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Nucleic Acids Research Advance Access published online on May 21, 2007
Nucleic Acids Research, doi:10.1093/nar/gkm315
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© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Disparate contributions of the Fanconi anemia pathway and homologous recombination in preventing spontaneous mutagenesis

John M. Hinz*, Peter B. Nham, Salustra S. Urbin, Irene M. Jones and Larry H. Thompson

Chemistry, Materials, & Life Sciences Directorate, L441, Lawrence Livermore National Laboratory, P.O. Box 808, Livermore, CA 94551-0808, USA

*To whom correspondence should be addressed. Tel: +1 925 424 3686; Fax: +1 925 422 2099; Email: hinz4{at}llnl.gov

Received February 27, 2007. Revised April 11, 2007. Accepted April 12, 2007.

Fanconi anemia (FA) is a chromosomal instability disorder in which DNA-damage processing defects are reported for translesion synthesis (TLS), non-homologous end joining (NHEJ) and homologous recombination (HR; both increased and decreased). To reconcile these diverse findings, we compared spontaneous mutagenesis in FA and HR mutants of hamster CHO cells. In the fancg mutant we find a reduced mutation rate accompanied by an increased proportion of deletions within the hprt gene. Moreover, in fancg cells gene amplification at the CAD and dhfr loci is elevated, another manifestation of inappropriate processing of damage during DNA replication. In contrast, the rad51d HR mutant has a greatly elevated rate of hprt mutations, >85% of which are deletions. Our analysis supports the concept that HR faithfully restores broken replication forks, whereas the FA pathway acts more globally to ensure chromosome stability by promoting efficient end joining of replication-derived breaks, as well as TLS and HR.


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