BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil, forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ, Stock No. 001026) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M, 1985). Mammary tumor incidence is normally low, but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains. BALB/cByJ has a deletion in the Qa2 subregion of the murine MHC.
This is a substrain of BALB (Bagg’s albino) derived initially from the BALB strain maintained by MacDowell at Cold Spring Harbor, eventually sent to Andervont as BALB/cAn and to NIH in 1951 where D.W. Bailey obtained the substrain in 1961 at generation F99 and maintained it through locations at the University of California Medical School at San Francisco and ultimately at The Jackson Laboratory. Histocompatibility was stabilized commencing at generation F105. In 1975 at generation F136 BALB/cBy mice were sent to JAX production facility upon hysterectomy derivation and maintained there as Stock No. 001026. BALB/cBy mice were cryopreserved in 2010 at generation F210.
The Andervont/Bailey lineage and the lineage giving rise to BALB/cJ were separated from the BALB/c line maintained by Snell at The Jackson Laboratory during the period of 1937 to 1939 around generation F36.
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|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 coding nucleotide position 753 of Cdh23 (SNP rs257098870). This hypomorphic allele changes splice donor site G-GT to A-GT, causing frame skipping of exon 7. This 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: 129S1/SvImJ, C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.|
|Allele Name||low response|
|Allele Type||Spontaneous (Hypomorph)|
|Gene Symbol and Name||If1, NDV-induced circulating interferon|
|Strain of Origin||BALB/c|
|Molecular Note||This phenotypic variation causing decreased interferon production in response to particular stimuli has been mapped to distal Chromosome 3|
When using the BALB/cBy mouse strain in a publication, please include JAX stock #000650 in your Materials and Methods section.