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.
BALB/c mice are particularly well known for the production of plasmacytoma on 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) typically are susceptible, while those descended from BALB/cJ are resistant. 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 neoplasm, 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. A deficiency of Acads (acyl-Coenzyme A dehydrogenase, short chain) leads to severe organic aciduria. BALB/cByJ develop a fatty liver upon fasting or dietary fat challenge and become hypoglycemic after an 18-hour fast. BALB/cByJ mice have the advantage of better reproductive performance and less aggression than mice of the BALB/cJ substrain.
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 where D.W. Bailey obtained the substrain and maintained it through locations at the University of California Medical School at San Francisco and ultimately at The Jackson Laboratory. In 1975 at generation F136 BALB/cBy (Stock No. 000650) mice were sent to JAX production facility upon hysterectomy derivation and became the BALB/cByJ substrain.
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||b-2 variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahb-2; Ahh|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Gene Synonym(s)||bHLHe76; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; Ahh; dioxin receptor; In; Ah; Ahre; inflammatory reactivity|
|Strain of Origin||BALB/cBy|
|General Note||C57BL/6 carries the responsive Ahrb allele; DBA/2 carries nonresponsive Ahrd. Heterozygotes (Ahrb/Ahrd) are responsive (J:5282). Later work identified a second (J:8895) and later a third (J:22144) allele conferring response. Thus the allele in C57, C58, and MA/My strains is now Ahrb-1; Ahrb-2 is carried by BALB/cBy, A, and C3H; and Ahrb-3 by Mus spretus, M. caroli, and MOLF/Ei. The nonresponsive strains AKR, DBA/2, and 129 carry Ahrd (J:22144). Nucleotide and amino acid sequence differences between Ahrb-1 and Ahrd have been determined (J:17460). |
Strain of origin - this allele was found in BALB/cByJ, A/J, C3H/HeJ, CBA strains
|Molecular Note||This allele encodes a high affinity, heat labile, 104 kDa receptor containing 848 amino acids. Sequencing studies of cDNA from C57BL/6J congenic mice homozygous for this allele identified nucleotide substitutions in the ORF that would cause 5 amino acid differences between the C57BL/6J and BALB/cBy peptides, and 2 amino acid differences between the BALB/cBy and DBA/2J peptides. A T to C transition in exon 11 replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the BALB/cBy allele. This change would extend translation of the BALB/cBy mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa, vs 95 kDa for the C57BL/6J allele).|
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|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.|
|Allele Name||deletion, Jackson|
|Allele Synonym(s)||Bcd-1c; Scad|
|Gene Symbol and Name||Acads, acyl-Coenzyme A dehydrogenase, short chain|
|Gene Synonym(s)||Hdlq8; AI196007; Bcd-1; Bcd1; butyryl CoA dehydrogenase 1; ACAD3; expressed sequence AI196007; HDL QTL 8; Hdlq8; SCAD; Bcd-1; Bcd1; Scad|
|Strain of Origin||BALB/cByJ|
|Molecular Note||A 278bp deletion occurs which starts in intron "A" and includes exon "B" and the first 78bp of exon "C". As a result of this deletion, mRNA transcription is reduced to about 35% of normal and includes two forms, a longer normal length transcript and a shorter misspliced form. If these mRNAs were translated they both would result in truncated products. Protein product is undetectable immunologically and there is a total absence of enzyme activity.|
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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