In Schizosaccharomyces pombe two different repair mechanisms remove UV-induced lesions from DNA, i.e. nucleotide excision repair (NER) and UV damage repair (UVDR). Here, the kinetics of removal of cyclobutane pyrimidine dimers (CPDs) by both pathways is determined at base resolution in the transcribed strand (TS) and the non-transcribed strand (NTS) of the sprpb2 +gene. UVDR does not remove lesions in a strand-specific manner, indicating that UVDR 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, NER is coupled to transcription. In repair-proficient S.pombe the TS is repaired very rapidly, as a consequence of two efficiently operating pathways, while the NTS is repaired more slowly, mainly by UVDR. Furthermore, we demonstrate that UVDR is not always faster than NER.