Mice that are homozygous null for the Irs3 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The inactivation of Irs3 appears not to perturb glucose homeostasis with the possible exception of young (9-13 weeks, postnatal) homozygous males. These mice exhibit a fasting plasma insulin level 60% that of wildtype controls. The difference is not observed in female or older (6 months) homozygous null mice.
A targeting vector containing a herpes simplex virus thymidine kinase gene and a neomycin resistance gene driven by the mouse phosphoglycerate kinase promoter was used to disrupt the Irs3 coding region sequence. The construct was electroporated into 129S4/SvJae-derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric male was bred to C57BL/6 females. Offspring animals were bred to homozygosity. This strain arose on a B6;129 background and is maintained on the same.
|Allele Name||targeted mutation 1, Gustav E Lienhard|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||IRS3-; IRS-3-|
|Gene Symbol and Name||Irs3, insulin receptor substrate 3|
|Strain of Origin||129S4/SvJae|
|Molecular Note||A neomycin resistance cassette disrupted the coding region of the gene.|
|Mutations Made By|| |
Gustav Lienhard, Dartmouth Medical School
When maintaining a live colony, these mice can be bred as homozygotes. The expected coat color from breeding is black.
When using the IRS-3 KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #003900 in your Materials and Methods section.