BALB/cByJ

Stock number: 001026
Strain synonyms: BALB Bailey Jackson, BALB/c Bailey Jackson, CByJ
Research areas: Cancer Research, Cardiovascular Research, Immunology, Inflammation and Autoimmunity Research, Neurobiology Research, Research Tools, Sensorineural Research

Description

Mice of this substrain of BALB/c, among other differences, have better reproductive performance and less aggression than mice of the BALB/cJ substrain (Stock No. 000651).

Detailed description

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. A 2022 study found vaginal septa in 21% of BALB/cByJ females.

BALB/c mice are predisposed to dystrophic cardiac calcinosis (mineralization of cardiac tissues). Using BALB/cByJ and BALB/cJ mice obtained from The Jackson Laboratory, a study by the laboratory of Dr. Steven Taffet reports that BALB/cByJ mice exhibited more frequent and severe calcium deposition (44/49; 90% at 5 weeks of age) than did BALB/cJ (1/6; 17% at 5 weeks of age) or other BALB/c substrains [Glass et al. 2013 Comp Med 63: 29 (PMID:23561935)].

Development

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

Symbol: Hld
Name: hippocampal lamination defect
MGI accession ID: MGI:2447987
Generation method: Spontaneous
Marker symbol: Hld
Marker name: hippocampal lamination defect
Chromosome: UN
Strain of origin: BALB/cJ

Allele

Symbol: Cdh23^ahl
Name: age related hearing loss 1
MGI accession ID: MGI:3028349
Generation method: Spontaneous
Marker symbol: Cdh23
Marker name: cadherin 23 (otocadherin)
Chromosome: 10
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

Symbol: Ahr^b-2
Name: b-2 variant
MGI accession ID: MGI:2667355
Generation method: Not Applicable
Marker symbol: Ahr
Marker name: aryl-hydrocarbon receptor
Chromosome: 12
Strain of origin: BALB/cBy
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).
General note: C57BL/6 carries the responsive Ahr^b allele; DBA/2 carries nonresponsive Ahr^d. Heterozygotes (Ahr^b/Ahr^d) 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 Ahr^b-1; Ahr^b-2 is carried by BALB/cBy, A, and C3H; and Ahr^b-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 Ahr^b-1 and Ahr^d have been determined (J:17460).

Strain of origin - this allele was found in BALB/cByJ, A/J, C3H/HeJ, CBA strains

Allele

Symbol: Acads^del-J
Name: deletion, Jackson
MGI accession ID: MGI:3029768
Generation method: Spontaneous
Attributes: Null/Knockout
Marker symbol: Acads
Marker name: acyl-Coenzyme A dehydrogenase, short chain
Chromosome: 5
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.

Allele

Symbol: If1^l
Name: low response
MGI accession ID: MGI:6201402
Generation method: Spontaneous
Attributes: Hypomorph
Marker symbol: If1
Marker name: NDV-induced circulating interferon
Chromosome: 3
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

Allele

Symbol: B2m^a
Name: a variant
MGI accession ID: MGI:6357680
Generation method: Spontaneous
Attributes: Not Applicable
Marker symbol: B2m
Marker name: beta-2 microglobulin
Chromosome: 2
Strain of origin: multiple strains
Molecular note: The a variant is slightly slower running on SDS PAGE and was found to have an aspartic acid at amino acid position 85. This allele is found in A, BALB/c, LP and most other strains.

Allele

MGI accession ID: MGI:96954
Marker symbol: Mdmg1
Marker name: mandibular morphogenesis 1
Chromosome: 17