NOR/LtJ

Stock number: 002050
Strain synonyms: NOR
Research areas: Diabetes and Obesity Research, Immunology, Inflammation and Autoimmunity Research, Neurobiology Research, Sensorineural Research

Description

NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/ShiLtJ mice (Stock No. 001976). NOR/LtJ mice are matched at the diabetogenic H2^g7 complex to NOD/ShiLtJ. In addition to serving as controls to the NOD/ShiLtJ strain, these mice are useful in studies of hearing loss.

Detailed description

NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/ShiLtJ mice (Stock No. 001976). NOR/LtJ mice are matched at the diabetogenic H2^g7 complex to NOD/ShiLtJ.

Development

NOR/LtJ is a recombinant congenic strain in which limited regions of the NOD/LtJ genome have been replaced by genome from the C57BLKS/J strain.

Allele

Symbol: Cdh23^ahl
Name: age related hearing loss 1
MGI accession ID: MGI:3028349
Generation method: Spontaneous
Synonyms: Cdh23^753A; mdfw
Marker symbol: Cdh23
Marker name: cadherin 23 (otocadherin)
Marker synonyms: 4930542A03Rik; ahl; bob; CDHR23; mdfw; nmf112; nmf181; nmf252; PITA5; sals; USH1D
Chromosome: 10
Strain of origin: multiple strains
Molecular note: Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has shown this is caused by a G to A transition at coding nucleotide position 753 of Cdh23 (SNP rs257098870). This hypomorphic allele changes splice donor site G-GT to A-GT, causing frame skipping of exon 7. This is predicted to delete part of the 2nd and 3rd ectodomains in the encoded peptide and cause reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD-1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LtJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: 129S1/SvImJ, C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.

Allele

Symbol: Gpr84^del
Name: deletion
MGI accession ID: MGI:5812913
Generation method: Spontaneous
Attributes: Null/Knockout
Marker symbol: Gpr84
Marker name: G protein-coupled receptor 84
Marker synonyms: EX33; GPCR4
Chromosome: 15
Strain of origin: multiple strains
Molecular note: This spontaneously arising frameshift deletion is located in exon 2 at position 103308576 bp (NCBI Build 37) and results in a premature stop codon. The mutation is predicted to result in a truncated protein lacking the transmembrane domains 4-7. The inbred strains BDP/J, DBA/1J, DBA/2J, I/LnJ, FVB/NJ, LG/J, MRL/MpJ, NODShi/LtJ, NOR/LtJ, P/J, PL/J, SKHIN/Sprd, SJL/J, SM/J are homozygous for the deletion. The allele is segregating in the outbred stocks ICR and CD-1.