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||B-cell maturation defect 1|
|Allele Synonym(s)||B-cell maturation defect 1; Tnfrsf13cBcmd1|
|Gene Symbol and Name||Tnfrsf13c, tumor necrosis factor receptor superfamily, member 13c|
|Gene Synonym(s)||Bcmd-1; Bcmd1; RIKEN cDNA 2010006P15 gene; 2010006P15Rik; 2010006P15Rik; CD268; BAFFR; BAFF-R; BROMIX; B-cell maturation defect 1; RGD1560810; CVID4; prolixin; Bcmd1; Lvis22; Baffr|
|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. This mutation is not present in A/J. 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||mutation 1|
|Allele Synonym(s)||Il3ram1; mutation 1|
|Gene Symbol and Name||Il3ra, interleukin 3 receptor, alpha chain|
|Gene Synonym(s)||Cyrl; SUT-1; hIL-3Ra; IL-3 receptor alpha chain; IL3R; IL3RAY; IL3RX; IL3RY; CD123|
|Strain of Origin||multiple strains|
|General Note||This allele has been identified in A/J, A/WySnJ, A/HeJ, C58/J, RF/J, AKR/J, SM/J, BUB/BnJ, CE/J, and NZB/B1NJ. see J:24918.|
|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 Synonym(s)||deficient; Hc0|
|Gene Symbol and Name||Hc, hemolytic complement|
|Gene Synonym(s)||He; CPAMD4; ECLZB; C5b; He; C5; C5a; C5D; C5; Hfib2; hepatic fibrogenesis 2; Hfib2|
|Strain of Origin||multiple strains|
|General Note|| |
This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, A/J, 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, A/J, AKR/J, DBA/2J, I/LnJ, KK/HlJ, MOLF/EiJ, NZB/B1NJ, RF/J, ST/bJ 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||cleft lip 1|
|Allele Synonym(s)||cleft lip 1; Wnt9bclf1|
|Gene Symbol and Name||Wnt9b, wingless-type MMTV integration site family, member 9B|
|Gene Synonym(s)||clf1; Wnt15; cleft lip; cleft lip 1; WNT14B; WNT15; clf; clf1; wingless-type MMTV integration site 15; clf; Wnt15; Wnt14b|
|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.|
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||age related hearing loss 1; Cdh23ahl|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||bob; bustling; bobby; nmf112; nmf252; nmf252; 4930542A03Rik; ahl; 4930542A03Rik; W; sals; mdfw; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; modifier of deaf waddler; age related hearing loss 1; v; USH1D; nmf181; RIKEN cDNA 4930542A03 gene; CDHR23; sals; waltzer; nmf112; nmf181; mdfw; neuroscience mutagenesis facility, 112; bus; ahl; bob; salsa; PITA5|
|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 nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7, which is predicted to delete part of the 2nd and 3rd ectodomains, 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: C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.|
When using the A Woolley Snell mouse strain in a publication, please include JAX stock #000647 in your Materials and Methods section.
|Inbred, 1 pair minimum will be supplied|
We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We 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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