Nature Communications (May 2019)

The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT)

  • Robert Lu,
  • Julienne J. O’Rourke,
  • Alexander P. Sobinoff,
  • Joshua A. M. Allen,
  • Christopher B. Nelson,
  • Christopher G. Tomlinson,
  • Michael Lee,
  • Roger R. Reddel,
  • Andrew J. Deans,
  • Hilda A. Pickett

DOI
https://doi.org/10.1038/s41467-019-10180-6
Journal volume & issue
Vol. 10, no. 1
pp. 1 – 14

Abstract

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ALT telomeres experience DNA damage that may drive recombination-based telomere elongation. Here, the authors reveal that FANCM plays a critical role in the suppression of ALT activity through its interaction with the BTR (BLM-TOP3A-RMI) complex.