This strain is homozygous for Adamts20bt, Bmp5se and Tgfawa1.
Mice homozygous for the Tgfawa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth.
Mice homozygous for the recessive Adamts20bt mutation have a dorsal and a ventral unpigmented patch posterior to the midline of the trunk with the dorsal patch usually being larger than the ventral patch. These patches run in a more transverse orientation across the mouse than lengthwise and often extend around the sides of the mouse to form a white belt. The size of the patches can vary from approximately 1 to 20 percent of the surface. Unlike other spotting mutations, no variability in phenotype was identified when belted was transferred onto the C57BL/6J or JU/CtLm backgrounds (Lamoreaux 1999). Murray and Snell reported finding a small belly spot on a few heterozygotes so the Adamts20bt mutation may not be entirely recessive.
In 1954 Drs. William Murray and George Snell reported the belted mutation (Adamts20bt) that arose spontaneously in strain DBA at The University of Maine. They combined the mutations pink-eyed dilution (p) and waved 1 (Tgfawa1) with belted into a linkage testing stock called BP. Waved 1 had been found in a mixed stock by Crew in 1933. Later in the 1960s brown (Tyrp1b) and short ear (Bmpsse) from the SEC/1 strain were added by Dr. Allan Griffin and the stock was called ABP. ABP was probably sibling mated although no records are available. It was used specifically for testing in irradiation experiments. In 1969 it was taken by P. Lane and inbred as a multiple recessive inbred strain ABP/Le. It was cryopreserved at F64 in 1978 by mating homozygotes.
|Allele Name||pink-eyed dilution|
|Allele Synonym(s)||p; R262X|
|Gene Symbol and Name||Oca2, oculocutaneous albinism II|
|Strain of Origin||Asiatic fancy mice|
|General Note|| |
Oca2p is a very old mutation carried in many varieties of fancy mice (J:12958). It has been suggested that the original mutation occurred in Japanese wild mice, Mus musculus molossinus (J:19782).
|Molecular Note||A nonsense substitution was identified to account for the phenotype. It is a C to T substitution in exon 7 in the codon for the 262nd amino acid of the OCA2 protein (p.R262*).|
|Gene Symbol and Name||Tyrp1, tyrosinase-related protein 1|
|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.|
|Allele Name||waved 1|
|Allele Synonym(s)||wa-1; waved|
|Gene Symbol and Name||Tgfa, transforming growth factor alpha|
|Strain of Origin||Not Specified|
|Molecular Note||This allele was identified by a noncomplementation test with Tgfatm1Unc. Although the specific molecular lesion has not been identified, Northern blot analysis revealed that expression of TGFalpha transcript was reduced in homozygous mice.|
|Allele Name||myxovirus susceptibility 1|
|Gene Symbol and Name||Mx1, MX dynamin-like GTPase 1|
|Strain of Origin||multiple strains|
|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 Mx1r.
The Mx1r 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 Mx1s1 allele which produces mRNA lacking exons 9, 10, and 11 of the Mx1r 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 Mx1s2 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).
|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.|
|Allele Name||short ear|
|Gene Symbol and Name||Bmp5, bone morphogenetic protein 5|
|Strain of Origin||mice from Abbie Lathrop mouse farm|
|General Note||Phenotypic Similarity to Human Syndrome: Ear, Patella, Short Stature Syndrome (Meier-Gorlin Syndrome) in homozygous mice (J:24474)|
|Molecular Note||The C to T substitution creates a stop codon at arginine codon 208 (p.R208*). The resulting truncated protein does not include the carboxy terminal signaling portion of the molecule.|
|Gene Symbol and Name||Adamts20, a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 20|
|Strain of Origin||DBA/2J|
|Molecular Note||The mutation was identified as C to T transition at position 1598 that generates a substitution of leucine for proline in the ADAM cysteine-rich domain.|
When using the ABP/LeJ mouse strain in a publication, please include JAX stock #000004 in your Materials and Methods section.
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