Cellular site and mode of Fv-2 gene action

Abstract

The Fv-2 genotype of erythroid progenitors directly determines whether they will undergo viral-induced transformation. This conclusion was reached from studies of allophenic mice compounded from congenic C57BL/6 strains differing at Fv-2 and an enzyme marker (GPI). Infection of these Fv-2ss in equilibrium Fv-2rr mosaic animals with the polycythemic strain of Friend virus results in the development of Friend disease. Concomitant with disease symptoms is a shift in the mosaic composition of the erythrocytes in favor of those of the susceptible strain. The observed viral-induced shift in the erythrocyte composition is paralleled by a similar change in the mosaic composition of the CFU-E pool but not the primitive (d8) BFU-E pool. Thus, with regard to this particular Fv-2 phenotype (susceptibility to FV-P-induced cellular hyperplasia), Fv-2 manifests itself specifically in the erythroid lineage, either in mature (d3) BFU-E or CFU-E.