibited by RNA polymerase II transcription. In contrast, in a UVDR-deficient strain the TS is repaired preferentially. This strong strand bias suggests that in S. pombe, as in other species, NE R is coupled to transcription. In repair-proficient S,pombe the TS is repai red very rapidly, as a consequence of two efficiently operating pathways, w hile the NTS is repaired more slowly, mainly by UVDR, Furthermore, we demon strate that UVDR is not always faster than NER.