International Mammalian Genome Society


The 13th International Mouse Genome Conference
October 31-November 3, 1999

Table of Contents * Structure * Bioinformatics * Sequence * Mapping * New Tools * Gene Discovery * Developmental * Mutagenesis * Functional Genomics

F45 Characterization of the Friend Virus Susceptibility Gene 2 (Fv2) Locus on Mouse Chromosome 9

Pam Correll1, Ed Melkin1, Paul Ney2 and Robert Paulson1. Department of Veterinary Science, The Pennsylvania State University1, University Park, PA and St Judes Hospital2, Memphis, TN

Friend erythroleukemia virus causes erythroleukemia in adult mice. The disease progresses through an initial stage where the expansion of infected erythroid progenitors is driven by an interaction between the envelope glycoprotein of Friend virus (gp55) and the erythropoietin receptor (EpoR). During the later stages of the disease, leukemic clones emerge that have acquired mutations in p53 and proviral insertions into the ets family genes Spi-1 and Fli-1. Because of the reproducible progression of Friend disease and the exquisite specificity of the virus for the erythroid lineage, a number of loci have been identified that affect susceptibility to Friend erythroleukemia. The Friend virus susceptibility gene 2 (Fv2) affects the early stage of Friend disease by regulating the expansion of infected cells mediated by the interaction between EpoR and gp55. Two mechanisms have been proposed for Fv2 function. First, Fv2 has been thought to be a component of the EpoR signaling complex because mutations in gp55 can overcome Fv2 mediated restriction of Friend disease. Second, it has been suggested that Fv2 regulates the cell cycle progression of the early erythroid progenitors (BFU-E) that are the target cells for Friend virus infection. In Fv2 resistant mice few BFU-E are actively cycling, thus fewer cells can be infected.

We have mapped Fv2 on mouse chromosome 9. Genetic analysis of the locus demonstrated that the two functions ascribed to Fv2, restriction of Friend erythroleukemia and the regulation of BFU-E cell cycling are encoded by linked genes. We will present data on the identification of the gene that is necessary for the early expansion of Friend virus infected cells and the gene that appears to regulate cell cycle progression of BFU-E and how they may act in concert during the development of Friend erythroleukemia.

 


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