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Description
Strain Information
Type Inbred Strain; Additional information on Inbred Strains. Visit our online Nomenclature tutorial. Mating System Sibling x Sibling (Female x Male) Species laboratory mouse H2 Haplotype d Generation F223p (03-JAN-08)
View larger imageAppearance
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 three months of age.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 three to four weeks of age) and becoming severe by two to three 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 three and four 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 six to seven months of age, all mice demonstrate significant widespread transillumination and thickening of the iris border. Elevation of IOP is evident in some females by six months of age. By nine 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.
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 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 000691 129X1/SvJ 000646 A/J 000647 A/WySnJ 003070 ALR/LtJ 003072 ALS/LtJ 004502 B6;AKR-Lxl2/GrsrJ 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/GrsrJ 004820 C57BL/6J-Kcne12J/J 004703 C57BL/6J-Kcnq2Nmf134/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
000957 AKXD28/TyJ
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 000674 I/LnJ 001303 NOD.CB17-Prkdcscid/J 001976 NOD/ShiLtJ 000684 NZB/BlNJ 000682 RF/J 000688 ST/bJ 000689 SWR/J
001005 AKXD1/TyJ 001003 AKXD11/TyJ 000765 AKXD13/TyJ 000779 AKXD14/TyJ 000954 AKXD15/TyJ 001093 AKXD18/TyJ 000776 AKXD2/TyJ 001062 AKXD21/TyJ 000947 AKXD22/TyJ 000949 AKXD25/TyJ 000764 AKXD27/TyJ 000959 AKXD3/TyJ 000285 B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J 000652 BDP/J 000036 BXD1/TyJ 000013 BXD16/TyJ 000015 BXD18/TyJ 000010 BXD19/TyJ 000077 BXD21/TyJ 000043 BXD22/TyJ 000081 BXD25/TyJ 006255 BXD25/TyJRwwJ 000029 BXD29/TyJ 000037 BXD5/TyJ 000007 BXD6/TyJ 000084 BXD8/TyJ 000105 BXD9/TyJ 000284 CWD/LeJ 000670 DBA/1J 000963 DBA/2J-Myo5ad+17J/Myo5ad/J 000964 DBA/2J-Myo5ad+18J/Myo5ad/J 000067 DBA/2J-Myo5ad+2J/Myo5ad/J 000673 HRS/J 000674 I/LnJ 001850 MEV-Q/TyJ 001855 MEV-V/TyJ 003345 MEV/2Ty-Emv64/J 000679 P/J 000644 SEA/GnJ 000390 STOCK Myo5ad Ds/J 000994 STOCK a Myo5ad Mregdsu/J 000286 STOCK a/a Myo5ad fd/+ +/J
000957 AKXD28/TyJ
002756 B6.CAST-Cdh23Ahl+/Kjn 002432 B6J x B6.C-H2-Kbm1/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
000664 C57BL/6J
000664 C57BL/6J
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
005012 A.B6 Tyr+-Myo5ad-l31J/J 001013 B10.D2/nSnJ-Myo5ad-n/J 000502 B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J 000963 DBA/2J-Myo5ad+17J/Myo5ad/J 000964 DBA/2J-Myo5ad+18J/Myo5ad/J 000067 DBA/2J-Myo5ad+2J/Myo5ad/J 000253 DLS/LeJ
000004 ABP/LeJ 008684 B6.Cg-Rag1tm1Mom Tyrp1B-w Tg(Tcra,Tcrb)9Rest/J 000571 B6.Cg-Whrnwi Tyrp1b/+ +/J 000027 B6.D-Tyrp1b Dock7m/J 000068 C57BL/6J-Tyrp1b-J/J 000093 C57BL/6J-Tyrp1b-cJ/J 000670 DBA/1J 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
Additional Web Information
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.
JAX® NOTES, Winter 2008; 512. DBA/2J, a multipurpose neurological disease model
National Center for Biotechnology Information / SNP Data
Phenotype
Phenotype Information
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
JAX® Physiological Data Summary [pdf]
JAX® Physiological Data Protocol [pdf]
Glaucoma-Related Pigment Dispersion Syndrome - Models with phenotypic similarity to human disease where etiologies are distinct.2
2 Human genes are associated with this disease. Orthologs of those genes do not appear in the mouse genotype(s).
assigned by genotype
GpnmbR150X/GpnmbR150X
DBA/2J
- vision/eye phenotype
- abnormal iris pigmentation (MGI Ref ID J:54013)
- pigment dispersion in the iris
- pigmentation phenotype
- abnormal iris pigmentation (MGI Ref ID J:54013)
- pigment dispersion in the iris
GpnmbR150X/GpnmbR150X Tyrp1isa/Tyrp1isa
DBA/2J
- vision/eye phenotype
- abnormal iris pigment epithelium (MGI Ref ID J:54013)
- atrophy
- abnormal iris stroma morphology (MGI Ref ID J:54013)
- atrophy
- optic nerve atrophy (MGI Ref ID J:54013)
- retinal ganglion cell degeneration (MGI Ref ID J:54013)
- loss of retinal ganglion cells
- pigmentation phenotype
- abnormal iris pigment epithelium (MGI Ref ID J:54013)
- atrophy
- nervous system phenotype
- optic nerve atrophy (MGI Ref ID J:54013)
- retinal ganglion cell degeneration (MGI Ref ID J:54013)
- loss of retinal ganglion cells
Tyrp1isa/Tyrp1isa
DBA/2J
- vision/eye phenotype
- abnormal iris stroma morphology (MGI Ref ID J:54013)
- atrophy
ahl8DBA/2J/ahl8DBA/2J
DBA/2J
- hearing/vestibular/ear phenotype
- decreased brainstem auditory evoked potential (MGI Ref ID J:139223)
- although DBA/2J is homozygous for both Cdh23
and ahl8, through linkage analysis with CAST/Ei, which is wild-type at Cdh23, ahl8 is shown to contribute up to 37% of the 16 kHz ABR threshold variation in 13 week old homozygotes - increased susceptibility to age-related hearing loss (MGI Ref ID J:139223)
- hearing loss is progressive and shows a much earlier onset than in C57BL/6J, with average 16 kHz ABR thresholds approximately 50 dB higher at 10 weeks of age than in 30 week old C57BL/6J
asp2/asp2
DBA/2J
- life span-post-weaning/aging
- premature death (MGI Ref ID J:11261)
- audiogenic seizures lead to death
- behavior/neurological phenotype
- audiogenic seizures (MGI Ref ID J:5094)
- induced by auditory stimuli
- hyperactivity (MGI Ref ID J:11261)
- wild running is induced by auditory stimuli
- nervous system phenotype
- audiogenic seizures (MGI Ref ID J:5094)
- induced by auditory stimuli
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Cdh23ahl | ||
|---|---|---|---|
| Allele Name | age related hearing loss 1 | ||
| Allele Type | QTL | ||
| Common Name(s) | Cdh23753A; mdfw; | ||
| Strain of Origin | multiple strains | ||
| 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; sals; salsa; 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, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, 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. [MGI Ref ID J:86905] | ||
| Allele Symbol | Fbrwt1DBA/2J | ||
| Allele Name | DBA/2J | ||
| Allele Type | QTL | ||
| Strain of Origin | DBA/2J | ||
| Gene Symbol and Name | Fbrwt1, forebrain weight 1 | ||
| Chromosome | 1 | ||
| Allele Symbol | Fbrwt2DBA/2J | ||
| Allele Name | DBA/2J | ||
| Allele Type | QTL | ||
| Strain of Origin | DBA/2J | ||
| Gene Symbol and Name | Fbrwt2, forebrain weight 2 | ||
| Chromosome | 11 | ||
| Gene Common Name(s) | Fbrwt11; | ||
| Allele Symbol | GpnmbR150X | ||
| Allele Name | iris pigment dispersion | ||
| Allele Type | Spontaneous | ||
| 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. [MGI Ref ID J:75398] | ||
| Allele Symbol | Hc0 | ||
| Allele Name | deficient | ||
| Allele Type | Spontaneous | ||
| 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. [MGI Ref ID J:23983] | ||
| Allele Symbol | Myo5ad | ||
| Allele Name | dilute | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | d; dv; maltese dilution; | ||
| Strain of Origin | old mutant of the mouse fancy | ||
| Gene Symbol and Name | Myo5a, myosin VA | ||
| Chromosome | 9 | ||
| Gene Common Name(s) | 9630007J19Rik; AI413174; AI661011; D; Dbv; Dop; GS1; MVa; MYH12; MYO5; MYR12; Myo5; MyoVA; RIKEN cDNA 9630007J19 gene; d; dilute; expressed sequence AI413174; expressed sequence AI661011; flail; flailer; flr; myosin V; nmf244; | ||
| General Note |
Mutations at the Myo5a locus lighten coat color through an abnormal morphology of melanocytes that causes uneven pigmentation of the hair shaft (J:11005). Most of these mutations also cause severe neurological defects; in some mutant forms, these defectslead to early death (J:12978), while in others life span is normal, but convulsions and loss of equilibrium occur after about four months of age (J:16915). Maltese dilution, as this mutation was originally called, is an old mutation of the mouse fancy. The blue-gray color of the hair produced by this mutation in nonagouti (a/a) mice is caused by clumping of the melanin pigment into a few large masses (J:12958). The melanocytes are misshapen, with fewer and thinner dendritic processes than wild-type melanocytes, and melanin granules are largely clumped around the nucleus (J:12970). Incorporation of tyrosine into melanin proceeds at a normal rate (J:12173), and the fine structure of the melanin granules is normal (J:5346). Cultured primary melanocytesfrom dilute homozygotes are normal in morphology but display clustering of melanosomes (J:37976). Griscelli disease (Chediak-Higashi-like syndrome, OMIM 214450) is a human autosomal recessive disorder whose symptoms include pigment dilution, immunodeficiency, and acute lethal lymphocyte and macrophage activation. Melanocyte malformation is characteristic of the pigment abnormality. The immunological abnormality includes absence of cutaneous hypersensitivity and impaired function of natural-killer cells. Griscelli disease resembles the dilute-lethal mouse mutant, except for the neurological disorder in the mouse. The locus for Griscelli disease colocalizes with the locus for myosin Va, which is mutated in at least some Griscelli patients. Griscelli disease is thus the homolog of mouse Maltese dilution (J:41253). The original Myo5ad mutation which identified the locuswas caused by insertion of an ecotropic murine leukemia virus (see Emv3) (J:6844, J:6587). All other mutations examined lack the virus. Reversions of Myo5ad to wild-type, which have been reported frequently, are caused by excision of the virusleaving exactly one long terminal repeat in place (J:7092). The virus is integrated into a noncoding region of the DNA (J:7751). | ||
| Molecular Note | This mutation is the result of the integration of the ecotropic murine leukemia virus Emv-3 into the normal Myo5ad gene. [MGI Ref ID J:6587] | ||
| Allele Symbol | Tyrp1isa | ||
| Allele Name | iris stromal atrophy | ||
| Allele Type | Spontaneous | ||
| 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. [MGI Ref ID J:75398] | ||
| Allele Symbol | a | ||
| Allele Name | nonagouti | ||
| Allele Type | Spontaneous | ||
| Strain of Origin | old mutant of the mouse fancy | ||
| Gene Symbol and Name | a, nonagouti | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | AGSW; AGTI; AGTIL; ASP; As; MGC126092; MGC126093; SHEP9; agouti; agouti signal protein; agouti suppressor; | ||
| 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. [MGI Ref ID J:16984] [MGI Ref ID J:24934] | ||
| Allele Symbol | ahl8DBA/2J | ||
| Allele Name | DBA/2J | ||
| Allele Type | QTL | ||
| Strain of Origin | DBA/2J | ||
| Gene Symbol and Name | ahl8, age related hearing loss 8 | ||
| Chromosome | 11 | ||
| General Note |
ahl8 interacts with Cdh23 | ||
| Molecular Note | This allele confers increased hearing loss severity at 6- and 13-weeks of age compared to C57BL/6J. [MGI Ref ID J:139223] | ||
| Allele Symbol | asp2 | ||
| Allele Name | audiogenic seizure prone 2 | ||
| Allele Type | Spontaneous | ||
| Strain of Origin | DBA/2 | ||
| Gene Symbol and Name | asp2, audiogenic seizure prone 2 | ||
| Chromosome | 4 | ||
| Gene Common Name(s) | asp; asp-2; audiogenic seizure prone; | ||
| General Note | This allele is carrried in DBA/2. C57BL/6 is resistant to audiogenic seizures. | ||
Genotyping
Genotyping Information
This strain will not have a genotyping protocol or one is not currently available.
Helpful Links
Genotyping resources and troubleshooting
References
References
Selected Reference(s)
Anderson 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] [MGI Ref ID J:75398]
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] [MGI Ref ID J:69682]
Howell GR; Libby RT; John SW. 2008. Mouse genetic models: an ideal system for understanding glaucomatous neurodegeneration and neuroprotection. Prog Brain Res 173:303-21. [PubMed: 18929118] [MGI Ref ID J:140472]
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] [MGI Ref ID 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] [MGI Ref ID 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] [MGI Ref ID 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] [MGI Ref ID 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] [MGI Ref ID J:109950]
Additional References
Belknap JK; Crabbe JC; Riggan J; O'Toole LA. 1993. Voluntary consumption of morphine in 15 inbred mouse strains. Psychopharmacology (Berl) 112(2-3):352-8. [PubMed: 7871041] [MGI Ref ID J:15468]
Chang B; Smith RS; Hawes NL; Anderson MG; Zabaleta A; Savinova O ; Roderick TH ; Heckenlively JR ; Davisson MT ; John SW. 1999. Interacting loci cause severe iris atrophy and glaucoma in DBA/2J mice. Nat Genet 21(4):405-9. [PubMed: 10192392] [MGI Ref ID J:54013]
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| Pricing for USA, Canada and Mexico shipping destinations |
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Weeks of Age Price (US dollars $) Gender 3 weeks $19.75 Female $18.20 Male 4 weeks $19.75 Female $18.20 Male 5 weeks $19.75 Female $18.20 Male 6 weeks $21.85 Female $20.30 Male 7 weeks $25.95 Female $24.40 Male 8 weeks $25.95 Female $24.40 Male 9 weeks $25.95 Female $26.50 Male 10 weeks $30.15 Female $28.60 Male 11 weeks $30.15 Female $28.60 Male 12 weeks $30.15 Female $28.60 Male 13 weeks $32.20 Female $30.65 Male 14 weeks $34.25 Female $32.70 Male 15 weeks $36.30 Female $34.75 Male
Additional Supply Details
| Supply Notes |
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| Pricing for International shipping destinations |
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Weeks of Age Price (US dollars $) Gender 3 weeks $25.70 Female $23.70 Male 4 weeks $25.70 Female $23.70 Male 5 weeks $25.70 Female $23.70 Male 6 weeks $28.50 Female $26.40 Male 7 weeks $33.80 Female $31.80 Male 8 weeks $33.80 Female $31.80 Male 9 weeks $33.80 Female $34.50 Male 10 weeks $39.20 Female $37.20 Male 11 weeks $39.20 Female $37.20 Male 12 weeks $39.20 Female $37.20 Male 13 weeks $41.90 Female $39.90 Male 14 weeks $44.60 Female $42.60 Male 15 weeks $47.20 Female $45.20 Male
Additional Supply Details
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Supply Details
| Standard Supply | Level 2. Up to 100 mice. Larger quantities or custom orders arranged upon request. |
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| Supply Notes |
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| Important 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 three months of age. | |
Payment Terms and Conditions
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
The Jackson Laboratory's Genotype Promise
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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Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
No Liability
In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. In purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.
MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.
Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.