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J. Biol. Chem., Vol. 268, Issue 27, 20105-20109, 09, 1993
CL Hsieh, CF Arlett and MR Lieber
Ataxia telangiectasia (AT) and Bloom's syndrome (BS) patients are
characterized by sensitivity to radiation, increased lymphoid malignancy,
and frequent translocations to the antigen receptor loci. Because of these
features, there has been a persistent question as to whether the V(D)J
recombinase might be abnormal in cells from these patients. Such
abnormalities might be due to inappropriate to inaccurate expression of
components of the V(D)J recombinase or due to mutation in a component
shared between V(D)J recombination and other cellular processes, such as
DNA repair. Bloom's syndrome is associated with a ligation deficiency, and
this activity may contribute in the end resolution steps of both
site-specific and general DNA-processing reactions. In the current study,
we have activated V(D)J recombination in normal, AT, and BS fibroblasts and
in fibroblasts from a patient with mutations that largely abolish DNA
ligase I activity. We find that the signal and coding joint formation of
the V(D)J recombination reaction are entirely normal in AT, BS, and DNA
ligase I mutant cells. In addition to ruling out abnormalities of the V(D)J
recombinase in AT, BS, and DNA ligase I mutant cells, these studies suggest
that DNA ligase I is unlikely to be required for signal or coding end
joining in the V(D)J recombination reaction.
V(D)J recombination in ataxia telangiectasia, Bloom's syndrome, and a DNA ligase I-associated immunodeficiency disorder
Department of Pathology, Stanford University School of Medicine, California 94305-5324.
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