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From the * Departments of Biochemistry and Molecular Biology; Recent experiments have strongly suggested that the process of somatic mutation is linked to
transcription initiation. It was postulated that a mutator factor loads onto the RNA polymerase and, during elongation, causes transcriptional arrest that activates DNA repair, thus occasionally
causing errors in the DNA sequence. We report the analysis of the role of one of the known
DNA repair systems, nucleotide excision repair (NER), in somatic mutation. Epstein-Barrvirus-transformed B cells from patients with defects in NER (XP-B, XP-D, XP-V, and CS-A)
were studied. Their heavy and light chain genes show a high frequency of point mutations in
the variable (V), but not in the constant (C) regions. This suggests that these B cells can undergo somatic hypermutation despite significant defects in NER. Thus, it is doubtful that NER
is an essential part of the mechanism of somatic hypermutation of Ig genes. As an aside, NER
seems also not involved in Ig gene switch recombination.
Departments of Molecular Genetics
and Cell Biology, University of Chicago, Chicago, Illinois, 60637; § Center for Molecular Biology and
Genetics, Kyoto University, Japan; Laboratoire d'Immuno Génétique Moléculaire, Centre National de
la Recherche Scientifique, UMR 5535, Université Montpellier, France
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