Overview

Also Known As:CBA Carter J, CBA/Ca

The CBA inbred strain was initially bred for longevity and a low incidence of spontaneous mammary tumors relative to C3H. CBA/CaJ mice are commonly used for leukemogenesis research because this strain has a low spontaneous incidence of leukemia while myeloid leukemia can readily be induced. CBA/CaJ mice carry viral proteins Mtv8, Mtv9, and Mtv14. Male CBA/CaJ mice develop a mild adult onset diabetes-obesity syndrome that is characterized by hyperglycemia, hyperinsulinemia and insulin resistance. Unlike the CBA/J substrain, CBA/CaJ mice do not carry the retinal degeneration 1 allele (Pde6b^rd1), and CBA/CaJ mice are not histocompatible with the CBA/J.

Genetic overview

Genetic Background	Generation

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Research Applications

Diabetes and Obesity Research
Cancer Research
Research Tools
Sensorineural Research
Reproductive Biology Research

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Base Price

Starting at:

$48.36 Domestic price for female 3-week

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Details

Detailed Description

CBA inbred mice are derived from a cross of an unpedigreed Bagg albino female and an early DBA progenitor male. C3H mice are descended from the same cross. The CBA inbred strain was initially bred for longevity and a low incidence of spontaneous mammary tumors (compared with C3H). Burdette and Strong reported that CBA mice were comparatively susceptible to tumor induction after a single subcutaneous injection of methylcholanthrene. The tumor types identified in this early work in CBA mice included spindle cell sarcoma, rhabdomyosarcoma, and epidermoid carcinoma. Strong and Smith reported finding benign hepatomas in aging CBA mice. Several groups confirmed this finding, and the majority of studies found a higher frequency of spontaneous hepatomas in males than in females.

CBA/CaJ mice are commonly used for leukemogenesis research because this strain has a low spontaneous incidence of leukemia but has a relatively high inducibility of myeloid leukemia in response to benzene and radiation exposure. Multiple reports using CBA, its F1 hybrids, and other strains, have indicated that deletions in a specific segment of chromosome 2 are linked to radiation and chemical induction of myeloid leukemia. This segment is reported to map to a 1 cM interval flanked by D2Mit126 and D2Mit185 which is homologous to human chromosome segment 11p11-12.

In addition, CBA/CaJ mice have been used for the assessment of cytostatic drug combination protocols and have also been utilized successfully as hosts for childhood rhabdomyosarcoma xenografts, after thymectomy and irradiation. CBA/CaJ mice carry viral proteins Mtv8, Mtv9, and Mtv14.

Male CBA/CaJ mice develop a mild adult onset diabetes-obesity syndrome that is characterized by hyperglycemia, hyperinsulinemia and insulin resistance. Pancreatic beta cells do not degenerate and circulating insulin levels remain high throughout life.

CBA/CaJ electroretinograms show a reduced amplitude of both scotopic and photopic b-waves but normal a-wave. This was found to be caused by a p.Met66Leu mutation in metabotropic glutamate receptor 6, Grm6^nob8. This substitution at a conserved methionine causes decreased glycosylation, and decreased expression in the depolarizing bipolar cell dendritic tips, the normal site of expression, with increased expression in the cell bodies. The decreased scotopic b-wave also has prominent high frequency oscillatory potentials. There are fewer visually responsive retinal ganglion cells and the time to peak of ON retinal ganglion cells is increased relative to C57BL/6J controls, although the time to peak of OFF is normal. Retinal structure is normal. The Grm6^nob8 mutation provides a model for congenital stationary night blindness type 1B that is more mild than that provided by Grm6 null alleles, which have no b-wave. Unlike the CBA/J substrain, CBA/CaJ mice do not carry the retinal degeneration 1 allele (Pde6b^rd1). CBA/CaJ mice are not histocompatible with the CBA/J substrain (Green and Kaufer, 1965).

Development

Beginning in 1920, Strong developed the CBA inbred strain from a cross of an unpedigreed Bagg albino female and an early DBA progenitor male. C3H mice are descended from the same cross. Progeny were selected for low mammary tumor incidence. Strong sent the CBA mice to Little at The Jackson Laboratory, then to Haldane and Gruneberg (university College, London) in 1932, to Carr and Carter (Institute of Animal Genetics, Edinburgh, Scotland) in 1947, and to Green at The Jackson Laboratory in 1950.

Selected References

Figueroa CD; Taberner PV. 1994. Pancreatic islet hypertrophy in spontaneous maturity onset obese-diabetic CBA/Ca mice. Int J Biochem 26(10-11):1299-303PubMed: 7851633 MGI: J:23005
Peachey NS; Hasan N; FitzMaurice B; Burrill S; Pangeni G; Karst SY; Reinholdt L; Berry ML; Strobel M; Gregg RG; McCall MA; Chang B. 2017. A MISSENSE MUTATION IN GRM6 REDUCES BUT DOES NOT ELIMINATE MGLUR6 EXPRESSION OR ROD DEPOLARIZING BIPOLAR CELL FUNCTION. J Neurophysiol:jn.00888.2016PubMed: 28490646 MGI: J:240996
Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11PubMed: 15081119 MGI: J:89298
Rithidech KN; Cronkite EP; Bond VP. 1999. Advantages of the CBA mouse in leukemogenesis research. Blood Cells Mol Dis 25(1):38-45PubMed: 10349512 MGI: J:53730

View All References

Genetics

Grm6^nob8

Allele Symbol: Grm6^nob8

Allele Name	no b wave 8
Allele Type	Spontaneous (Hypomorph)
Allele Synonym(s)
Gene Symbol and Name	Grm6, glutamate receptor, metabotropic 6
Gene Synonym(s)
Strain of Origin	CBA/CaJ
Chromosome	11
Molecular Note	This spontaneous A-to-T transversion at position Chr11:50851337 (GRCm38) results in a missense mutation at position 66, changing methionine to leucine (p.M66L). This residue lies in the glutamate binding region and is invariant across many mammals including human.

Rmcf^r

Allele Symbol: Rmcf^r

Allele Name	MCF resistant
Allele Type	Spontaneous
Allele Synonym(s)
Gene Symbol and Name	Rmcf, resistance to MCF virus
Gene Synonym(s)
Strain of Origin	multiple strains
Chromosome	5
General Note	This locus controls resistance and susceptibility of cells in tissue culture to infection by mink cell focus-forming murine leukemia viruses. The allele Rmcf^r determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcf^s determines susceptibility and occurs in strains AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB, 129/J, and many others. Heterozygotes are as resistant as the resistant parent or nearly so. Rmcf is different from and independent of Fv1, a locus that controls susceptibility to infection by ecotropic viruses. Rmcf is located on Chr 5 close to Hm near the centromeric end (J:7108). Rmcf^r protects (AKR x CBA/Ca)F1 and (AKR x DBA/2)F1 hybrids from development of spontaneous thymic lymphomas and reduces the incidence of MCF-induced thymic lymphomas (J:7175). It also reduces susceptibility of cells of Sxv^s/Sxv^r mice to exogenous xenotropic viruses (J:7951). In addition, in strains susceptible to Friend virus-induced erythroleukemia, a condition thought to be due to the replication of MCF virus, Rmcf^r increases resistance to the virus-induced erythroleukemia. It may cause resistance by coding for or regulating the production of an MCF-related envelope glycoprotein that blocks the receptor for MCF viruses (J:8074). This conclusion is reinforced by the findings of Buller et al. (J:8497), who showed that the Rmcf^r allele contains an endogenous MCF gp70 env gene and that the Rmcf^s allele, at least in some strains (C57BL/6, CBA/J, and A/WySn), contains a xenotropic gp70 env gene. Presumably the MCF gp70 inhibits exogenous MCF infection in vitro by a mechanism of viral interference.
Molecular Note	This locus controls resistance of cells to infection by mink cell focus-forming murine leukemia viruses. The dominant r (resistance) allele is found in strains DBA/1, DBA/2 and CBA/Ca.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

congenital stationary night blindness 1B

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Diabetes and Obesity Research
- Insulin Resistance
  - males
- Obesity With Diabetes
  - males
- Hyperinsulinemia
  - adult onset, males
- Hyperglycemia
  - adult onset, males
- Type 2 Diabetes (NIDDM)
  - adult onset, males
Cancer Research
- Increased Tumor Incidence
  - Hepatomas
  - Leukemia
  - Lymphomas
  - Mammary Gland Tumors: late onset
  - Mammary Gland Tumors
Research Tools
- General Purpose
Reproductive Biology Research
- Meiotic Nondisjunction Studies

Genotype: Grm6^nob8 related

Sensorineural Research
- Eye Defects

Mammalian Phenotype Terms by Genotype

The following phenotype relates to a compound genotype created using this strain

Genotype: Grm6^nob8/Grm6^nob8
CBA/CaJ

vision/eye phenotype

decreased b wave amplitude
- The a-wave is normal, but the scotopic b-wave is reduced although not abolished, with prominant high frequency oscillatory potentials, and the photopic b-wave is reduced nearly to the levels caused by null alleles. This point mutation causes the protein to have decreased glycosylation and mislocalization to the retinal bipolar cell soma instead of the dendritic tips.

Phenotype Information

Festing Inbred Strain Characteristics: CBA

References

Figueroa CD; Taberner PV. 1994. Pancreatic islet hypertrophy in spontaneous maturity onset obese-diabetic CBA/Ca mice. Int J Biochem 26(10-11):1299-303PubMed: 7851633 MGI: J:23005
Peachey NS; Hasan N; FitzMaurice B; Burrill S; Pangeni G; Karst SY; Reinholdt L; Berry ML; Strobel M; Gregg RG; McCall MA; Chang B. 2017. A MISSENSE MUTATION IN GRM6 REDUCES BUT DOES NOT ELIMINATE MGLUR6 EXPRESSION OR ROD DEPOLARIZING BIPOLAR CELL FUNCTION. J Neurophysiol:jn.00888.2016PubMed: 28490646 MGI: J:240996
Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11PubMed: 15081119 MGI: J:89298
Rithidech KN; Cronkite EP; Bond VP. 1999. Advantages of the CBA mouse in leukemogenesis research. Blood Cells Mol Dis 25(1):38-45PubMed: 10349512 MGI: J:53730

Additional References

Festing MF; Roderick TH. 1989. Correlation between genetic distances based on single loci and on skeletal morphology in inbred mice. Genet Res 53(1):45-55PubMed: 2714645 MGI: J:280888
Geuther BQ; Deats SP; Fox KJ; Murray SA; Braun RE; White JK; Chesler EJ; Lutz CM; Kumar V. 2019. Robust mouse tracking in complex environments using neural networks. Commun Biol 2:124PubMed: 30937403 MGI: J:275426
International Nomenclature Committee. 1952. COMMITTEE on Standardized Nomenclature for Inbred Strains of Mice Cancer Res 12(8):602-13PubMed: 14945054 MGI: J:166288
Liu H; Li G; Lu J; Gao YG; Song L; Li GL; Wu H. 2019. Cellular Differences in the Cochlea of CBA and B6 Mice May Underlie Their Difference in Susceptibility to Hearing Loss. Front Cell Neurosci 13:60PubMed: 30873008 MGI: J:276076
Liu JL; Wang TS; Zhao M. 2016. Genome-Wide Association Mapping for Female Infertility in Inbred Mice. G3 (Bethesda) 6(9):2929-35PubMed: 27449513 MGI: J:244239
Park HJ; Kim MJ; Rothenberger C; Kumar A; Sampson EM; Ding D; Han C; White K; Boyd K; Manohar S; Kim YH; Ticsa MS; Gomez AS; Caicedo I; Bose U; Linser PJ; Miyakawa T; Tanokura M; Foster TC; Salvi R; Someya S. 2019. GSTA4 mediates reduction of cisplatin ototoxicity in female mice. Nat Commun 10(1):4150PubMed: 31515474 MGI: J:279409
Vazquez AE; Luebke AE; Martin GK; Lonsbury-Martin BL. 2001. Temporary and permanent noise-induced changes in distortion product otoacoustic emissions in CBA/CaJ mice. Hear Res 156(1-2):31-43PubMed: 11377880 MGI: J:71311
Xue Y; Shen SQ; Corbo JC; Kefalov VJ. 2015. Circadian and light-driven regulation of rod dark adaptation. Sci Rep 5:17616PubMed: 26626567 MGI: J:239226
Yan W; Long P; Chen T; Liu W; Yao L; Ren Z; Li X; Wang J; Xue J; Tao Y; Zhang L; Zhang Z. 2018. A Natural Occurring Mouse Model with Adgrv1 Mutation of Usher Syndrome 2C and Characterization of its Recombinant Inbred Strains. Cell Physiol Biochem 47(5):1883-1897PubMed: 29961073 MGI: J:273686
Zheng QY; Tong YC; Alagramam KN; Yu H. 2007. Tympanometry assessment of 61 inbred strains of mice. Hear Res 231(1-2):23-31PubMed: 17611057 MGI: J:123543

Additional - Grm6^nob8 related

Additional - Rmcf^r related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- End Point Analysis:Crb1End Point
- Standard PCR:Generic Pde6b Alternate1
- Probe:Pde6b Probe
- Genotyping resources and troubleshooting
Inbred mouse strains are maintained through sibling (sister x brother) matings; no genotyping required.
Breeding Considerations

This strain is a good breeder.
- Additional Breeding and Husbandry Support
Mating System
- Sibling x Sibling
Appearance
- agouti
  Related Genotype: A/A
Citation
When using the CBA/Ca mouse strain in a publication, please include JAX stock #000654 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX27 (Maximum)

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Readily Available

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Live Mouse

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weeks

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