BALB/cJ

Stock number: 000651
Product name: BALBc
Strain synonyms: C, BALB, BALB/c
Research areas: Cancer Research, Cardiovascular Research, Hematological Research, Immunology, Inflammation and Autoimmunity Research, Mouse/Human Gene Homologs, Neurobiology Research, Research Tools, Sensorineural Research

Description

BALB/cJ is a commonly used inbred. Key traits include a susceptibility to developing the demyelinating disease upon infection with Theiler's murine encephalomyelitis virus. The BALB/cJ substrain is susceptible to Listeria, all species of Leishmania, and several species of Trypanosoma, but is resistant to experimental allergic orchitis (EAO).

Detailed description

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) 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. This strain was found to be susceptible to infection by Listeria monocytogenes, with a 3 day median time to death in females (Cheers and McKenzie, 1978).

White et al. reported a variation in thioglycolate medium-induced peritoneal leukocyte recruitment in 4 analyzed strains. The response of total leukocyte recruitment, from greatest to least, was C57BL/6J>BALB/c>CD1>129X1/SvJ. Variations were also found in the timeline of response and cell types most impacted.

BALB/c mice immunized with PLP_180-199 develop an atypical form of experimental autoimmune encephalomyelitis (EAE) in which susceptibility is determined by location. In the spinal cord 60-70% mice develop pathological lesions and in the brain and cerebellum 100% of mice develop sever lesions.

Dorso-ventral vaginal septa is observed in some BALB/cJ females, and may contribute to non-productive females in this strain. (Cunliffe-Beamer T, Lab Anim Sci, 1976)

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)].

Mice may often exhibit yellow fur, particularly around genital region (presumably the result of urination stains), which may be accompanied by localized hair loss and more prominent in older mice.

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 G.D. Snell at the University of Texas and brought by Snell to the Jackson Laboratory in 1932 at generation F26. Three branches from Snell’s BALB/c were separated during the period 1937-1939, Andervont (BALB/cAn), Scott (BALB/cSc), and Green (BALB/cGn). The lineage from BALB/cSc eventually became BALB/cJ in 1941 at generation F41.

Allele

Symbol: Micrlⁿ
Name: non-responder
MGI accession ID: MGI:5014256
Generation method: QTL
Marker symbol: Micrl
Marker name: microwave induced increase in complement receptor B cells
Chromosome: 5
Strain of origin: multiple strains
General note: The following inbred strains are homozygous for the recessive QTL, Micrl, and do not respond to microwave exposure by increasing splenic C3 receptor-bearing B cells: A/J, BALB/cJ, C3HeB/FeN, C57BL/6J, C57BL/10J (inferred from the response of two congenic lines "B10.BR", "B10.D2", "B10.D2"), C58/J, AK.B6-H2^b, and B6.AK-H2^k. These recombinant inbred strains are also non-responding: BXH2/Ty, BXH6/Ty, BXH7/Ty, BXH12/Ty, and BXH14/Ty.

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: Mx1^s1
Name: myxovirus susceptibility 1
MGI accession ID: MGI:3715154
Generation method: Spontaneous
Attributes: Null/Knockout
Marker symbol: Mx1
Marker name: MX dynamin-like GTPase 1
Chromosome: 16
Strain of origin: multiple strains
Molecular note: Many inbred mouse strains have an exon 9 to 11 deletion, resulting in a null allele and susceptibility to myxoviruses, including: A/J, ABP/Le, AKR/J, AU/SsJ, BALB/cJ, BDP/J, BUB/BnJ, C3H/HeJ, C57BL/6J, C57BL/10J, C57BL/KsJ, C57L/J, C58/J, DA/HuSn, DBA/2J, FSB/GnEi, FVB/NJ, LIS/A, LP/J, MA/MyJ, MAS/A, NZB/BINJ, P/J, PL/J, RIIIS/J, RF/J, SEA/GnJ, SEC1/ReJ, SJL/J, ST/bJ, TS1/A, TW1/A. YBR/Ei, 020/A, 129/J, SF/CamEi and SK/CamEi.
General note:

The Mx genes determine resistance to the lethal effects of various myxoviruses including neurotropic avian influenza A virus injected intracerebrally, pneumotropic strains injected intranasally, and a hepatotropic strain injected intraperitoneally (J:5645, J:13136). Resistance is not dependent on presence of the thymus and is not abolished by immunosuppression or by inhibitors of macrophage function (J:5735, J:5478, J:5645). Resistance is specific for the orthomyxoviruses (J:6265). It is dependent on the presence of interferon-alpha and -beta but not -gamma (J:7365).

The resistance allele at the Mx1 locus, under induction by alpha/beta interferon, produces the 75 kDa protein MX-1, which confers resistance to the influenza virus, in the nuclei of cells carrying the allele. Susceptibility alleles do not produce the protein (J:8273). The protein is located in the nucleus (J:7703) and produces its antiviral effect by preventing synthesis of viral mRNA in the nucleus (J:7992). Nuclear localization is necessary for anti-influenza virus activity (J:1417), but mutations induced in Mx1 showed that nuclear position was not sufficient for the effect; mutations in several domains can cause its loss (J:11840). The MX-1 protein is a GTPase containing a GTP binding domain (J:1417) and this binding core is also necessary (J:21243).

Resistance is expressed by macrophages and other cells in vitro (J:6649, J:5940) but could not be transferred to susceptible animals by transfer of macrophages from resistant mice (J:6149).

Resistance to infection with two tick-borne viruses, Thogoto virus (J:8273) and Dhori virus (J:27760), is also conferred by Mx1^r.

The Mx1^r allele occurs only in strains A2G, SL/NiA, and T9, the latter being a strain derived from an influenza-resistant wild stock, and CAST/Ei, derived from Mus musculus castaneus. Most inbred strains, including C57BL/6J, C3H/HeJ, and BALB/cJ, carry an influenza susceptible Mx1^s1 allele which produces mRNA lacking exons 9, 10, and 11 of the Mx1^r allele. This large deletion apparently renders the protein incapable of providing resistance to influenza. The CBA/J, CE/J, I/LnJ, and PERA/Ei strains, also susceptible to the virus, have another form of the Mx1^s2 allele in which there is a nonsense mutation (J:9452).

Interferon is induced by viral infection and in turn induces the Mx protein (J:7703). Although some interferon-induced genes respond directly to virus invasion as well as indirectly through induction by virus-induced interferon, this primary response is very weak for the MX-1 protein in response to either influenza or Newcastle disease viruses (J:1892).

Allele

Symbol: Cox7a2l^s
Name: short
MGI accession ID: MGI:6276120
Generation method: Not Applicable
Attributes: Not Specified
Marker symbol: Cox7a2l
Marker name: cytochrome c oxidase subunit 7A2 like
Chromosome: 17
Strain of origin: multiple strains
Molecular note: This allele contains a 6 bp microdeletion causing the loss of two amino acids and truncating the protein to 111 amino acids instead of 113 amino acids. It is found in BALB/cAnCrl, BALB/cJ, C57BL/6Cr, C57BL/6JCrl, C57BL/6JOlaHsd, C57BL/6NCrl, C57BL/6NJcl, C57BL/6NHsd, C57BL/6NTac, C57BL/6NJ, B6(CG)-Tyr/J, C57BL/6JClr, C57BL/6JArc, C57BL/6JJcl, C57BL/6JJmsSlc, C57BL/6JOla, C57BL/6JOlaHsd, C57BL/6JRcc, C57BL/6JRccHsd, C57BL/6JBom, and C57BL/6JBomTac mice.
General note: Querying the sequences of the Sanger Mouse Genomes Project reveals that the short allele with its 6 bp deletion exists in C57BL/6J, C57BL/10J, C57BL/6NJ, C58/J, BALB/cJ, C3H/HeH, 129S5/SvEvBrd, NZW/LacZ, and SEA/GnJ, but the long allele lacking the deletion exists in 129S1/SvImJ, A/J, AKR/J, BTBR T⁺ Itpr3^tf/J, BUB/BnJ, C3H/HeJ, C57BR/cdJ, C57L/J, CAST/EiJ, CBA/J, DBA/1J, DBA/2J, FVB/NJ, I/LnJ, KK/HiJ, LEWES/EiJ, LP/J, MOLF/EiJ, NOD/ShiLtJ, NZB/BlNJ, NZO/HlLtJ, PWK/PhJ, RF/J, SPRET/EiJ, ST/bJ, WSB/EiJ, ZALENDE/EiJ.

Allele

Symbol: Hbb^d
Name: d
MGI accession ID: MGI:1858119
Generation method: Not Applicable
Marker symbol: Hbb
Marker name: hemoglobin beta chain complex
Chromosome: 7
Strain of origin: BALB/c

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.