CBA/Ca2J

Stock number: 027000
Research areas: Cancer Research, Diabetes and Obesity Research, Reproductive Biology Research, Research Tools, Sensorineural Research

Description

This subline of CBA/CaJ was derived from a 2002 bankstock and lacks the Grm6^nob8 mutation so does not have the diminished electroretinogram b-wave that CBA/CaJ mice have.

Detailed description

This strain came from a 2002 crypreserved bankstock of CBA/CaJ. The Grm6^nob8 point mutation, which causes diminished b-wave amplitude in CBA/CaJ mice, arose spontaneously after 2002 so is absent from CBA/Ca2J, which have a normal b-wave (Peachey et al, 2017, Fig 2C).

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. Please see Stock No. 000654 for the CBA/CaJ strain.

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, who sent the strain to to Haldane and Gruneberg (university College, London) in 1932, who sent it to Carter (Institute of Animal Genetics, Edinburgh, Scotland) in 1947, who sent it to Green at The Jackson Laboratory in 1950. In 2002 the inbred strain CBA/CaJ was cryopreserved at generation F181. In 2016, when the Grm6^nob8 mutation was identified in the CBA/CaJ colony still maintained on the shelf, it was found that this 2002 bankstock lacked the Grm6^nob8 mutation. This Grm6⁺ 2002 bankstock was reanimated and bred for colony expansion then embryos were generated for cryopreservation within 2 generations of the thaw and this bankstock is CBA/Ca2J. Please see Stock No. 000654 for the CBA/CaJ strain that is homozygous for the Grm6^nob8 mutation.

Allele

Symbol: Grm6⁺
Name: wild type
MGI accession ID: MGI:2176771
Generation method: Not Specified
Marker symbol: Grm6
Marker name: glutamate receptor, metabotropic 6
Marker synonyms: CSNB1B; GPRC1F; mGlu6; mGluR6; nerg1; nob3
Chromosome: 11
Strain of origin: Not Applicable