Overview
BUB/BnJ is an inbred strain of mouse that exhibits immunological abnormalities and serves as a model for arthritis.[1]
History
The ancestry of BUB/BnJ is not well known. Random inbreeding of albino mice was conducted by Wilson at Brown University, US in 1945. The descendents of the offspring were brought to the Jackson Laboratory at generation 46, and have now passed through over 160 generations.[1]
Physical Characteristics
BUB/BnJ mice are albino, and so have completely white fur with red eyes. They also have quite a high body weight compared to most strains.[2]
Behavioral Characteristics & Handling
The Jackson Laboratory handbook describes this strain as “docile”.[2] While detailed information on their ease of handling is not given, the descriptor “docile” suggests that researchers can have high confidence in dealing with these mice.
In a two-bottle choice experiment, BUB/BnJ mice show an intermediate amount of nicotine consumption (higher than A/J but lower than C57BL/6J). This result was associated with the slow development of nicotine tolerance in BUB/BnJ.[3]
These mice also show reasonably high immobility in the forced swim test (higher than CBA/J, A/J, and many other strains), as well as an intermediate distance, travelled in the open field.[4] It seems likely that these results are manifestations of locomotor difficulties experienced by the strains as a consequence of its arthritic phenotype.
Health Characteristics
The most important health characteristic of BUB/BnJ mice is its disease phenotype resembling rheumatoid arthritis. This strain has a mutation in T cell receptor V beta which acts in concert with a number of other uncharacterized genetic modifiers to bring about collagen-induced inflammation of the joints. The disease is seen in 76% of males immunized at six to eight weeks of age.[2]
In tandem with arthritis, these mice exhibit other immune system abnormalities: they have high complement activity in the serum, and in response to challenge display nephritis with glomerular inflammation, protein in the urine and tubulointerstitial disease.[2]
They are homozygous for the mutant allele frings of G protein-coupled receptor 98, conferring susceptibility to audiogenic seizures when under 25 days of age, and hearing impairment from three to four weeks. Like many inbred strains, they also express the mutant rd1 allele of phosphodiesterase b causing progressive retinal degeneration.[2]
BUB/BnJ mice do not express any murine leukemia virus DNA sequences.[2]
Major Experimental Uses
As detailed above, BUB/BnJ is of most interest as a model for arthritis, specifically, type II collagen-induced arthritis. They can be applied to research in the field of immunology more generally, especially for issues surrounding inflammation, and can also be used in the study of epilepsy, hearing defects, retinal degeneration, and cancer.[1][2]
References
- 000653 – BUB/BnJ. 2018. 000653 – BUB/BnJ. [ONLINE] Available at: https://www.jax.org/strain/000653. [Accessed 21 December 2018].
- The Jackson Laboratory Handbook on Genetically Standardized Mice. 6th ed. 2009. [ONLINE]. Available at: http://jackson.jax.org/rs/444-BUH-304/images/JAX%20Handbook%20Genetically%20Standardized%20Mice.pdf.
- F. Clementi, D. Fornasari, C. Gotti. Neuronal Nicotinic Receptors. Springer Science & Business Media, 2012. pp. 570-571.
- Miller BH, Schultz LE, Gulati A, Su AI, Pletcher MT. 2010. Phenotypic Characterization of a Genetically Diverse Panel of Mice for Behavioral Despair and Anxiety. PLoS ONE 5(12): e14458.