Strain BDP has frequent mammary tumors and polycystic or granular kidneys with large kidney/body weight ratio. Erythrocytes have a high agglutin ability. Serum complement activity is high and plasma cholesterol is high at 12 and 24 weeks. Harderian gland has low porphyrin content. Mice of this strain have high susceptibility to audiogenic and electroconvulsive seizures. BDP mice have a novel disease phenotype with recovery of immune function after a period of profound immune suppression. This is inherited as a dominant character in crosses with both susceptible and resistant strains.
This strain is homozygous for the retinal degeneration allele Pde6brd1. See article "Genetic Background Effects: Can Your Mice See?", JAX® NOTES Spring 2002, No. 485.
Strain BDP has frequent mammary tumors and polycystic or granular kidneys with large kidney/body weight ratio. Erythrocytes have a high agglutin ability. Serum complement activity is high and plasma cholesterol is high at 12 and 24 weeks. Harderian gland has low porphyrin content. Mice of this strain have high susceptibility to audiogenic and electroconvulsive seizures. BDP mice have a novel disease phenotype with recovery of immune function after a period of profound immune suppression. This is inherited as a dominant character in crosses with both susceptible and resistant strains.
Allele Name | dilute |
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Allele Type | Spontaneous |
Allele Synonym(s) | blue dilution; d; dv; Maltese dilution |
Gene Symbol and Name | Myo5a, myosin VA |
Gene Synonym(s) | |
Strain of Origin | old mutant of the mouse fancy |
Chromosome | 9 |
Molecular Note | This mutation is the result of the integration of ecotropic murine leukemia virus Emv-3 into a noncoding region of the Myo5ad gene. Reversions of Myo5ad to wild-type are caused by excision of the virus leaving exactly one long terminal repeat in place. |
Allele Name | short ear |
---|---|
Allele Type | Spontaneous |
Allele Synonym(s) | seGnJ |
Gene Symbol and Name | Bmp5, bone morphogenetic protein 5 |
Gene Synonym(s) | |
Strain of Origin | mice from Abbie Lathrop mouse farm |
Chromosome | 9 |
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. |
Allele Name | retinal degeneration 1 |
---|---|
Allele Type | Spontaneous |
Allele Synonym(s) | Pdebrd1; rd; rd1; rd-1; rodless retina |
Gene Symbol and Name | Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide |
Gene Synonym(s) | |
Strain of Origin | various |
Chromosome | 5 |
General Note | The following inbred strains are known to be homozygous for Pde6b |
Molecular Note | Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C-to-A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain, has been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested. |
Allele Name | d variant |
---|---|
Allele Type | Not Applicable |
Allele Synonym(s) | ah; Ahd; Ahk; Ahhn; AhRd; in |
Gene Symbol and Name | Ahr, aryl-hydrocarbon receptor |
Gene Synonym(s) | |
Strain of Origin | Not Applicable |
Chromosome | 12 |
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. |
Allele Name | p variant |
---|---|
Allele Type | Not Applicable |
Allele Synonym(s) | |
Gene Symbol and Name | H2, histocompatibility-2, MHC |
Gene Synonym(s) | |
Strain of Origin | various |
Chromosome | 17 |
Molecular Note | The p haplotype of the H2 complex is known to be present in the inbred strains F/St, NB, and P/J. |
Allele Name | deletion |
---|---|
Allele Type | Spontaneous (Null/Knockout) |
Allele Synonym(s) | |
Gene Symbol and Name | Gpr84, G protein-coupled receptor 84 |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 15 |
Molecular Note | This spontaneously arising frameshift deletion is located in exon 2 at position 103308576 bp (NCBI Build 37) and results in a premature stop codon. The mutation is predicted to result in a truncated protein lacking the transmembrane domains 4-7. The inbred strains BDP/J, DBA/1J, DBA/2J, I/LnJ, FVB/NJ, LG/J, MRL/MpJ, NODShi/LtJ, NOR/LtJ, P/J, PL/J, SKHIN/Sprd, SJL/J, SM/J are homozygous for the deletion. The allele is segregating in the outbred stocks ICR and CD-1. |
Allele Name | myxovirus susceptibility 1 |
---|---|
Allele Type | Spontaneous (Null/Knockout) |
Allele Synonym(s) | |
Gene Symbol and Name | Mx1, MX dynamin-like GTPase 1 |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 16 |
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. |
When using the BDP/J mouse strain in a publication, please include JAX stock #000652 in your Materials and Methods section.
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