Mice homozygous for the Fcer1gtm1Rav targeted mutation are viable and fertile. Immune system defects include: inability to phagocytose Ab-coated particles despite normal binding, defective NK cell-mediated Ab-dependent cytotoxicity and mast cell-mediated allergic responses. T cell development is normal. Inflammatory response to immune complexes is attentuated (lack of Arthus response). Homozygotes are completely resistant to experimental immune thrombocytopenia induced by mouse anti-platelet antibodies.
A targeting vector containing a NEO cassette was used to disrupt exon 2, which created a new stop codon 239 bp downstream of the integration site. The construct was electroporated into 129P2/OlaHsd derived E14 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice, and maintained on the mixed B6;129P2 background.
|Allele Name||targeted mutation 1, Jeffrey V Ravetch|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Fcepsilonrgamma-; Fcer1gtm1; Fcer1gtm1Ra; Fcerg1tm1; FcgammaR-; FcR-; FcR gamma-; FcRg-; FcRgamma-; FcRgammanl; FcRgammac-; FcRgamma-chain-; FcRKO; gamma-|
|Gene Symbol and Name||Fcer1g, Fc receptor, IgE, high affinity I, gamma polypeptide|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||A neomycin selection cassette was inserted into exon 2, creating a new stop codon 239 bp downstream of the integration site. RT-PCR analysis on RNA isolated from activated macrophages, mast cells and NK cells of homozygous mice demonstrated that no detectable transcript was produced from this allele. Western blot analysis on lysates derived from activated macrophages, mast cells and NK cells of homozygous mice confirmed that no protein is encoded by this allele.|
|Mutations Made By|| |
Dr. Jeffrey Ravetch, Memorial Sloan Kettering Cancer Center
When using the FcRg- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002847 in your Materials and Methods section.