The Mst1r gene encodes for a receptor tyrosine kinase that binds the macrophage-stimulating protein and is involved in wound healing (epithelial cell migration) and innate immune response. These mice carry a mutation of the Mst1r gene in which the alternative truncated short-length protein is not expressed, only the full length form of the protein is expressed. No short-length/truncated gene product (mRNA) is detected by RT-PCR analysis of bone marrow, spleen or testis from homozygotes, and Northern blot analysis of testicular RNA from homozygotes. Mice homozygous for the mutation are less susceptible to Friend leukemia viral infection. When challenged with ConA induced T-cell mediated acute liver injury, homozygotes exhibit higher levels of serum IFN-gamma and have a more severe liver injury response when compared to wildtype controls. 
Mice that are homozygous for the targeted mutation are viable and fertile. 
 In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

These FL-RON mutant mice express only the full-length protein, and do not express the truncated isoform.  They are suitable for use in studies of the role of the alternate forms of this receptor tyrosine kinase in the innate immune response.

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FVB.129P2(Cg)-Mst1r<tm2(Mst1r*)Sew>/J Frozen Embryo