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.
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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.
In 2019-2020, researchers at The Jackson Laboratory discovered this inbred strain contains the Trem2S148E allele - a naturally occurring variant at position 48351151-48351152 on Chr 17 (rs108080490 and rs107649577; Ensembl GRCm38.p6). This TC to GA transition results in a serine to glutamic acid substitution at amino acid 148 (S148E).
SJL mice were developed by James Lambert at The Jackson Laboratory in 1955 from three different sources of Swiss Webster mice.
Allele Name | pink-eyed dilution |
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Allele Type | Spontaneous |
Allele Synonym(s) | p; R262X |
Gene Symbol and Name | Oca2, oculocutaneous albinism II |
Gene Synonym(s) | |
Strain of Origin | Asiatic fancy mice |
Chromosome | 7 |
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*). |
Allele Name | retinal degeneration 1 |
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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 | inflammatory myopathy |
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Allele Type | Spontaneous (Null/Knockout) |
Allele Synonym(s) | SJL-Dysf |
Gene Symbol and Name | Dysf, dysferlin |
Gene Synonym(s) | |
Strain of Origin | SJL |
Chromosome | 6 |
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 Name | d variant |
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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 | hepatitis virus (MHV-4) resistance |
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Allele Type | Spontaneous |
Allele Synonym(s) | Ceacam1b |
Gene Symbol and Name | Ceacam1, carcinoembryonic antigen-related cell adhesion molecule 1 |
Gene Synonym(s) | |
Strain of Origin | SJL/J |
Chromosome | 7 |
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 Name | deletion |
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Allele Type | Spontaneous |
Allele Synonym(s) | Disc1129S6; Disc1delta6 |
Gene Symbol and Name | Disc1, disrupted in schizophrenia 1 |
Gene Synonym(s) | |
Strain of Origin | various |
Chromosome | 8 |
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 in exon 6 causes a frame shift in the reading frame, resulting in 13 novel amino acids and a premature stop codon in exon 7. |
Allele Name | MCF sensitive |
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Allele Type | Spontaneous |
Allele Synonym(s) | |
Gene Symbol and Name | Rmcf, resistance to MCF virus |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 5 |
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. |
Allele Name | mutation 1 |
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Allele Type | Spontaneous |
Allele Synonym(s) | |
Gene Symbol and Name | Il2, interleukin 2 |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 3 |
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 | deletion |
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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 | mutation 1 |
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Allele Type | Spontaneous (Not Applicable) |
Allele Synonym(s) | OGG1-R336H |
Gene Symbol and Name | Ogg1, 8-oxoguanine DNA-glycosylase 1 |
Gene Synonym(s) | |
Strain of Origin | various |
Chromosome | 6 |
Molecular Note | A G-to-A change at the fifty-ninth nucleotide in exon 7 resulted in a substitution of arginine with histidine at position 336 (p.R336H) in a putative nuclear localization signal. The mutation led to disruption of the nuclear localization of the enzyme, although the activity remained normal. |
Allele Name | mutation 2 |
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Allele Type | Spontaneous (Null/Knockout) |
Allele Synonym(s) | OGG1-R304W |
Gene Symbol and Name | Ogg1, 8-oxoguanine DNA-glycosylase 1 |
Gene Synonym(s) | |
Strain of Origin | various |
Chromosome | 6 |
Molecular Note | A C-to-T change at the twelfth nucleotide in exon 6 results in a substitution of arginine with tryptophan at postion 304 (p.R304W). |
Allele Name | b variant |
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Allele Type | Spontaneous (Not Applicable) |
Allele Synonym(s) | CD5.2; Ly-1.2 |
Gene Symbol and Name | Cd5, CD5 antigen |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 19 |
Molecular Note | This variant is found in many inbred strains including C57BL/6J, C58/J, AKR/J, SJL/J, SWR. Sequence analysis shows that relative to the a variant of C3H/HeJ the b variant has point mutations that result in isoleucine instead of valine at amino acid 9, glutamine instead of leucine at amino acid 52, and phenylalanine instead of isoleucine at amino acid 71, all within the amino terminal scavenger receptor cysteine-rich D1 domain, in addition to 7 silent point mutations. |
Allele Name | myxovirus susceptibility 1 |
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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 SJL mouse strain in a publication, please include JAX stock #000686 in your Materials and Methods section.
Facility Barrier Level Descriptions
MP16 (Standard) |
MP13 (Maximum) |
RB04 (Maximum) |
QUANTITY | Volume Pricing |
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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.
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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