This inbred strain has been described (Mouse Genome Database; Inbred Strains of Mice and Rats, Michael Festing) as exhibiting at least 50% amyloid with obesity in crosses with other strains, low tumor incidence, and lacks microsomal glucuronidases. The extant strain has no yellow or dilute alleles.
The stock from which this strain eventually derived was described by C.C. Little in 1934 (J Exp Med, v59 p229) as Ay/a B/br D/db, the black-eyed yellow offspring of a cross between an early DBA and Dunn's derivative of Brooke's English Stock, which was Ay/a B/br D/D (heterozygous for yellow, brown, and wildtype for dilute). This stock was shared by C. C. Little, at The Jackson Laboratory, with H. B. Andervont, at NCI, Bethesda in 1936, who sent it to W. E. Heston, NCI in 1946, when inbreeding had reach generation F30. Heston sent it to J. W. Wilson, Brown University in 1948, who sent it to T. S. Hauschka, Roswell Park Memorial Institute, Buffalo, NY in 1951, who gave it to V. M. Chapman, also at Roswell Park Memorial Institute, in1973, and he sent it to EM Eicher, at The Jackson Laboratory in 1979. The strain that arrived in the laboratory of Eva Eicher was nonagouti brown, with no yellow or dilute alleles (a/a b/b D/D). In 1980, with 25 generations of additional sibling inbreeding after arrival, this inbred strain was transferred to The Jackson Laboratory Mouse Mutant Resource and in 1989 embryos were cryopreserved at generation ?+F25+13.
|Allele Name||d variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahd; Ahk; AhRd; Ahhn; ah; in|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Gene Synonym(s)||Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity|
|Strain of Origin||Not Applicable|
|General Note|| |
Strain of origin - this allele was found in DBA/2J, AKR/J, 129, SWR, RF, NZB strains
|Molecular Note||This allele encodes a 104 kDa receptor that is stabilized by molybdate and has an affinity for ligand 10-100 fold lower than that of the receptor produced by the C57BL/6J allele. PCR sequencing of cDNA revealed ten nucleotide differences between the coding sequences of the DBA/2J and C57BL/6J receptors. Five of the ten differences would cause amino acid changes. One of these, an apparent T to C transition replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the DBA/2J allele. This change would extend translation of the DBA/2J mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa vs 95 kDa for the C57BL/6J allele). A second T to C transition changes a leucine codon in the C57BL/6J allele to a proline codon in the DBA/2J allele, and would likely change secondary structure of the peptide and thus ligand affinity.|
|Gene Symbol and Name||Tyrp1, tyrosinase-related protein 1|
|Gene Synonym(s)||B; CAS2; CATB; GP75; OCA3; Oca3; TRP; TRP-1; TRP1; TYRP; Tyrp; Tyrp; b; b-PROTEIN; brown; iris stromal atrophy; isa; isa; tyrosinase-related protein|
|Strain of Origin||old mutant of the mouse fancy|
|Molecular Note||A G-to-A transition point mutation at position 329 was shown by revertant analysis to be responsible for the mutant phenotype seen in the brown mutant. This mutation is predicted to change a cysteine residue to a tyrosine in the encoded protein. Three other point mutations in the brown sequence were identified, but do not contribute to the mutant phenotype.|
When using the YBR/EiJ mouse strain in a publication, please include JAX stock #000933 in your Materials and Methods section.
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