Strain Name: |
DBA/2J |
|---|---|
Stock Number: |
000671 |
Availability: | Level 1 |
General Terms and Conditions |
| Strain Common Names | D2; D2J; |
| Genes & Alleles | Cdh23; Cdh23ahl; Gpnmb; GpnmbR150X; Hc; Hc0; Tyrp1; Tyrp1isa; |
Product Information
Strain Details
Type Inbred Strain Additional information on Inbred Strains. Mating System Sibling x Sibling (Female x Male) Species laboratory mouse H2 Haplotype d Generation F223p (03-JAN-08) Appearance
dilute brown
Related Genotype: a/a Tyrp1b/Tyrp1b Myo5ad/Myo5adImportant Note
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss that is already severe by 3 months of age.Strain Description
DBA/2J is a widely used inbred strain that is valuable in a large number of research areas, including cardiovascular biology, neurobiology, and sensorineural research. Its characteristics are often contrasted with those of the C57BL/6J inbred strain (Stock No. 000664). DBA/2J mice show a low susceptibility to developing atherosclerotic aortic lesions (20 to 350 um2 atherosclerotic aortic lesions /aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). They also exhibit high-frequency hearing loss beginning roughly at the time of weaning/adolescence (between 3-4 weeks of age) and becoming severe by 2-3 months of age. This strain possesses three recessive alleles that cause progressive cochlear pathology initially affecting the organ of Corti. Decreasing anteroventral cochlear nucleus volume decreases and neuron loss parallel the progression of peripheral hearing loss. Young DBA/2J inbred mice are also susceptible to audiogenic seizures.Aging DBA/2J mice develop progressive eye abnormalities that closely mimic human hereditary glaucoma. Defects include iris pigment dispersion, iris atrophy, anterior synechia (adhesion of the iris to the cornea), and elevated intraocularpressure (IOP). The onset of disease symptoms begins between 3 and 4 months of age with 56% of females and 15% of males showing signs of iris pigment epithelium loss and transillumination of the peripheral iris. By 6 to 7 months of age, all mice demonstrate significant widespread transillumination and thickening of the iris border. Elevation of IOP is evident in some females by 6 months of age. By 9 months of age, both sexes exhibit elevated IOP, with pressures higher in females (mean: 20.3 +/-79; 1.8 mmHg) compared to males (mean: 16.2 +/-79; 1.4 mmHg). Retinal histopathology reveals retinal ganglion cell, as well as GABAergic and cholinergic amacrine cell, loss. (Moon JI, et al., 2005). Two alleles contribute to the eye phenotype, GpnmbR150X and Tyrp1isa; both are present in DBA/2J mice.
DBA/2J mice also show an extreme intolerance to alcohol and morphine. In 2002, Vance et al. reported that NK cells in DBA/2J exhibit the unique characteristic that they lack surface expression of CD94/NKG2A receptors. CD94/NKG2 receptors are normally expressed on the surface of most fetal NK cells. Expression of CD94/NKG2 is thought to play a role in self tolerance and the ability of NK cells to distinguish between MHC Ilow and MHC Ihigh target cells. CD94 is the product of the mouse Klrd1 locus, on mouse Chromosome 6. A subsequent publication by Wilhelm and coworkers identified a deletion in the 3' end of the Klrd1 gene of DBA/2J mice. This ~2.4 kb deletion does not prevent transcription of the gene, but prevents translation and cell surface expression of the CD94 protein. Analysis of DNA samples held at The Jackson Laboratory (unpublished results) confirmed the presence of the deletion of Klrd1 in the DBA/2J strain. The deletion, which occurred sometime between 1984 and 1989, is homozygous within our colonies, making DBA/2J mice naturally CD94 deficient.
Strain Development
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 is most likely results from residual heterozygosity in the strain when the substrains were separated.
Related Disease (OMIM) Terms |
Mammalian Phenotype Terms assigned by genotype |
Gene & Allele Details
| Allele Symbol | Cdh23ahl | ||
|---|---|---|---|
| Allele Name | age related hearing loss 1 | ||
| Common Name(s) | Cdh23753A; mdfw; | ||
| Strain of Origin | C57BL/6J | ||
| Gene Symbol and Name | Cdh23, cadherin 23 (otocadherin) | ||
| Chromosome | 10 | ||
| Gene Common Name(s) | 4930542A03Rik; DFNB12; DKFZp434P2350; FLJ00233; FLJ36499; KIAA1774; KIAA1812; MGC102761; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; bob; bobby; bus; bustling; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf181; nmf252; v; waltzer; | ||
| 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, 129/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129/ScJ, NOR/LtJ, A/J, C57BL/6, NOD/LyJ, 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. [J:86905] | ||
| Allele Symbol | GpnmbR150X | ||
| Allele Name | iris pigment dispersion | ||
| Common Name(s) | Gpnmbipd; | ||
| Strain of Origin | DBA/2J | ||
| Gene Symbol and Name | Gpnmb, glycoprotein (transmembrane) nmb | ||
| Chromosome | 6 | ||
| Gene Common Name(s) | Dchil; HGFIN; NMB; Osteoactivin; dendritic cell associated heparan sulfate proteoglycans dependent integrin ligand; ipd; iris pigment dispersion; | ||
| General Note |
The mouse strain DBA/2J develops glaucoma associated with iris stromal atrophy and iris pigment dispersion phneotypes. Genetic studies defined two separate loci that contribute to the overall phenotype in the DBA/2J mouse, ipd and isa. Either mutation in a homozygous state contributes to glaucoma, while mice homozygous for both mutations develop an earlier onset and more severe iris disease. | ||
| Molecular Note | The underlying mutation responsible for the phenotype in the iris pigment dispersion mouse was identified as a C to T substitution that resulted in a nonsense mutation, Arg150stop. [J:75398] | ||
| Allele Symbol | Hc0 | ||
| Allele Name | deficient | ||
| Common Name(s) | C5-; C5-d; C5-def; C5-deficient; hco; | ||
| Gene Symbol and Name | Hc, hemolytic complement | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | C5; C5a; CPAMD4; FLJ17816; FLJ17822; He; MGC142298; RGD1561905; | ||
| General Note |
This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ Hc was identified as a candidate gene for Abhr2 in a microarray analysis of lung mRNA from A/J, C3H/HeJ, and (A/J x C3H/HeJ)F1 x A/J backcross animals. Hc genotype shows statistically significant correlation to allergen-induced bronchial hyperresponsive phenotype. The A/J allele contains a 2 bp deletion resulting in deficient Hc mRNA and protein production and is associated with susceptibility to allergen-induced bronchial hyperresponsiveness. (J:108211) | ||
| Molecular Note | A 2 base "TA" deletion at positions 62 and 63 of an 83 base pair exon near the 5' end of the gene is found in the following mouse strains: A/HeJ, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ. The consequence of this deletion is the creation of a stop codon starting four bases after the deletion. A truncated product of 216 amino acids is predicted as a result although contradictory reports exist that a larger pro-C5 protein may be synthesized. Nevertheless, macrophages from mouse strains carrying this allele do not secrete complement 5. [J:23983] | ||
| Allele Symbol | Tyrp1isa | ||
| Allele Name | iris stromal atrophy | ||
| Common Name(s) | isa; | ||
| Strain of Origin | DBA/2J | ||
| Gene Symbol and Name | Tyrp1, tyrosinase-related protein 1 | ||
| Chromosome | 4 | ||
| Gene Common Name(s) | B; CAS2; CATB; GP75; TRP; TRP-1; TRP1; TYRP; Tyrp; b; b-PROTEIN; brown; iris stromal atrophy; isa; tyrosinase-related protein; | ||
| General Note |
The mouse strain DBA/2J develops glaucoma associated with iris stromal atrophy and iris pigment dispersion phneotypes. Genetic studies defined two separate loci that contribute to the overall phenotype in the DBA/2J mouse, ipd and isa. Either mutation in a homozygous state contributes to glaucoma, while mice homozygous for both mutations develop an earlier onset and more severe iris disease. | ||
| Molecular Note | Expression of a BAC containing the wild type Tyrp1 gene rescues the phenotype of isa mice. The isa phenotype has been identified in numerous aged stocks carrying Tyrp1b allele. It is therefore most probable, that the Tyrp1b alleleis responsible for the isa phenotype. [J:75398] | ||
Colony Maintenance
| Diet Information | LabDiet® 5K54 |
|---|
Related Strains
DBA Strains
000670 DBA/1J 001140 DBA/1LacJ 001907 DBA/2BiJ 000052 DBA/2DeJ 000973 DBA/2HaSmnJ 002860 DBA/8BiDsmJ View DBA Strains (6 strains)
001137 129P1/ReJ 000690 129P3/J 002065 129T2/SvEmsJ 000691 129X1/SvJ 000646 A/J 000647 A/WySnJ 003070 ALR/LtJ 003072 ALS/LtJ 004502 B6;AKR-Lxl2/J 001026 BALB/cByJ 000653 BUB/BnJ 005494 C3.129S1(B6)-Grm1rcw/J 000664 C57BL/6J 004764 C57BL/6J-Cdh23v-8J/J 003129 C57BL/6J-Epha4rb-2J/J 004820 C57BL/6J-Kcne12J/J 004703 C57BL/6J-Nmf134/J 004811 C57BL/6J-nmf110/J 004812 C57BL/6J-nmf111/J 004747 C57BL/6J-nmf118/J 004656 C57BL/6J-nmf88/J 004391 C57BL/6J-Chr 13A/J/NaJ 004385 C57BL/6J-Chr 7A/J/NaJ 000662 C57BLKS/J 000667 C57BR/cdJ 000668 C57L/J 000669 C58/J 000657 CE/J 000670 DBA/1J 001140 DBA/1LacJ 007048 DBA/2J-Gpnmb+/SjJ 002106 KK/HlJ 000675 LG/J 000676 LP/J 000677 MA/MyJ 001976 NOD/ShiLtJ 002050 NOR/LtJ 000679 P/J 002747 SENCARB/PtJ 002335 SKH2/J 003392 STOCK Crb1rd8/J
000645 A/HeJ 000646 A/J 000647 A/WySnJ 000648 AKR/J 000460 B10.D2-Hc0 H2d H2-T18c/o2SnJ 000461 B10.D2-Hc0 H2d H2-T18c/oSnJ 000657 CE/J 007048 DBA/2J-Gpnmb+/SjJ 001800 FVB/NJ 001491 FVB/NMob 001303 NOD.CB17-Prkdcscid/J 001976 NOD/ShiLtJ 000684 NZB/BlNJ 000682 RF/J 000688 ST/bJ 000689 SWR/J
002756 B6.CAST-Cdh23Ahl+/Kjn 002432 B6J x B6.C-H2bm1/ByJ-Cdh23v-J/J 002552 C57BL/6J-Cdh23v-2J/J 004764 C57BL/6J-Cdh23v-8J/J 004819 C57BL/6J-Cdh23v-9J/J 005016 CByJ;B6-Cdh23v-10J/J 000275 V/LeJ
007048 DBA/2J-Gpnmb+/SjJ
000470 AK.M-H2m H2-T18a/nSnJ 005308 B10.Cg-H2d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ 000463 B10.D2-Hc1 H2d H2-T18c/nSnJ 003147 B10.D2-Hc1 H2d H2-T18c/nSnJ-Tg(DO11.10)10Dlo/J 004306 NOD.CBALs-Hc1/LtJ
000004 ABP/LeJ 000571 B6.Cg-Whrnwi Tyrp1b/+ +/J 000027 B6.D-Tyrp1b m/J 000068 C57BL/6J-Tyrp1b-J/J 000093 C57BL/6J-Tyrp1b-cJ/J 003588 LT/SvEi 006252 LT/SvEiJ 000265 MY/HuLeJ 001045 SI/Col Tyrp1b Dnahc11iv/J 002142 STOCK 11R30m/J 000064 STOCK a Tyrp1b Sisi/J 002238 STOCK a Tyrp1b shmy/J 001432 STOCK a/a Tyrp1b sks/Tyrp1b +/J 000594 STOCK T(2;8)26H a/T(2;8)26H a Tyrp1+/Tyrp1b/J 001101 STOCK T(3;4)5Rk Tyrp1b/J 000274 TSJ/LeJ
Phenotypic Data
Body Weight Information - JAX® Mice Strain DBA/2J (000671)Mouse Phenome Database
(This chart reflects the typical correlation between body weight and age for mice maintained in production colonies at The Jackson Laboratory.)
Mouse Phenome Database - atherogenic diet
Mouse Phenome Database - body weight
Mouse Phenome Database - cardiovascular
Mouse Phenome Database - cholesterol
Mouse Phenome Database - disease susceptibility
Mouse Phenome Database - food and water intake
Mouse Phenome Database - hearing
Mouse Phenome Database - hematology
Mouse Phenome Database - hormones
Mouse Phenome Database / SNP Facility
Festing Inbred Strain Characteristics: DBA
NEW -- JAX® Physiological Data Summary
NEW -- JAX® Physiological Data Protocol
Additional Web Information
NEW -- JAX® Physiological Data Protocol
NEW -- JAX® Physiological Data Summary
Genetic Quality Control Annual Report
JAX Notes, April 1988; 433. H-2 Haplotypes of Mice from Jackson Laboratory Production Colonies.
JAX Notes, Fall 2003; 491. JAX West Expansion
JAX Notes, Fall 2004; 495. CD94 Deletion Verified in JAX® Mice Strain DBA/2J.
JAX Notes, Spring 1990; 441. Imperforate Vagina and Mucometra in Mice.
JAX Notes, Spring 2002; 485. Genes Implicated in a Mouse Model for Pigmentary Glaucoma.
JAX Notes, Spring 2003; 489. Malocclusion in the Laboratory Mouse.
JAX Notes, Summer 2003; 490. Hydrocephalus in Laboratory Mice.
JAX Notes, Winter 2006; 504. JAX® Mice: the Gold Standard Just Got Better.
National Center for Biotechnology Information / SNP Data
Animal Health Reports
Room Number AX3
Room Number AX9
Room Number MP14
Room Number WR3
Research Applications
This mouse can be used to support research in many areas including:
Cdh23ahl relatedCardiovascular Research
Diet-Induced Atherosclerosis (Relatively Resistant)
Developmental Biology Research
Lymphoid Tissue Defects (hematopoietic defects)
Neurobiology Research
Epilepsy (audiogenic seizures)
Vestibular and Hearing Defects (Age related hearing loss)
Research Tools
General Purpose
Immunology and Inflammation Research (specific complement deficiency) (C5 complement)
Sensorineural Research
Eye Defects (hereditary glaucoma)
Vestibular and Hearing Defects (Age related hearing loss)
Hc0 relatedNeurobiology Research
Vestibular and Hearing Defects (Age related hearing loss)
Sensorineural Research
Vestibular and Hearing Defects (Age related hearing loss)
Immunology and Inflammation Research
Immunodeficiency (specific complement deficiency)
Research Tools
Immunology and Inflammation Research (specific complement deficiency) (C5 complement)
References
Selected Reference(s)
Additional ReferencesAnderson MG; Smith RS; Hawes NL; Zabaleta A; Chang B; Wiggs JL; John SW. 2002. Mutations in genes encoding melanosomal proteins cause pigmentary glaucoma in DBA/2J mice. Nat Genet 30(1):81-5. [PubMed: 11743578] [J:75398]
Doering CH; Shire JG; Kessler S; Clayton RB. 1973. Genetic and biochemical studies of the adrenal lipid depletion phenotype in mice. Biochem Genet 8(1):101-11. [PubMed: 4348256] [J:5333]
Drake TA; Schadt E; Hannani K; Kabo JM; Krass K; Colinayo V; Greaser LE rd; Goldin J; Lusis AJ. 2001. Genetic loci determining bone density in mice with diet-induced atherosclerosis. Physiol Genomics 5(4):205-15. [PubMed: 11328966] [J:69682]
Kirk EA; Moe GL; Caldwell MT; Lernmark JA; Wilson DL; LeBoeuf RC. 1995. Hyper- and hypo-responsiveness to dietary fat and cholesterol among inbred mice: searching for level and variability genes. J Lipid Res 36(7):1522-32. [PubMed: 7595076] [J:28648]
Nishina PM; Wang J; Toyofuku W; Kuypers FA; Ishida BY; Paigen B. 1993. Atherosclerosis and plasma and liver lipids in nine inbred strains of mice. Lipids 28(7):599-605. [PubMed: 8355588] [J:13267]
Paigen B. 1995. Genetics of responsiveness to high-fat and high- cholesterol diets in the mouse. Am J Clin Nutr 62(2):458S-462S. [PubMed: 7625360] [J:28248]
Paigen B; Ishida BY; Verstuyft J; Winters RB; Albee D. 1990. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis 10(2):316-23. [PubMed: 2317166] [J:22615]
Paigen B; Morrow A; Brandon C; Mitchell D; Holmes P. 1985. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis 57(1):65-73. [PubMed: 3841001] [J:109950]
Price and Supply Information
| Strain Name: | DBA/2J |
| Stock Number: | 000671 |
Price Details
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Supply Details
| Standard Supply | Level 1. JAX Ready Strain® (readily available). |
|---|---|
| Supply Notes |
Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available. Strains that must be genotyped are not available until five to seven weeks of age. This strain is available from some international Charles River Laboratories (CRL) breeding facilities in Japan and/or Europe. For more information, see the Worldwide Distributor List for JAX® Mice. Genomic DNA is available for this strain from the Mouse DNA Resource. |
| Licensing | See General Terms and Conditions below |
General Terms and Conditions
View JAX® Mice & Services Conditions of Use.
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.Ordering and Purchasing Information
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