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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Mismatch repair co-opted by hypermutation.

Mice homozygous for a disrupted allele of the mismatch repair gene Pms2 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 lambda 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.[1]


  1. Mismatch repair co-opted by hypermutation. Cascalho, M., Wong, J., Steinberg, C., Wabl, M. Science (1998) [Pubmed]
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