000933 - Strain Details

Inbred Strain

Originating Article

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. MacDearmid et al (2006) found that YBR/EiJ mice can be infected by mouse mammary tumor virus and transmit infectious MMTV, but virus production is attenuated relative to that seen in other inbred mice and YBR/EiJ mice clear the infection in successive generations. This dominant trait is not the result of antiviral antibody production, as is the case with I/LnJ mice, but rather is mediated by YBR/EiJ T cells. Nair et al (2016) mapped 2 alleles in YBR/EiJ that cause mice of this strain to develop a progressive depigmenting iris disease, elevated intraocular pressure, and glaucoma. The progressive pigment-dispersing iris stromal atrophy maps to the Tyrp1^b allele on Chromosome 4, but is less severe than that found in DBA/2J, which has an additional mutation in Gpnmb. Only the iris stroma is prone to degeneration, not the iris pigment epithelium, which degenerates in DBA/2J. Independent of Tyrp1^b, there is also a locus on YBR/EiJ Chromosome 17 between 73,461,956 bp and 86,112, 456 bp that causes high intraocular pressure to develop and when combined with Tyrp1^b the consequence is compounded. Independent of Tyrp1^b on a mixed B6;YBR background this Chromosome 17 locus may provide a model for open-angle glaucoma with no iris disease. Piletz et al. (1981) found that YBR carries an electrophoretic variant of whey acidic protein that is not found in 58 other inbred strains and may be caused by a cysteine to arginine substitution. Zheng et al (1999) found late onset hearing loss in YBR/EiJ, and slightly larger than average external ear canal volume (2007).

The stock from which this strain eventually derived was described by C.C. Little in 1934 (J Exp Med, v59 p229) as A^y/a B/b^r D/d^b, the black-eyed yellow offspring of a cross between an early DBA and Dunn’s derivative of Brooke’s English Stock, which was A^y/a B/b^r 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.

Genetic Background
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Generation
Generation Definitions >

(Last Updated: June 25th 2019)

Allele Symbol Ahr^d

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Strain of Origin

Chromosome

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.

General Note

Strain of origin - this allele was found in DBA/2J, AKR/J, 129, SWR, RF, NZB strains

Mutations Made By

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Allele Symbol Tyrp1^b

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Strain of Origin

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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 changes cysteine to tyrosine at position 110 (p.C110Y) in the encoded protein. Three other point mutations in the brown sequence were identified, but do not contribute to the mutant phenotype.

General Note

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Mutations Made By

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Allele Symbol Ces1e^h

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Strain of Origin

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Molecular Note

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General Note

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Mutations Made By

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Allele Symbol Mx1^s1

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Strain of Origin

Chromosome

Molecular Note

Many inbred mouse strains have an exon 9 to 11 deletion, resulting in a null allele and susceptibility to myxoviruses, including: A/J, ABP/Le, AKR/J, AU/SsJ, BALB/cJ, BDP/J, BUB/BnJ, C3H/HeJ, C57BL/6J, C57BL/10J, C57BL/KsJ, C57L/J, C58/J, DA/HuSn, DBA/2J, FSB/GnEi, FVB/NJ, LIS/A, LP/J, MA/MyJ, MAS/A, NZB/BINJ, P/J, PL/J, RIIIS/J, RF/J, SEA/GnJ, SEC1/ReJ, SJL/J, ST/bJ, TS1/A, TW1/A. YBR/Ei, 020/A, 129/J, SF/CamEi and SK/CamEi.

General Note

The Mx genes determine resistance to the lethal effects of various myxoviruses including neurotropic avian influenza A virus injected intracerebrally, pneumotropic strains injected intranasally, and a hepatotropic strain injected intraperitoneally (J:5645, J:13136). Resistance is not dependent on presence of the thymus and is not abolished by immunosuppression or by inhibitors of macrophage function (J:5735, J:5478, J:5645). Resistance is specific for the orthomyxoviruses (J:6265). It is dependent on the presence of interferon-alpha and -beta but not -gamma (J:7365).

The resistance allele at the Mx1 locus, under induction by alpha/beta interferon, produces the 75 kDa protein MX-1, which confers resistance to the influenza virus, in the nuclei of cells carrying the allele. Susceptibility alleles do not produce the protein (J:8273). The protein is located in the nucleus (J:7703) and produces its antiviral effect by preventing synthesis of viral mRNA in the nucleus (J:7992). Nuclear localization is necessary for anti-influenza virus activity (J:1417), but mutations induced in Mx1 showed that nuclear position was not sufficient for the effect; mutations in several domains can cause its loss (J:11840). The MX-1 protein is a GTPase containing a GTP binding domain (J:1417) and this binding core is also necessary (J:21243).

Resistance is expressed by macrophages and other cells in vitro (J:6649, J:5940) but could not be transferred to susceptible animals by transfer of macrophages from resistant mice (J:6149).

Resistance to infection with two tick-borne viruses, Thogoto virus (J:8273) and Dhori virus (J:27760), is also conferred by Mx1^r.

The Mx1^r allele occurs only in strains A2G, SL/NiA, and T9, the latter being a strain derived from an influenza-resistant wild stock, and CAST/Ei, derived from Mus musculus castaneus. Most inbred strains, including C57BL/6J, C3H/HeJ, and BALB/cJ, carry an influenza susceptible Mx1^s1 allele which produces mRNA lacking exons 9, 10, and 11 of the Mx1^r allele. This large deletion apparently renders the protein incapable of providing resistance to influenza. The CBA/J, CE/J, I/LnJ, and PERA/Ei strains, also susceptible to the virus, have another form of the Mx1^s2 allele in which there is a nonsense mutation (J:9452).

Interferon is induced by viral infection and in turn induces the Mx protein (J:7703). Although some interferon-induced genes respond directly to virus invasion as well as indirectly through induction by virus-induced interferon, this primary response is very weak for the MX-1 protein in response to either influenza or Newcastle disease viruses (J:1892).

Mutations Made By

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YBR/EiJ

How it's Made

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