Affiliation:
1. From the Departments of Biochemistry and Molecular Biology; 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
Abstract
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.
Publisher
Rockefeller University Press
Subject
Immunology,Immunology and Allergy
Cited by
43 articles.
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