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Mutagenesis vol. 19 no. 3 pp. 237-244, May 2004
© 2004 UK Environmental Mutagen Society/Oxford University Press

Characterization of the hamster FancG/Xrcc9 gene and mutations in CHO UV40 and NM3{dagger}

Jane E. Lamerdin, Nazumi A. Yamada, James W. George, Brian Souza, Allen T. Christian, Nigel J. Jones1 and Larry H. Thompson2

BBR Program, L441, Lawrence Livermore National Laboratory, PO Box 808, Livermore, CA 94550-0808, USA and 1School of Biological Sciences, Biosciences Building, Crown Street, University of Liverpool, Liverpool L69 7ZB, UK

The human FANCG/XRCC9 gene, which is defective in Fanconi anemia complementation group G (FA-G) cells, was first cloned by genetic complementation of the mitomycin C (MMC) sensitivity of CHO mutant UV40. The CHO NM3 mutant was subsequently assigned to the same complementation group. The parental AA8 CHO cells are hemizygous at the FancG locus, and we identified frameshift mutations that result in N-terminal truncations of the protein in both UV40 and NM3. Hypersensitivity to DNA cross-linking agents, such as MMC, typically characterizes FA cells. By introducing the native CHO FancG gene into mutant NM3, we demonstrate that hamster FancG fully corrects the 3-fold sensitivity to methyl methanesulfonate (MMS) as well as the 10-fold sensitivity to MMC, whereas resistance to ionizing radiation did not increase appreciably. In contrast, hamster cDNA transformants showed incomplete correction for both MMC and MMS sensitivity. The constitutively expressed FancG protein is present in the cytoplasmic, nuclear and chromatin fractions. FancG protein levels and subcellular localization do not change appreciably as a function of cell cycle position. Our results are consistent with roles of FancG in both the nuclear and cytoplasmic compartments to maintain genomic stability in response to various genotoxic agents.

2To whom correspondence should be addressed. Tel: +1 925 422 5658; Fax: +1 925 422 2099; Email: thompson14{at}llnl.gov
{dagger}This publication is dedicated to the memory and scientific contributions of Dr David B.Busch, who isolated the UV40 mutant in his large-scale UV mutant screens. David developed leukemia and passed away in April 2002.

Received on December 9, 2003; revised on January 22, 2004; accepted on January 23, 2004


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