Hildebrandt A L, Cantwell A M, Rule M C, King T R
Department of Biological Sciences, Central Connecticut State University, 1615 Stanley Street, New Britain, CT 06050, USA.
Immunogenetics. 1999 Jul;49(7-8):666-72. doi: 10.1007/s002510050663.
The recessive male sterility and histoincompatibility mutation (mshi) arose spontaneously in the standard inbred mouse strain BALB/cBy. In addition to generating sterility in homozygous males, mshi controls the loss of a minor histocompatibility antigen designated H-mshi. To determine whether the H-mshi antigen normally expressed by the BALB/cBy strain (H-mshi(c)) is the same as or different from the antigen (H-mshi(x)) expressed by the standard inbred C57BL/6J strain or the wild-derived CAST/Ei and SPRET/Ei strains, animals heterozygous for the mutant antigen-loss allele (H-mshi-) and H-mshi(x) were grafted with tail skin from BALB/cBy mice. The long-term retention of grafts by these hosts indicates that the H-mshi antigen encoded by the BALB/cBy, C57BL/6J, CAST/Ei, and SPRET/Ei strains is histogenically identical. Conservation of this minor histocompatibility antigen among these evolutionarily diverse strains suggests that H-mshi encodes a functionally important cellular product(s).