Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM

Seiki Hirano, Kazuhiko Yamamoto, Masamichi Ishiai, Mitsuyoshi Yamazoe, Masayuki Seki, Nobuko Matsushita, Mioko Ohzeki, Yukiko M. Yamashita, Hiroshi Arakawa, Jean Marie Buerstedde, Takemi Enomoto, Shunichi Takeda, Larry H. Thompson, Minoru Takata

Research output: Contribution to journalArticlepeer-review

97 Scopus citations


Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2-fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fance cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC-induced formation of GFP-BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair.

Original languageEnglish (US)
Pages (from-to)418-427
Number of pages10
JournalEMBO Journal
Issue number2
StatePublished - Jan 26 2005
Externally publishedYes


  • Bloom syndrome
  • Fanconi anemia
  • Homologous recombination
  • Sister chromatid exchange
  • Translesion synthesis

ASJC Scopus subject areas

  • Genetics
  • Cell Biology


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