Mismatch Repair Co-opted by Hypermutation

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Science  20 Feb 1998:
Vol. 279, Issue 5354, pp. 1207-1210
DOI: 10.1126/science.279.5354.1207

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Mice homozygous for a disrupted allele of the mismatch repair genePms2 have a mutator phenotype. When this allele is crossed into quasi-monoclonal (QM) mice, which have a very limited B cell repertoire, homozygotes have fewer somatic mutations at the immunoglobulin heavy chain and λ chain loci than do heterozygotes or wild-type QM mice. That is, mismatch repair seems to contribute to somatic hypermutation rather than stifling it. It is suggested that at immunoglobulin loci in hypermutable B cells, mismatched base pairs are “corrected” according to the newly synthesized DNA strand, thereby fixing incipient mutations instead of eliminating them.

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