| First Author | Behringer RR | Year | 1985 |
| Journal | Cell | Volume | 40 |
| Issue | 2 | Pages | 441-7 |
| PubMed ID | 3855388 | Mgi Jnum | J:7711 |
| Mgi Id | MGI:56180 | Doi | 10.1016/0092-8674(85)90158-8 |
| Citation | Behringer RR, et al. (1985) Cellular site and mode of Fv-2 gene action. Cell 40(2):441-7 |
| abstractText | 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. |
