BLM is an early responder to DNA double-strand breaks

Parimal Karmakar, Masayuki Seki, Makoto Kanamori, Kazunari Hashiguchi, Makoto Ohtsuki, Eriko Murata, Eri Inoue, Shusuke Tada, Li Lan, Akira Yasui, Takemi Enomoto

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)


Bloom syndrome (BS) is an autosomal recessive disorder characterized by a marked predisposition to cancer and elevated genomic instability. The defective protein in BS, BLM, is a member of the RecQ helicase family and is believed to function in various DNA transactions, including in replication, repair, and recombination. Here, we show that both endogenous and overexpressed human BLM accumulates at sites of laser light-induced DNA double-strand breaks within 10 s and colocalizes with γH2AX and ATM. Like its RecQ helicase family member, WRN, the defective protein in Werner syndrome, dissection of the BLM protein revealed that its HRDC domain is sufficient for its recruitment to the damaged sites. In addition, we confirmed that the C-terminal region spanning amino acids 1250-1292 within the HRDC domain is necessary for BLM recruitment. To identify additional proteins required for the recruitment of BLM, we examined the recruitment of BLM in various mutants generated from chicken DT40 cells and found that the early accumulation of BLM was not dependent on the presence of ATM, RAD17, DNA-PKcs, NBS1, XRCC3, RAD52, RAD54, or WRN. Thus, HRDC domain in DNA helicases is a common early responder to DNA double-strand breaks, enabling BLM and WRN to be involved in DNA repair.

Original languageEnglish
Pages (from-to)62-69
Number of pages8
JournalBiochemical and biophysical research communications
Issue number1
Publication statusPublished - 2006 Sept 15
Externally publishedYes


  • BLM protein
  • DNA double-strand break repair
  • DT40 cells
  • HRDC domain
  • Laser micro-irradiation
  • RecQ helicase

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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