Telomere shortening by cisplatin in yeast nucleotide excision repair mutant

Kenji Ishii, Weng Lang Yang, Mary Ellen Cvijic, Yoshihiro Kikuchi, Ichiro Nagata, Khew Voon Chin

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Telomeres are unique DNA tandem repeats that form the ends of eukaryotic chromosomes to protect the chromosomes from degradation and illegitimate recombination. In yeast, loss of telomere may be compensated for through the acquisition of new telomere by RAD52-mediated or RAD52-independent recombinational repair. In this report, the effects of cis-dichlorodiammine- platinum (II) (cisplatin) on telomere length and the role of nucleotide excision repair in telomere maintenance were examined in the yeast Saccharomyces cerevisiae. We showed that the SSL2 (RAD25) DNA repair yeast mutant exhibited a gradual shortening of the telomere in the presence of cisplatin. Further telomere shortening was prevented upon the withdrawal of cisplatin. Complementation of the mutant with the wild-type SSL2 (RAD25) gene abolished the cisplatin-induced telomere degradation. These results suggest that telomeres are susceptible to cisplatin-induced intrastrand crosslinks and that Ssl2 (Rad25) or the nucleotide excision repair pathway may play a critical role in the repair and the maintenance of telomere integrity. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)95-101
Number of pages7
JournalExperimental Cell Research
Issue number1
StatePublished - Feb 25 2000
Externally publishedYes


  • Cisplatin
  • Nucleotide excision repair
  • SSL2 (RAD25)
  • Saccharomyces cerevisiae
  • Telomere

ASJC Scopus subject areas

  • Cell Biology


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