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Publication Detail
Hot spot focusing of somatic hypermutation in MSH2-deficient mice suggests two stages of mutational targeting.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Rada C, Ehrenstein MR, Neuberger MS, Milstein C
  • Publication date:
    07/1998
  • Pagination:
    135, 141
  • Journal:
    Immunity
  • Volume:
    9
  • Issue:
    1
  • Status:
    Published
  • Country:
    United States
  • Print ISSN:
    1074-7613
  • PII:
    S1074-7613(00)80595-6
  • Language:
    eng
  • Keywords:
    Animals, B-Lymphocytes, Binding Sites, Cell Line, DNA-Binding Proteins, Female, Genes, Immunoglobulin, Immunoglobulin Heavy Chains, Male, Mice, Mice, Knockout, MutS Homolog 2 Protein, Mutation, Proto-Oncogene Proteins
Abstract
Likely creation of mismatches during somatic hypermutation has stimulated interest in the effect of mismatch repair deficiency on the process. Analysis of unselected mutations in the 3' flank of VH rearrangements in germinal center B cells revealed that MSH2 deficiency caused a 5-fold reduced mutation accumulation. This might reflect ectopic effects of the Msh2 disruption; indeed, the mice exhibit other perturbations within the B cell compartment. However, that MSH2 (or factors dependent upon it) plays a role in the mechanism of mutation fixation is indicated by a strikingly increased focusing of the mutations on intrinsic hot spots. We propose two phases to hypermutation targeting. The first is hot spot focused and MSH2 independent; the second, MSH2-dependent phase yields a more even spread of mutation fixation.
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