Evidence for mutation in an I–A gene

Abstract

Mutant mouse strains are important tools for immunogenetic studies of the regulation, structure and function of major histocompatibility (H–2) antigens^1–2 Several inbred strains have been established which carry H–2-linked mutations that cause changes in cell surface antigens as recognized by cytotoxic T cells and sometimes antibodies. Using intra-H–2 recombinant haplotypes in skin graft complementation studies, lesions in several of these mutant strains have been genetically mapped to genes encoded in the K- or D-end of the H–2 complex³. More precise mapping has often not been possible as many of the available mutant strains possessed lesions in the K-end of the H–2^b haplotype and a recombinant separating the K^b and I–A^b regions was not previously available. The genetic locations of the lesions in some of these mutant strains could therefore only be inferred when a serological and/or structural alteration was detected (see refs 1, 2). We describe here the use of a newly established recombinant strain, B10.MBR (ref. 4), for skin graft complementation studies to map K-end mutations. These studies provide the first genetic evidence that the B6.C-H-2^bm12 mutation involves an I–A^b gene and also confirm that the lesions in two other mutants can be mapped to a gene in the K^b region.