PMID:15955838

Citation	Min, IM, Rothlein, LR, Schrader, CE, Stavnezer, J and Selsing, E (2005) Shifts in targeting of class switch recombination sites in mice that lack mu switch region tandem repeats or Msh2. J. Exp. Med. 201:1885-90
Abstract	The mechanisms that target class switch recombination (CSR) to antibody gene switch (S) regions are unknown. Analyses of switch site locations in wild-type mice and in mice that lack the Smu tandem repeats show shifts indicating that a 4-5-kb DNA domain (bounded upstream by the Imu promoter) is accessible for switching independent of Smu sequences. This CSR-accessible domain is reminiscent of the promoter-defined domains that target somatic hypermutation. Within the 4-5-kb CSR domain, the targeting of S site locations also depends on the Msh2 mismatch repair protein because Msh2-deficient mice show an increased focus of sites to the Smu tandem repeat region. We propose that Msh2 affects S site location because sequences with few activation-induced cytidine deaminase targets generate mostly switch DNA cleavages that require Msh2-directed processing to allow CSR joining.
Links	PubMed PMC2212040 Online version:10.1084/jem.20042491
Keywords	Animals; Antibody Diversity/genetics; DNA Primers; DNA-Binding Proteins/genetics; DNA-Binding Proteins/metabolism; Immunoglobulin Class Switching/genetics; Immunoglobulin Class Switching/immunology; Immunoglobulin Switch Region/genetics; Mice; Mice, Knockout; Models, Genetic; MutS Homolog 2 Protein; Polymerase Chain Reaction/methods; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins/metabolism; Tandem Repeat Sequences/genetics
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