Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozyous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 12.5-15.5. No gene product (mRNA) is detected by RT-PCR or RNase protection assay analysis of homozygous embryos aged E12.5. Defects in the cardiac development of homozygotes include dilated atria, atrial septal defect, thin ventricular myocardium, common atrioventricular canal, absence of coronary vasculature, subpulmonic stenosis and subaortic ventricular septal defect. Lung development defects are also observed in homozygous embryos. This mutant mouse strain may be useful in studies of Tetralogy of Fallot, cardiovascular and pulmonary development.
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.
A targeting vector containing a loxP site flanked neomycin-cytidine deaminase cassette was used to disrupt all exons encoding the Zinc-finger domains. The construct was electroporated into 129Sl/Sv-p+ Tyr+ Kitl+ derived CJ7 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to Cre-deleter mice to remove the selection cassette, and then backcrossed to DBN2J for 13 generations.
|Allele Name||targeted mutation 1, Stuart Orkin|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Fog2-; FOG-2-|
|Gene Symbol and Name||Zfpm2, zinc finger protein, multitype 2|
|Strain of Origin||129S1/Sv-Oca2+ Tyr+ Kitl+|
|Molecular Note||The gene was disrupted by replacement of sequences encoding all of the zinc finger motifs with a floxed neomycin-cytidine deaminase cassette. The floxed cassette was removed by crossing mutant animals to a cre deleter strain. Homozygous mutant embryos were detected by Southern blot analysis up to day E15.5. RNase protection assay showed an absence of Zfpm2 mRNA in hearts of E12.5 homozygous mutant embryos.|
|Mutations Made By|| |
Stuart Orkin, Harvard University
When maintaining a live colony, these mice are bred as heterozygotes. Homozygotes
have an embryonic lethal phenotype.
When using the FOG-2- mouse strain in a publication, please cite the originating article(s) and include JAX stock #006838 in your Materials and Methods section.