Abstract
Nucleotide-excision repair (NER) and mismatch repair (MMR) are prominent examples of highly conserved DNA repair systems which recognize and replace damaged and/or mispaired nucleotides in DNA. In humans, inheritable defects in components of the NER system are associated with severe diseases such as xeroderma pigmentosum (XP) and Cockayne syndrome1 (CS), whereas inactivation of MMR is accompanied by predisposition to certain types of cancer2. In Schizosaccharomyces pombe, the msh2- and pms1-dependent long-patch MMR system efficiently corrects small insertion/deletion loops and all base-base mismatches, except C/C. Up to 70% of C/C mismatches generated in recombination intermediates, and to a lesser extent also other base-base mismatches, are thought to undergo correction by a minor, short-patch excision repair system3,4. We identify here the NER genes rhp14, swi10 and rad16 as components of this repair pathway and show that they act independently of msh2 and pms1.
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Acknowledgements
This work was supported by the Swiss National Science Foundation and a fellowship of the Deutsche Forschungsgemeinschaft to O.F.
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Fleck, O., Lehmann, E., Schär, P. et al. Involvement of nucleotide-excision repair in msh2 pms1-independent mismatch repair. Nat Genet 21, 314–317 (1999). https://doi.org/10.1038/6838
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DOI: https://doi.org/10.1038/6838
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