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in Somatic Hypermutation Determined by Analysis of Mutations in a Patient with Xeroderma Pigmentosum Variant
* Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892; and
Basic Research Laboratory, National Cancer Institute, Bethesda, MD 20892
To determine the possible role of polymerase 
(pol )
in somatic hypermutation of B cells, a mutational analysis of 24
nonproductive rearrangements from a patient with xeroderma pigmentosum
variant with a defect in pol was conducted. Although the mutational
frequency of A and T bases decreased in WA (A/T, A) motifs, regardless
of their RGYW (purine, G; pyrimidine, A/T) context, the overall
mutational frequency of A or T bases was not affected. Moreover, the
overall mutational frequency of the sequences examined was not
decreased. There was an apparent increase in the number of insertions
and deletions. The results are consistent with the conclusion that pol
specifically targets WA motifs. However, its overall contribution
to the somatic hypermutational process does not appear to be
indispensable and in its absence other mechanisms maintain mutational
activity.
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