RESUMO
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).
Assuntos
Infertilidade Masculina/genética , Antígenos de Histocompatibilidade Menor/genética , Animais , Animais Selvagens , Feminino , Rejeição de Enxerto , Imunofenotipagem , Infertilidade Masculina/imunologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos , Camundongos Mutantes , Transplante de Pele/imunologiaRESUMO
The recessive male sterility and histoincompatibility (mshi) mutation in the mouse generates pleiotropic effects on graft transplantation and male reproduction. Previous analysis of backcross mice typed for mshi either by testicular morphology or by allograft rejection has located each trait to a 20-cM region on proximal mouse Chr 10. Here we present the microsatellite polymorphism analysis of a new 276-member intraspecific backcross panel--including a set of 135 males typed for sterility and histoincompatibility--that places both features controlled by mshi within a 1.7-cM interval between markers D10Mit51/168/212 and D10Mit213. In addition, this analysis has allowed an explicit test of a two-gene model for the mshi locus and has provided a measurement of the penetrance of the mshi-generated histogenic phenotype in both male (88.4 +/- 3.9%) and female (91.0 +/- 3.5%) mutants. The fine-structure map presented should facilitate a chromosome walk across this region and, ultimately, the molecular identification of the gene or genes affected by this interesting mutation.