Cutting edge: Hypermutation in Ig V genes from mice deficient in the MLH1 mismatch repair protein

Quy H. Phung, David B. Winter, Rudaina Alrefai, Patricia J. Gearhart

Research output: Contribution to journalArticlepeer-review

Abstract

During somatic hypermutation of Ig V genes mismatched nucleotide substitutions become candidates for removal by the DNA mismatch repair pathway. Previous studies have shown that V genes from mice deficient for the MSH2 and PMS2 mismatch repair proteins have frequencies of mutations that are comparable with those from wild-type (wt) mice; however, the pattern of mutation is altered. Because the absence of MSH2 and PMS2 produced different mutational spectra, we examined the role of another protein involved in mismatch repair, MLH1, on the frequency and pattern of hypermutation. MLH1- deficient mice were immunized with oxazolone Ag, and splenic B cells were analyzed for mutations in their VκOx1 light chain genes. Although the frequency of mutation in MLH1-deficient mice was twofold lower than in wt mice, the pattern of mutation in Mlh1(-/-) clones was similar to wt clones. These findings suggest that the MLH1 protein has no direct effect on the mutational spectrum.

Original languageEnglish (US)
Pages (from-to)3121-3124
Number of pages4
JournalJournal of Immunology
Volume162
Issue number6
StatePublished - Mar 15 1999

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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