Nucleic Acids Research, Vol 27, Issue 14 2868-2874, Copyright © 1999 by Oxford University Press
M Lombaerts, M Tijsterman, JA Brandsma, RA Verhage and J Brouwer
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.
ARTICLES
Removal of cyclobutane pyrimidine dimers by the UV damage repair and nucleotide excision repair pathways of Schizosaccharomyces pombe at nucleotide resolution
Medical Genetic Centre, Department of Molecular Genetics, Leiden Institute of Chemistry, Gorlaeus Laboratories, Leiden University, PO Box 9502, 2300 RA Leiden, The Netherlands.
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