SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene resulting in decreased levels of dysferlin protein in SJL/J mice and making this strain a good model for limb girdle muscular dystrophy 2B. SJL mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice. SJL are immunocompetent but have elevated levels of circulating T cells.Read More +
This strain is homozygous for the retinal degeneration allele Pde6brd1.
SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology including muscle fibers with central nuclei, size variation, splitting, inflammatory infiltrate, necrosis, and eventual replacement of muscle fiber with fat. While muscle weakness can be detected as early as three weeks of age the greatest pathology occurs after six months of age. SJL/J mice have also been shown to have an increased rate of muscle regeneration after injury when compared to BALB/c mice. Due to a mutation in Ceacam1 SJL/J mice are resistant to infection by certain strains of mouse hepatitis virus MHV-4.
SJL mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687). SJL/J are also useful as a control strain for studying immune defects in NOD/ShiLtJ mice (Stock No. 001976), a model for type 1 diabetes (IDDM). Both NOD and SJL/J are derived from Swiss mice; SJL are immunocompetent but have elevated levels of circulating T cells.
SJL mice were developed by James Lambert at The Jackson Laboratory in 1955 from three different sources of Swiss Webster mice.
|Allele Name||d variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahd; Ahk; AhRd; Ahhn; ah; 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||Not Applicable|
|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||hepatitis virus (MHV-4) resistance|
|Gene Symbol and Name||Ceacam1, carcinoembryonic antigen-related cell adhesion molecule 1|
|Gene Synonym(s)||BGP; BGP1; BGPI; BGPR; Bgp; Bgp; Bgp1; Bgp1; C-CAM; CD66a; Cc1; Ccam1; Cea-1; Cea-1; Cea-7; Cea-7; Cea1; Cea1; Cea7; Cea7; Hv-2; Hv-2; Hv2; Hv2; MHVR1; Mhv-1; Mhv-1; biliary glycoprotein; biliary glycoprotein 1; carcinoembryonic antigen 1; carcinoembryonic antigen 7; hepatitis virus (MHV-4) susceptibility; mCEA1; mmCGM1; mmCGM2; resistance to MHV (A59) replication in macrophages|
|Strain of Origin||SJL/J|
|General Note|| |
Previously called Mhv-1, Hv2. This locus controls resistance of neurons and macrophages to infection by the JHM and A59 strains of mouse hepatitis virus MHV-4. The allele Ceacam1Hv2-r determines resistance and has been found only in the SJL/J strain; the strains A/J, C57BL/10, BALB/c, NZB, DBA/2, AKR/J, CBA/J, C3H/He, and SWR are all susceptible to infection (Ceacam1Hv2-s. Heterozygotes are fully susceptible (J:6451, J:14870, J:7456).
|Molecular Note||This allele determines resistance to infection by the A59 strains of mouse hepatitis virus MHV-4, and is found only in the SJL/J strain. The protein encoded by this allele differs in the first 27 of the 108 amino acids of the first Ig domain compared to the susceptible allele. This region is thought to be important for virus binding.|
|Allele Synonym(s)||Disc1129S6; Disc1delta6|
|Gene Symbol and Name||Disc1, disrupted in schizophrenia 1|
|Gene Synonym(s)||C1orf136; SCZD9|
|Strain of Origin||various|
|General Note||This deletion appears in multiple strains of the 129 superfamily, 101/RI, BTBR T+ tf/J, LP/J, FVB/NJ, SJL/J, SWR/J and DDY/JclSidSeyFrkJ (J:111837, J:195189).|
|Molecular Note||A 25 bp deletion of the locus causes a frame shift in the reading frame, resulting in 13 novel amino acids and a premature stop codon at exon 7.|
|Allele Name||inflammatory myopathy|
|Gene Symbol and Name||Dysf, dysferlin|
|Gene Synonym(s)||2310004N10Rik; 2310004N10Rik; AI604795; D6Pas3; DNA segment, Chr 6, Pasteur Institute 3; FER1L1; LGMD2B; MMD1; RIKEN cDNA 2310004N10 gene; expressed sequence AI604795|
|Strain of Origin||SJL|
|Molecular Note||The molecular basis for the mutation is due to a splicing mutation in the gene, resulting from a 141 bp deletion of a small tandem repeat in an intron. This splicing mutation results in the deletion of an exon from the encoded mRNA. This results in a 171 bp in-frame deletion in the encoded mRNA, and is predicted to remove 57 amino acids from the corresponding protein. This region corresponds to most of the fourth C2 domain of the protein, and the deletion likely results in instability of the protein.|
|Allele Type||Spontaneous (Not Specified)|
|Gene Symbol and Name||Gpr84, G protein-coupled receptor 84|
|Gene Synonym(s)||EX33; GPCR4|
|Strain of Origin||multiple strains|
|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||mutation 1|
|Gene Symbol and Name||Il2, interleukin 2|
|Gene Synonym(s)||IL-2; Il-2; TCGF; lymphokine|
|Strain of Origin||multiple strains|
|Molecular Note||This hypoactive polymorphism, found in MRL/MpJ, SJL/J, and NOD/ShiLtJ inbred strains, includes a smaller polyglutamine tract predicted to shorten the first alpha helix, which forms part of the IL2 receptor binding site.|
|Allele Name||retinal degeneration 1|
|Allele Synonym(s)||Pdebrd1; rd; rd-1; rd1; rodless retina|
|Gene Symbol and Name||Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide|
|Gene Synonym(s)||CSNB3; CSNBAD2; GMP-PDEbeta; PDEB; Pdeb; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; r; rd; rd; rd-1; rd1; rd1; rd10; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10|
|Strain of Origin||various|
|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 also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested.|
|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.|
When using the SJL mouse strain in a publication, please include JAX stock #000686 in your Materials and Methods section.
Volume Pricing Program
Quantities: Volume pricing is automatically applied when a minimum quantity per strain for a shipment is reached
Sexes: Sexes of the same strain may be combined to reach minimum quantity levels to receive the volume pricing
Shipment: All shipping destinations qualify
This strain is available from some international Charles River (CR) breeding facilities in Japan and/or Europe. For more information, see the Worldwide Distributor List for JAX® Mice.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
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