C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis and highly responsive to phytohemagglutinin. In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions following 14 weeks on an atherogenic diet. On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis.Read More +
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset prior to three months of age.
C57L/J mice are used widely in research as a general purpose strain. Mice have a high incidence of Hodgkin's-like reticulum cell neoplasm at 18 months of age and pituitary tumors in old multiparous females. C57L/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE) and highly responsive to phytohemagglutinin. In addition, C57L/J mice are highly susceptible to developing atherosclerotic aortic lesions (4500 to 8000 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat) (Paigen et al. 1990). On a lithogenic diet, C57L/J mice develop gallstones as a result of abnormal regulation of cholesterol synthesis (Xua et al. 2004). C57L/J mice carry no detectable endogenous ecotropic MuLV DNA sequences.
C57L/J mice were inbred following a mutation in a now extinct substrain of C57BR at F22. Inbreeding was carried out by J Murray at The Jackson Laboratory beginning in 1933. They were transferred to the production facility in 1947 at F45. The current generation of inbreeding is F203+.
|Allele Name||b-1 variant|
|Allele Type||Not Applicable (Not Applicable)|
|Allele Synonym(s)||Ah; Ahb-1; Ahb; Ahhi; Ahrb; 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||C57BL/6J|
|General Note||C57BL/6 carries the responsive Ahrb allele; DBA/2 carries nonresponsive Ahrd. Heterozygotes (Ahrb/Ahrd) are responsive (J:5282). Later work identified a second (J:8895) and later a third (J:22144) allele conferring response. Thus the allele in C57, C58, and MA/My strains is now Ahrb-1; Ahrb-2 is carried by BALB/cBy, A, and C3H; and Ahrb-3 by Mus spretus, M. caroli, and MOLF/Ei. The nonresponsive strains AKR, DBA/2, and 129 carry Ahrd (J:22144). Nucleotide and amino acid sequence differences between Ahrb-1 and Ahrd have been determined (J:17460). |
Strain of origin - this allele was found in C57BL/6, C58/J, C57BR, MA/My strains
|Molecular Note||This allele encodes a high affinity, relatively heat stabile, 95 kDa receptor. 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, a C to T transition in exon 11 would change the arginine codon in the DBA/2J allele to an opal termination codon in the C57BL/6J allele. This change would prevent the 43 amino acid extension of mRNA translation predicted for the DBA/2J allele and account for the smaller size of the peptide produced by this allele (95 kDa vs 104 kDa for the DBA/2J allele). A second C to T transition changes a proline codon in the DBA/2J allele to leucine codon in the C57BL/6J allele, and would likely change secondary structure of the peptide and thus ligand affinity.|
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||4930542A03Rik; 4930542A03Rik; CDHR23; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; ahl; bob; bob; bobby; bus; bustling; mdfw; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf112; nmf181; nmf181; nmf252; nmf252; sals; sals; salsa; v; waltzer|
|Strain of Origin||multiple strains|
|Molecular Note||Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has shown this is caused by a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7, which is predicted to delete part of the 2nd and 3rd ectodomains, and cause reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LtJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.|
|Gene Symbol and Name||Mlph, melanophilin|
|Gene Synonym(s)||2210418F23Rik; 5031433I09Rik; AW228792; D1Wsu84e; D1Wsu84e; DNA segment, Chr 1, Wayne State University 84, expressed; SLAC2-A; Slac-2a; expressed sequence AW228792; leaden; ln|
|Strain of Origin||C57BR|
|Molecular Note||This allele has a C to T transition at mRNA nucleotide position 266. This introduces a stop codon in the sequence of the normally spliced transcript and it also creates a new splice donor site in exon 2. Use of this alternative splice site yields a transcript with an in-frame 21 base pair deletion that deletes 7 amino acids from the translated protein. Northern blots failed to detect this size difference and did not find any change from normal in transcript expression level.|
|Gene Symbol and Name||Obq4, obesity QTL 4|
|Strain of Origin||C57L/J|
|General Note||Obq4 may also be consistent with an additive mode of inheritance.|
|Molecular Note||This allele confers increased adiposity in male animals compared to AKR/J, and accounts for 11.7% of the phenotypic variance in male inguinal fat pad weight (percentage).|
|Allele Name||MCF sensitive|
|Gene Symbol and Name||Rmcf, resistance to MCF virus|
|Strain of Origin||multiple strains|
|General Note|| |
This locus controls resistance and susceptibility of cells in tissue culture to infection by mink cell focus-forming murine leukemia viruses. The allele Rmcfr determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcfs determines susceptibility and occurs in strains AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB, 129/J, and many others. Heterozygotes are as resistant as the resistant parent or nearly so. Rmcf is different from and independent of Fv1, a locus that controls susceptibility to infection by ecotropic viruses. Rmcf is located on Chr 5 close to Hm near the centromeric end (J:7108). Rmcfr protects (AKR x CBA/Ca)F1 and (AKR x DBA/2)F1 hybrids from development of spontaneous thymic lymphomas and reduces the incidence of MCF-induced thymic lymphomas (J:7175). It also reduces susceptibility of cells of Sxvs/Sxvr mice to exogenous xenotropic viruses (J:7951). In addition, in strains susceptible to Friend virus-induced erythroleukemia, a condition thought to be due to the replication of MCF virus, Rmcfr increases resistance to the virus-induced erythroleukemia. It may cause resistance by coding for or regulating the production of an MCF-related envelope glycoprotein that blocks the receptor for MCF viruses (J:8074). This conclusion is reinforced by the findings of Buller et al. (J:8497), who showed that the Rmcfr allele contains an endogenous MCF gp70 env gene and that the Rmcfs allele, at least in some strains (C57BL/6, CBA/J, and A/WySn), contains a xenotropic gp70 env gene. Presumably the MCF gp70 inhibits exogenous MCF infection in vitro by a mechanism of viral interference.
|Molecular Note||This locus controls resistance of cells to infection by mink cell focus-forming murine leukemia viruses. The recessive s (susceptible) allele is found in AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB and 129/J.|
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