Both CASA/RkJ and CAST/EiJ (Stock No. 000928) were derived from wild mice trapped in Thailand. Like CAST, CASA is resistant to flavivirus infection. The flavivirus family includes pathogens responsible for dengue, yellow fever and several forms of encephalitis. Most common laboratory mice are sensitive to flavivirus infection. Resistance/sensitivity is conferred through the oligoA synthase Oas1b locus. In a comparison of multiple strains, CASA and CAST exhibit reduced numbers of retinal ganglion cells as compared to common laboratory strains and other wild-derived strains. Wild-derived mice are genetically distinct from common laboratory mice for a number of complex phenotypic characteristics and are valuable tools for genetic mapping, evolution and systematics research.
In 2019-2020, researchers at The Jackson Laboratory discovered this inbred strain contains the Trem2S148E allele - a naturally occurring variant at position 48351151-48351152 on Chr 17 (rs108080490 and rs107649577; Ensembl GRCm38.p6). This TC to GA transition results in a serine to glutamic acid substitution at amino acid 148 (S148E).
The founders were trapped in a grain warehouse, in Thonburi, Thailand by Dr. Joseph T Marshall, and mice were sent to Dr. Vernon Chapman and Dr. Frank Ruddle at Yale University, and, from there, to Dr. Eva Eicher and Dr. Thomas Roderick at The Jackson Laboratory in 1971. Dr. Eicher's colony were maintained by inbreeding to generate CAST/Ei and Dr. Roderick's colony were maintained by inbreeding to generate CASA/Rk and CASB/Rk. (Roderick, 1982; Chapman and Ruddle, 1972.)
|Allele Name||flavivirus resistance|
|Gene Symbol and Name||Oas1b, 2'-5' oligoadenylate synthetase 1B|
|Strain of Origin||various|
|General Note||The majority of mouse strains carry the susceptibility allele. Only the Det, BSVR, BRVR, CASA/RK, CAST/Ei, and PRI carry the resistance allele. The MOLD/Rk strain carried the allele for minor resistance. |
Genbank ID for this allele: AF481734
|Molecular Note||This allele confers resistance to flavivirus infection. Susceptible mouse strains produce a protein lacking 30% of the C-terminal region due a nucleotide substitution. The T-to-C transition in resistant strains results in the change of a premature stop codon to an arginine codon at position 253 (p.*253R).|