DBA/1J mice are widely used as a model for rheumatoid arthritis: immunization with type II collagen leads to the development of severe polyarthritis mediated by an autoimmune response. DBA/1J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions on an atherogenic diet. In response to challenge, DBA/1J mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease.
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset after 10 months of age.
DBA/1J mice are widely used as a model for rheumatoid arthritis: immunization with type II collagen leads to the development of severe polyarthritis mediated by an autoimmune response. The incidence of collagen induced arthritis varies by experimental protocol, but is less than 100%. Similar to the human condition, mice with collagen-induced arthritis display synovitis and erosions of cartilage and bone. In addition, susceptibility in both humans and mice is linked to the expression of specific MHC class II molecules. DBA/1J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions on an atherogenic diet. In response to challenge, DBA/1J mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). There is high incidence of calcified lesions of the tongue with age. This strain is among the least responsive to phytohemagglutinin (Heiniger et al., 1975).
The DBA inbred strain is the oldest of all inbred strains of mice. Dr. CC Little began inbreeding in 1909 from a mouse colony segregating for coat color. During 1929 and 1930 crosses were made among substrains, and several new substrains were established including DBA/1 and DBA/2. DBA/1 and DBA/2 differ at a large number of loci (including the MHC H2 haplotype) which most likely results from residual heterozygosity in the strain when the substrains were separated.
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||4930542A03Rik; 4930542A03Rik; CDHR23; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; ahl; bob; bob; bobby; bus; bustling; mdfw; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf112; nmf181; nmf181; nmf252; nmf252; sals; sals; salsa; v; waltzer|
|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 identified an association between ahl and a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7 and reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD1, 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: C3H/HeSnJ, I/LnJ,YBR/Ei, MRL/MpJ.|
|Allele Synonym(s)||Maltese dilution; blue dilution; d; dv|
|Gene Symbol and Name||Myo5a, myosin VA|
|Gene Synonym(s)||9630007J19Rik; 9630007J19Rik; AI413174; AI661011; D; Dbv; Dbv; Dop; GS1; MVa; MYH12; MYO5; MYR12; Myh12; Myo5; Myo5; MyoVA; RIKEN cDNA 9630007J19 gene; d; dilute; expressed sequence AI413174; expressed sequence AI661011; flail; flail; flailer; flr; myosin V; nmf244|
|Strain of Origin||old mutant of the mouse fancy|
|Molecular Note||This mutation is the result of the integration of ecotropic murine leukemia virus Emv-3 into a noncoding region of the Myo5ad gene. Reversions of Myo5ad to wild-type are caused by excision of the virus leaving exactly one long terminal repeat in place.|
|Gene Symbol and Name||P2rx7, purinergic receptor P2X, ligand-gated ion channel, 7|
|Gene Synonym(s)||AI467586; P2X(7); P2X7; P2X7 receptor; P2X7R; expressed sequence AI467586|
|Strain of Origin||various|
|Molecular Note||A proline to leucine change at amino acid residue 451 is caused by a T to C transition at nucleic acid base 1352. This mutation is found in C57BL/6, C57BL/10, DBA/1, and DBA/2 and contrasts with the condition in BALB/c, NZW, NOD, 129, Mus caroli, M. spretus, M. musculus, and M. poschiavinus. The mutation lies within a C-terminal cytoplasmic domain homologous with the TNFR 1-death domain and with an SH3 binding protein.|
|Allele Name||MCF resistant|
|Gene Symbol and Name||Rmcf, resistance to MCF virus|
|Strain of Origin||multiple strains|
|General Note|| |
This locus controls resistance and susceptibility of cells in tissue culture to infection by mink cell focus-forming murine leukemia viruses. The allele Rmcfr determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcfs determines susceptibility and occurs in strains AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB, 129/J, and many others. Heterozygotes are as resistant as the resistant parent or nearly so. Rmcf is different from and independent of Fv1,a locus that controls susceptibility to infection by ecotropic viruses. Rmcf is located on Chr 5 close to Hm near the centromeric end (J:7108). Rmcfr protects (AKR x CBA/Ca)F1 and (AKR x DBA/2)F1 hybrids from development of spontaneous thymic lymphomas and reduces the incidence of MCF-induced thymic lymphomas (J:7175). It also reduces susceptibility of cells of Sxvs/Sxvr mice to exogenous xenotropic viruses (J:7951). In addition, in strains susceptible to Friend virus-induced erythroleukemia, a condition thought to be due to the replication of MCF virus, Rmcfr increases resistance to the virus-induced erythroleukemia. It may cause resistance by coding for or regulating the production of an MCF-related envelope glycoprotein that blocks the receptor for MCF viruses (J:8074). This conclusion is reinforced by the findings of Buller et al. (J:8497), who showed that the Rmcfr allele contains an endogenous MCF gp70 env gene and that theRmcfs allele, at least in some strains (C57BL/6, CBA/J, and A/WySn), contains a xenotropic gp70 env gene. Presumably the MCF gp70 inhibits exogenous MCF infection in vitro by a mechanism of viral interference.
|Molecular Note||This locus controls resistance of cells to infection by mink cell focus-forming murine leukemia viruses. The dominant r (resistance) allele is found in strains DBA/1, DBA/2 and CBA/Ca.|
|Gene Symbol and Name||Tyrp1, tyrosinase-related protein 1|
|Gene Synonym(s)||B; CAS2; CATB; GP75; OCA3; Oca3; TRP; TRP-1; TRP1; TYRP; Tyrp; Tyrp; b; b-PROTEIN; brown; iris stromal atrophy; isa; isa; tyrosinase-related protein|
|Strain of Origin||old mutant of the mouse fancy|
|Molecular Note||A G-to-A transition point mutation at position 329 was shown by revertant analysis to be responsible for the mutant phenotype seen in the brown mutant. This mutation is predicted to change a cysteine residue to a tyrosine in the encoded protein. Three other point mutations in the brown sequence were identified, but do not contribute to the mutant phenotype.|
|Gene Symbol and Name||a, nonagouti|
|Gene Synonym(s)||AGSW; AGTI; AGTIL; ASP; As; As; SHEP9; agouti; agouti signal protein; agouti suppressor|
|Strain of Origin||old mutant of the mouse fancy|
|General Note||Phenotypic Similarity to Human Syndrome: Metabolic Syndrome in mice homozygous for Apoetm1Unc and heterozygous for Ay and a (J:177084) |
|Molecular Note||Characterization of this allele shows an insertion of DNA comprised of a 5.5kb virus-like element, VL30, into the first intron of the agouti gene. The VL30 element itself contains an additional 5.5 kb sequence, flanked by 526 bp of direct repeats. The host integration site is the same as for at-2Gso and Aw-38J and includes a duplication of four nucleotides of host DNA and a deletion of 2 bp from the end of each repeat. Northern analysis of mRNA from skin of homozygotes shows a smaller agouti message and levels 8 fold lower than found in wild-type.|
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