These double knock-out Line F mice carry two knock-out insulin genes, Ins1 and Ins2 along with a transgene expressing a mutated insulin. Female transgenic mice fail to produce insulin autoantibodies, and show no diabetes or insulitis. Sialitis is expressed at a higher level than Line B (Stock No. 005524).
George Eisenbarth, U of Colorado
Genetic Background | Generation |
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|
Allele Type | Gene Symbol | Gene Name |
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Targeted (Null/Knockout) | Ins1 | insulin I |
Allele Type | Gene Symbol | Gene Name |
---|---|---|
Targeted (Reporter, Null/Knockout) | Ins2 | insulin II |
Allele Type |
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Transgenic (Inserted expressed sequence) |
Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. In contrast, transgenic mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005).
This stock is useful to study insulin-reactive autoimmunity.
NOD-Tg(Ins2*Y16A)3Ell/GseJ expresses the rat insulin 7 promoter fused to a mutated preproinsulin II cDNA, where the tyrosine at position 16 of the b chain was replaced with alanine. This transgene was inserted by Nakayama et al, 2004 directly into NOD/MrkTac oocytes. Offspring from the founder line F was further crossed to NOD.Ins1-/- and NOD.Ins2-/- prior to intercrossing for homozygosity of the Ins1 and Ins2 targeted mutations. In 2006, the T1DR received NOD.Cg-Tg(Ins2*Y16A)3Ell Ins1tm1Jja Ins2tm1Jja/GseJ at generation N10F9.
Expressed Gene | lacZ, beta-galactosidase, E. coli |
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Site of Expression | |
Expressed Gene | Ins2, insulin 2, rat |
Site of Expression |
Allele Name | targeted mutation 1, Jacques Jami |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | Ins1- |
Gene Symbol and Name | Ins1, insulin I |
Gene Synonym(s) | |
Strain of Origin | 129S2/SvPas |
Chromosome | 19 |
Molecular Note | The majority of the coding region was replaced with a neomycin selection cassette. RT-PCR analysis showed an absence of transcript in homozygous mutant mice. |
Mutations Made By | Jacques Jami, INSERM |
Allele Name | targeted mutation 1, Jacques Jami |
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Allele Type | Targeted (Reporter, Null/Knockout) |
Allele Synonym(s) | Ins2-; proins-2-; proinsulin 2- |
Gene Symbol and Name | Ins2, insulin II |
Gene Synonym(s) | |
Expressed Gene | lacZ, beta-galactosidase, E. coli |
Strain of Origin | 129S2/SvPas |
Chromosome | 7 |
Molecular Note | The majority of the coding region was replaced by the insertion of a lacZ-neo fusion gene. The expression of lacZ was found to be under the control of the endogenous promoter via cytochemical assays. |
Mutations Made By | Jacques Jami, INSERM |
Allele Name | transgene insertion 3, John F Elliot |
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Allele Type | Transgenic (Inserted expressed sequence) |
Allele Synonym(s) | tg B:16 alanine, line F |
Gene Symbol and Name | Tg(Ins2*Y16A)3Ell, transgene insertion 3, John F Elliot |
Gene Synonym(s) | |
Promoter | Ins2, insulin 2, rat |
Expressed Gene | Ins2, insulin 2, rat |
Strain of Origin | NOD/MrkTac |
Chromosome | UN |
Molecular Note | This transgenic construct contains the rat insulin7 construct of the rat insulin 2 gene fused to a mutated preproinsulin II cDNA where the tyrosine at position 16 of the B chain was replaced with alanine. The transgene is expressed in pancreatic beta cells. |
Mutations Made By | John Elliott, University of Alberta |
Genotypes available: Tg/?, Ins1-/-, Ins2-/-
Breeders available: Tg/?, Ins1-/-, Ins2-/- female x Tg/?, Ins1-/-, Ins2-/- male
Affected mutant: Tg/?, Ins1-/-, Ins2-/-
TJL mating scheme: Tg/?, Ins1-/-, Ins2-/- female x Tg/?, Ins1-/-, Ins2-/- male
When using the NOD.Tg B:16 alanine, line F (high), Ins1null, Ins2null mouse strain in a publication, please cite the originating article(s) and include JAX stock #005525 in your Materials and Methods section.
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