These NOD mice contain a ZFN-mediated mutation that disrupts the MHC class II I-Ag7 molecule.
Yi-Guang Chen, The Medical College of Wisconsin
NOD.H2-Ab-/- line 11 mice contain a ZFN-mediated mutation targeted to exon 2 of the H2-Ab1 (histocompatibility 2, class II antigen A, beta 1) gene. The mutation disrupts the expression of the diabetes susceptible MHC class II I-Ag7 molecule uniquely expressed in NOD mice. I-Ag7 is involved in antigen presentation and T-cell activation, contributing to the development of Insulin-dependent diabetes mellitus (IDDM). NOD.H2-Ab-/- line 11 mice exhibit greatly reduced numbers of CD4 single positive T cells in the thymus and spleen.
This zinc finger nuclease induced mutation targets exon 2 of the H2-Ab1
(histocompatibility 2, class II antigen A, beta 1) gene, creating a 17 bp deletion that disrupts normal expression of the MHC class II I-Ag7 molecule. The mRNA encoding the ZFN was injected into NOD/ShiLtJ (Stock No. 001976) one cell embryos and a mouse from founder line 11 was bred back to NOD/ShiLtJ. Resulting offspring were intercrossed. Upon arrival at The Jackson Laboratory, mice were bred to NOD/ShiLtJ for at least one generation to establish the colony.
|Allele Name||endonuclease-mediated mutation 1, Yi-Guang Chen|
|Allele Type||Endonuclease-mediated (Null/Knockout)|
|Allele Synonym(s)||H2-Ab- line 11|
|Gene Symbol and Name||H2-Ab1, histocompatibility 2, class II antigen A, beta 1|
|Strain of Origin||NOD/ShiLtJ|
|Molecular Note||Zinc-finger nuclease technology generated a 17 bp deletion in exon 2 that disrupts normal expression of this diabetes susceptibility allele.|
When maintaining a live colony, homozygous mice may be bred together.
When using the NOD.H2-Ab-/- line 11 mouse strain in a publication, please cite the originating article(s) and include JAX stock #027057 in your Materials and Methods section.