Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 191, Issue 3, Pages 579-584Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.191.3.579
Keywords
DNA mismatch repair; immunoglobulin genes; germinal center; Msh3; Msh6
Categories
Funding
- NCI NIH HHS [R01 CA072649, 5R37CA39838, T32 CA009173, R01CA72649, R01CA76329, R01 CA076329] Funding Source: Medline
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Although the primary function of the DNA mismatch repair (MMR) system is to identify and correct base mismatches that have been erroneously introduced during DNA replication, recent studies have further implicated several MMR components in somatic hypermutation of immunoglobulin (Ig) genes. We studied the immune response in mice deficient in MutS homologue (MSH)3 and MSH6, two mutually exclusive partners of MSH2 that have not been examined previously for their role in Ig hypermutation. In Msh6(-/-) and Msh3(-/-)/Msh6(-/-) mice, base substitutions are preferentially targeted to G and C nucleotides and to an RGYW hot spot, as has been shown previously in Msh2(-/-) mice. In contrast, Msh3(-/-) mice show no differences from their littermate controls. These findings indicate that the MSH2-MSH6 heterodimer, but not the MSH2-MSH3 complex, is responsible for modulating Ig hypermutation.
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