International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)

Table of Contents * Complex Genetics * Developmental Genetics * Gene Annotation * Gene Discovery * Genome Sequencing * Functional Genomics * Mutagenesis * Presentations * Verne Chapman Memorial Lecture

Dr. Christine Kozak
Natl. Inst. Of Allergy and Infectious Diseases
NIAID, LMM, Bldg 4, Room 329
4 Center Drive MSC 0460
Bethesda, MD
20892-0460
USA

Co-Authors: 1)T. Wu, 2)C.G. Lee, 1)M. C. Adamson
Institutions: 1)National Institute of Allergy and Infectious Diseases, National Institutes of Health, 2)Yale University

Most strains of laboratory mice contain a serum factor capable of inactivating some subgroups of murine leukemia viruses. Previous studies had shown that this leukemia virus inactivating factor (LIF) is distinct from immunoglobulin and complement, and that it is found in the lipoprotein containing serum fractions and may be an apolipoprotein. We screened the various virus subgroups for sensitivity to LIF inactivation. Although initially described as xenotropic-specific, LIF most efficiently inactivated polytropic isolates. Xenotropic viruses vary in LIF sensitivity, and amphotropic and ecotropic viruses are unaffected by LIF. Use of chimeras between amphotropic and polytropic viruses suggests that the VRA region of the viral envelope is the target of LIF inactivation. We screened 30 inbred strains for the presence of serum LIF. LIF was identified in all mice tested except the inbred NIH Swiss strain, NFS/N. Analysis of backcross mice showed LIF to be under control of a single gene on distal Chr 10 at or near the gene encoding a minor serum apolipoprotein, apolipoprotein F (ApoF). To evaluate this gene as a potential candidate for LIF, mouse ApoF was cloned and sequenced and its expression was assessed in LIF positive and negative mice; however, no obvious differences were detected suggesting that LIF is governed by a distinct linked gene.