The C57BL/10J substrain is similar to the C57BL/6J substrain, but allelic variants have been described at the H9, Igh2 and Lv loci. C57BL/10J mice are a valuable immunological research tool. They have a high lymphocyte phytohaemagglutinin response, a good immune response to ovalbumin, a poor response to DNP-keyhole limpet haemocyanin and are resistant to induction of passive cutaneous anaphylaxis (IgG1- and IgE- mediated). They are susceptible to immunosuppression of contact hypersensitivity by ultraviolet light, highly susceptible to TNBS-induced colitis and moderately susceptible to experimental allergic encephalomyelitisRead More +
C57BL/10J is a substrain of C57BL, and shares a common origin with C57BL/6J (Stock No. 000664), which is one of the most widely used inbred strains. Coat color is black (non-agouti), a/a. The C57BL/10J substrain is similar to the C57BL/6J substrain, but allelic variants have been described at the H9, Igh2 and Lv loci. C57BL/10J mice have a long life-span (826 +/-29 days in males, 693 +/- 31 days in females). Overall tumor incidence is 33% in males and 31% in females, most of which is due to lymphoma. C57BL/10J mice are prone to dermatitis, which is a common problem in the C57BL strain. C57BL/10J mice are a valuable immunological research tool. They have a high lymphocyte phytohaemagglutinin response, a good immune response to ovalbumin, a poor response to DNP-keyhole limpet haemocyanin and are resistant to induction of passive cutaneous anaphylaxis (IgG1- and IgE- mediated). They are susceptible to immunosuppression of contact hypersensitivity by ultraviolet light, highly susceptible to TNBS-induced colitis and moderately susceptible to experimental allergic encephalomyelitis.
The C57BL strain created by C.C. Little in the 1920's gave rise to the C57BL/6 and C57BL/10 substrains sometime before 1937, and the C57BL/10J substrain was separated from other C57BL/10 substrains in 1947.
|Allele Synonym(s)||P451L; P2rx7P451L|
|Gene Symbol and Name||P2rx7, purinergic receptor P2X, ligand-gated ion channel, 7|
|Gene Synonym(s)||P2X(7); AI467586; P2X7 receptor; P2X7R; P2X7; expressed sequence AI467586|
|Strain of Origin||various|
|Molecular Note||A proline to leucine change at amino acid residue 451 is caused by a T to C transition at nucleic acid base 1352. This mutation is found in C57BL/6, C57BL/10, DBA/1, and DBA/2 and contrasts with the condition in BALB/c, NZW, NOD, 129, Mus caroli, M. spretus, M. musculus, and M. poschiavinus. The mutation lies within a C-terminal cytoplasmic domain homologous with the TNFR 1-death domain and with an SH3 binding protein.|
|Allele Name||myxovirus susceptibility 1|
|Allele Synonym(s)||Mx1s1; myxovirus susceptibility 1|
|Gene Symbol and Name||Mx1, MX dynamin-like GTPase 1|
|Gene Synonym(s)||Mx; Mx-1; Mx; Mx-1; AI893580; myxovirus (influenza) resistance 1 polypeptide; expressed sequence AI893580; IFI-78K; MxA; MX; IFI78; MXB; lncMX1-215|
|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 Synonym(s)||Micrln; non-responder|
|Gene Symbol and Name||Micrl, microwave induced increase in complement receptor B cells|
|Strain of Origin||multiple strains|
|General Note||The following inbred strains are homozygous for the recessive QTL, Micrl |
|Allele Type||Not Applicable (Not Specified)|
|Allele Synonym(s)||Cox7a2ls; short|
|Gene Symbol and Name||Cox7a2l, cytochrome c oxidase subunit 7A2 like|
|Gene Synonym(s)||COX7RP; SIG-81; SIG81; silica-induced gene 81; Silg81; COX7AR; EB1|
|Strain of Origin||multiple strains|
|General Note||Querying the sequences of the Sanger Mouse Genomes Project reveals that the short allele with its 6 bp deletion exists in C57BL/6J, C57BL/10J, C57BL/6NJ, C58/J, BALB/cJ, C3H/HeH, 129S5/SvEvBrd, NZW/LacZ, and SEA/GnJ, but the long allele lacking the deletion exists in 129S1/SvImJ, A/J, AKR/J, BTBR T+ Itpr3tf/J, BUB/BnJ, C3H/HeJ, C57BR/cdJ, C57L/J, CAST/EiJ, CBA/J, DBA/1J, DBA/2J, FVB/NJ, I/LnJ, KK/HiJ, LEWES/EiJ, LP/J, MOLF/EiJ, NOD/ShiLtJ, NZB/BlNJ, NZO/HlLtJ, PWK/PhJ, RF/J, SPRET/EiJ, ST/bJ, WSB/EiJ, ZALENDE/EiJ.|
|Molecular Note||This allele contains a 6 bp microdeletion causing the loss of two amino acids and truncating the protein to 111 amino acids instead of 113 amino acids. It is found in BALB/cAnCrl, BALB/cJ, C57BL/6Cr, C57BL/6JCrl, C57BL/6JOlaHsd, C57BL/6NCrl, C57BL/6NJcl, C57BL/6NHsd, C57BL/6NTac, C57BL/6NJ, B6(CG)-Tyr |
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