Telomere shortening by cisplatin in yeast nucleotide excision repair mutant

Telomeres are unique DNA tandem repeats that form the ends of eukaryotic ch romosomes to protect the chromosomes from degradation and illegitimate reco mbination. In yeast, loss of telomere may be compensated for through the ac quisition of new telomere by RAD52-mediated or RAD52-independent recombinat ional repair. In this report, the effects of cis-dichlorodiammine-platinum (II) (cisplatin) on telomere length and the role of nucleotide excision rep air in telomere maintenance were examined in the yeast Saccharomyces cerevi siae. We showed that the SSL2 (RAD25) DNA repair yeast mutant exhibited a g radual shortening of the telomere in the presence of cisplatin. Further tel omere shortening was prevented upon the withdrawal of cisplatin. Complement ation of the mutant with the wild-type SSL2 (RAD25) gene abolished the cisp latin-induced telomere degradation. These results suggest that telomeres ar e susceptible to cisplatin-induced intrastrand crosslinks and that SsI2 (Ra d25) or the nucleotide excision repair pathway may play a critical role in the repair and the maintenance of telomere integrity, (C) 2000 Academic Pre ss.