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 (Pde6brd1), and CBA/CaJ mice are not histocompatible with the CBA/J.Read More +
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, Grm6nob8. 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 Grm6nob8 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 (Pde6brd1). CBA/CaJ mice are not histocompatible with the CBA/J substrain (Green and Kaufer, 1965).
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.
|Allele Name||no b wave 8|
|Allele Type||Spontaneous (Hypomorph)|
|Allele Synonym(s)||no b wave 8; Grm6nob8|
|Gene Symbol and Name||Grm6, glutamate receptor, metabotropic 6|
|Gene Synonym(s)||nob4; nob3; gene model 3, (NCBI); nob3; cDNA sequence BC021919; CSNB1B; GPRC1F; nerg1; no b wave 3; mGlu6; MGLUR6; Gm3; no b wave 4; BC021919; mGluR6|
|Strain of Origin||CBA/CaJ|
|Molecular Note||This spontaneous A to T transversion at position Chr:11:50851337 (GRCm38) results in a missense mutation at position 66, changing methionine to leucine. This residue lies in the glutamate binding region and is invariant across many mammals including human.|
|Allele Name||MCF resistant|
|Allele Synonym(s)||Rmcfr; MCF resistant|
|Gene Symbol and Name||Rmcf, resistance to MCF virus|
|Strain of Origin||multiple strains|
|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 Rmcfr determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcfs 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). Rmcfr 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 Sxvs/Sxvr 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, Rmcfr 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 Rmcfr allele contains an endogenous MCF gp70 env gene and that the Rmcfs 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.|
When using the CBA/Ca mouse strain in a publication, please include JAX stock #000654 in your Materials and Methods section.
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