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.
The A inbred strain, from which this substrain is derived, is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains.
Unlike A/J mice, A/WySnJ mice carry a spontaneous mutation in Tnfrsf13c and exhibit a significant loss of mature B cells (Miller, et al., 1991, Lentz et al., 1996, Shulga-Morskaya et al., 2004).
This strain is a substrain of the A strain that was developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino. The substrain branch leading to A/WySnJ has been separated from the original A strain and the branch leading to the A/J substrain since about 1930.
|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)||C5-; C5-d; C5-def; C5-deficient; hco|
|Gene Symbol and Name||Hc, hemolytic complement|
|Gene Synonym(s)||C5; C5; C5D; C5a; C5b; CPAMD4; ECLZB; He; He|
|Strain of Origin||multiple strains|
|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.|
|Allele Name||mutation 1|
|Allele Synonym(s)||Il3raA/J; Il3ran|
|Gene Symbol and Name||Il3ra, interleukin 3 receptor, alpha chain|
|Gene Synonym(s)||CD123; Cyrl; IL-3 receptor alpha chain; IL3R; IL3RAY; IL3RX; IL3RY; SUT-1; hIL-3Ra|
|Strain of Origin||A/J|
|Molecular Note||Sequence analysis revealed A/J mice lack the sequence corresponding to exon 8, which encodes 10 amino acid residues in the extracellular domain. Aberrant splicing was due to a 5 base pair deletion at the branch point in intron 7.|
|Allele Name||B-cell maturation defect 1, A/WySnJ|
|Allele Synonym(s)||Baffrm; Bcmd1A/WySnJ|
|Gene Symbol and Name||Tnfrsf13c, tumor necrosis factor receptor superfamily, member 13c|
|Gene Synonym(s)||2010006P15Rik; 2010006P15Rik; B-cell maturation defect 1; BAFF-R; BAFFR; BROMIX; Baffr; Bcmd-1; Bcmd1; Bcmd1; CD268; CVID4; Lvis22; RGD1560810; RIKEN cDNA 2010006P15 gene; prolixin|
|Strain of Origin||A/WySnJ|
|Molecular Note||In the A/WySnJ strain of mice, an intracisternal type A particle retrotransposon insertion occurred in exon 3, resulting in the replacememt of the final 8 amino acids of the encoded protein with 21 amino acids from the inserted element. FACS analysis indicated that an aberrant fusion protein was expressed from this allele that appeared on the cell surface; however, the protein appeared to be nonfuctional.|
|Allele Name||cleft lip 1|
|Gene Symbol and Name||Wnt9b, wingless-type MMTV integration site family, member 9B|
|Gene Synonym(s)||WNT14B; WNT15; Wnt14b; Wnt15; Wnt15; cleft lip; cleft lip 1; clf; clf; clf1; clf1; wingless-type MMTV integration site 15|
|Strain of Origin||A/WySn|
|General Note||Unequal duplicate epistasis - the normal allele at clf1 is a dominant suppressor of the recessive phenotype at clf2, and the normal allele at clf2 is a semidominant suppressor of the recessive phenotype at the clf1 locus.|
|Molecular Note||This mutation is a novel insertion of an IAP transposon 3' from the gene. In addition, a standard genetic test of allelism between clf1 and a Wnt9b targeted mutation demonstrated noncomplementation, showing clf1 is an allele of Wnt9b.|
|Please inquire about possible genotypes.|
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of
each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders
are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in
order to provide the minimum number of animals, animals will ship within 25 weeks.
The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.
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