Surviving Telomere Attrition with the MiDAS Touch

Rachel L. Flynn, Christopher M. Heaphy

Research output: Contribution to journalShort surveypeer-review

1 Scopus citations


Cancer cells maintain telomere lengths through telomerase activity or by alternative lengthening of telomeres (ALT). Using an engineered model system, a recent study by Min et al. reveals that the combination of BLM-mediated DNA resection and telomere clustering, a characteristic of ALT telomeres, catalyzes RAD52-dependent mitotic DNA synthesis (MiDAS) specifically at telomeres to drive ALT activity.

Original languageEnglish (US)
Pages (from-to)783-785
Number of pages3
JournalTrends in Genetics
Issue number11
StatePublished - Nov 2019


  • BLM
  • RAD52
  • SUMO
  • alternative lengthening of telomeres
  • mitotic DNA synthesis

ASJC Scopus subject areas

  • Genetics


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