This strain carries a targeted knockout of the Apod (apolipoprotein D) gene. Evidence suggests that this gene acts in a cardioprotective capacity.
Jonathan D Smith, Cleveland Clinic Lerner College of Med.
Apod (apolipoprotein D) is a glycoprotein member of the lipocalin family, associated with the transport of small hydrophobic ligands. Expression of the gene increases 80-fold in an Scarb1/Apoe double knockout model of atherosclerotic coronary artery disease. Evidence suggests that Apod acts in a cardioprotective capacity.
This targeted mutation strain carries a deletion of the second exon. Homozygous mice show no significant differences in plasma levels of cholesterol or triglycerides, but show increased mortality under conditions of cardiac ischemia. Loss of APOD is also associated with a significant increase in cardiac infarct area, as compared to wildtype.
A targeting vector was designed to replace exon 2, including the translational start and signal peptide needed for protein secretion, with a neomycin resistance cassette. (129X1/SvJ x 129S1/Sv)F1- Kitl+-derived R1 embryonic stem (ES) cells were used to create the mutation. This strain was backcrossed to C57BL/6 for more than 10 generations by the donating lab (see SNP note below).
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background.
|Allele Name||targeted mutation 1, Jan L Breslow|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||ApoD-; Apodtm1Hhmd|
|Gene Symbol and Name||Apod, apolipoprotein D|
|Strain of Origin||(129X1/SvJ x 129S1/Sv)F1-Kitl+|
|Molecular Note||A targeting vector was designed to replace exon 2, including the translational start and signal peptide needed for protein secretion, with a neomycin resistance cassette.|
Homozygotes and heterozygotes are viable and fertile.
When using the B6.129-Apodtm1Bres/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #018292 in your Materials and Methods section.