The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/2000/2/579/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 3, February 7, 2000 579-584

Brief Definitive Report

Somatic Hypermutation in Muts Homologue (Msh)3-, Msh6-, and Msh3/Msh6-Deficient Mice Reveals a Role for the Msh2–Msh6 Heterodimer in Modulating the Base Substitution Pattern

Margrit Wiesendangera, Burkhard Kneitza, Winfried Edelmanna, and Matthew D. Scharffa

a Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461
Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461.718-430-8574718-430-3527

scharff{at}aecom.yu.edu

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.

Key Words: DNA mismatch repair • immunoglobulin genes • germinal center • Msh3 • Msh6

© 2000 The Rockefeller University Press


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