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Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
Functional relationships of FANCC to homologous recombination, translesion synthesis and BLM.
EMBO J. 24, 418-427 (2005)
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 fancc 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.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
bloom syndrome; fanconi anemia; homologous recombination; sister chromatid exchange; translesion synthesis
ISSN (print) / ISBN
0261-4189
e-ISSN
1460-2075
Journal
EMBO Journal, The
Quellenangaben
Volume: 24,
Issue: 2,
Pages: 418-427
Publisher
Springer
Publishing Place
Heidelberg, Germany
Reviewing status
Peer reviewed
Institute(s)
Institute of Molecular Radiation Biology (IMS)