The expression of the major histocompatibility complex (MHC) class II gene family is developmentally regulated and, in generaI, in a coordinate manner. In this study, we show that the expression of the entire repertoire of human class II genes, otherwise transcriptionally silent in the bare Iymphocyte syndrome-derived BLSI celI Iine, can be rescued by somatic celI hybridization with normai mouse spleen celIs. The analysis of the interspecies celI hybrids revealed a par-ticularly important and unprecedented aspect. A return to the BLSI-like, human MHC class Il-negative phenotype due to segregation of mouse chromosomes was accompanied in certain hybrids by Ioss of lE, but not lA celI surface antigen expression. At the molecular IeveI, this was the result of Iack of Ea-specific mRNA in the presence of E{3-, Aa- and A{3-specific mRNA. Thus, the mouse trans-acting function operating across species barriers and able to complement the defect of human BLSI celIs diverged in mice to contrai Ea, but not Eh, Aa and Ah gene expression. These findings suggest that evolutionary pressure has maintained the expression of the MHC class II multigene family under the con-trai of quite distinct species-specific transcriptionai mechanisms.
Divergent evolution in the mechanisms controlling MHC class II gene transcription in mouse and human.
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