Protection of internal (TTAGGG)n repeats in Chinese hamster cells by telomeric protein TRF1.

Raisa Ivanovna Krutilina, Alexandra Nikolaevna Smirnova, Olga Stanislavovna Mudrak, Nadezhda Mikhailovna Pleskach, Maria Pavlovna Svetlova, Shiao Li Oei, Peter M. Yau, Edwin Morton Bradbury, Andrey Olegovich Zalensky, Nikolai Viktorovich Tomilin

Research output: Contribution to journalArticlepeer-review


Chinese hamster cells have large interstitial (TTAGGG) bands (ITs) which are unstable and should be protected by an unknown mechanism. Here, we expressed in Chinese hamster V79 cells green fluorescent protein (GFP)-tagged human TRF1, and found that a major fraction of GFP-TRF1 bound to ITs is diffusionally mobile. This fraction strongly decreases after treatment of cells with wortmannin, a protein kinase inhibitor, and this drug also increases the frequency of chromosome aberrations. Ionizing radiation does not induce detectable translocation of GFP-TRF1 to the sites of random double-strand breaks visualized using antibodies against histone gamma-H2AX. TRF1 is known to be eliminated from telomeres by overexpression of tankyrase 1 which induces TRF1 poly(ADP-ribosyl)ation. We transfected V79 cells by plasmid encoding tankyrase 1 and found that the frequency of chromosome rearrangements is increased in these cells independently of their treatment by IR. Taken together, our results suggest that TRF1 is involved in sequence-specific protection of internal nontelomeric (TTAGGG)n repeats.

Original languageEnglish
Pages (from-to)6690-6698
Number of pages9
Issue number43
Publication statusPublished - Oct 2 2003

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

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