The H2-Kbm1 allele is a spontaneous variant from the parental H2b haplotype derived from C57BL/6By. This variant differs from the parental sequence by 7 nucleotide substitutions causing 3 codon changes, E152A, R155Y, L156Y, which are located in the alpha helix but not in the peptide binding groove, likely impacting the peptide binding domain and T cell receptor interaction (Sim et al., 1997). This strain has been used in models of allograft rejection/tolerance and characterization of antigenic peptide selection.
Dr. Donald Bailey, then at University of California Medical Center in San Francisco, began to generate a panel of congenic lines with differential loci that determine histocompatibility including lines carrying histocompatibility mutations. To reveal histocompatibility mutations, orthotopic tailskin grafts were made between F1 mice of a cross between C57BL/6By and BALB/cBy. The pattern of rejected grafts between F1 recipients showed whether the histocompatibility mutation determined a gain or loss of antigenicity, and subsequent grafts from the two parental strains onto a mutant carrier indicated in which genome the mutation occurred. Backcrossing, with testing, was carried out until siblings at backcross generation 11 or more were intercrossed to breed the congenic interval to homozygosity and each strain was maintained by sibling inbreeding (Bailey, 1975). Dr. Bailey transferred the mice to The Jackson Laboratory when he joined the staff in 1967. The strain was cryopreserved in 1981.
|Allele Name||b haplotype mutation 1|
|Allele Synonym(s)||bm1; H(z1); H-2ba; H-2bm1; Kbm1|
|Gene Symbol and Name||H2-K, histocompatibility 2, K region|
|Strain of Origin||C57BL/6By|
|General Note||Genbank ID for this allele: X56624|
|Molecular Note||The bm1 mutation contains 7 nucleotide differences resulting in amino acid substitutions at codon 152 (glutamate to alanine), codon 155 (arginine to tyrosine) and codon 156 (leucine to tyrosine).|