SJL/J

Stock number: 000686
Product name: SJL
Strain synonyms: Swiss Jim Lambert
Research areas: Cancer Research, Cardiovascular Research, Dermatology Research, Diabetes and Obesity Research, Hematological Research, Immunology, Inflammation and Autoimmunity Research, Metabolism Research, Mouse/Human Gene Homologs, Neurobiology Research, Research Tools, Sensorineural Research, Virology Research

Description

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.

Detailed description

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 Dysf^im 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 Trem2^S148E 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).

Development

SJL mice were developed by James Lambert at The Jackson Laboratory in 1955 from three different sources of Swiss Webster mice.

Allele

Symbol: Disc1^del
Name: deletion
MGI accession ID: MGI:3623217
Generation method: Spontaneous
Marker symbol: Disc1
Marker name: disrupted in schizophrenia 1
Chromosome: 8
Strain of origin: various
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.
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).

Allele

Symbol: Ceacam1^Hv2-r
Name: hepatitis virus (MHV-4) resistance
MGI accession ID: MGI:3053078
Generation method: Spontaneous
Marker symbol: Ceacam1
Marker name: carcinoembryonic antigen-related cell adhesion molecule 1
Chromosome: 7
Strain of origin: SJL/J
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.
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 Ceacam1^Hv2-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 (Ceacam1^Hv2-s. Heterozygotes are fully susceptible (J:6451, J:14870, J:7456).

Allele

Symbol: Il2^m1
Name: mutation 1
MGI accession ID: MGI:4352594
Generation method: Spontaneous
Marker symbol: Il2
Marker name: interleukin 2
Chromosome: 3
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

Symbol: Rmcf^s
Name: MCF sensitive
MGI accession ID: MGI:3798962
Generation method: Spontaneous
Marker symbol: Rmcf
Marker name: resistance to MCF virus
Chromosome: 5
Strain of origin: multiple strains
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.
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 Rmcf^r determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcf^s 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). Rmcf^r 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 Sxv^s/Sxv^r 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, Rmcf^r 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 Rmcf^r allele contains an endogenous MCF gp70 env gene and that the Rmcf^s 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.

Allele

Symbol: Ahr^d
Name: d variant
MGI accession ID: MGI:2667196
Generation method: Not Applicable
Marker symbol: Ahr
Marker name: aryl-hydrocarbon receptor
Chromosome: 12
Strain of origin: Not Applicable
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.
General note:

Strain of origin - this allele was found in DBA/2J, AKR/J, 129, SWR, RF, NZB strains

Allele

Symbol: Pde6b^rd1
Name: retinal degeneration 1
MGI accession ID: MGI:1856373
Generation method: Spontaneous
Marker symbol: Pde6b
Marker name: phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Chromosome: 5
Strain of origin: various
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.
General note: The following inbred strains are known to be homozygous for Pde6b: C3H sublines, CBA/J, FVB/NJ, PL/J, SB, SJL/J, and SWR/J.

Allele

Symbol: Dysf^im
Name: inflammatory myopathy
MGI accession ID: MGI:1857883
Generation method: Spontaneous
Attributes: Null/Knockout
Marker symbol: Dysf
Marker name: dysferlin
Chromosome: 6
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

Symbol: Gpr84^del
Name: deletion
MGI accession ID: MGI:5812913
Generation method: Spontaneous
Attributes: Null/Knockout
Marker symbol: Gpr84
Marker name: G protein-coupled receptor 84
Chromosome: 15
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

Symbol: Ogg1^m1
Name: mutation 1
MGI accession ID: MGI:6157073
Generation method: Spontaneous
Attributes: Not Applicable
Marker symbol: Ogg1
Marker name: 8-oxoguanine DNA-glycosylase 1
Chromosome: 6
Strain of origin: various
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

Symbol: Ogg1^m2
Name: mutation 2
MGI accession ID: MGI:6157074
Generation method: Spontaneous
Attributes: Null/Knockout
Marker symbol: Ogg1
Marker name: 8-oxoguanine DNA-glycosylase 1
Chromosome: 6
Strain of origin: various
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

Symbol: Cd5^b
Name: b variant
MGI accession ID: MGI:6157523
Generation method: Spontaneous
Attributes: Not Applicable
Marker symbol: Cd5
Marker name: CD5 antigen
Chromosome: 19
Strain of origin: multiple strains
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

Symbol: Mx1^s1
Name: myxovirus susceptibility 1
MGI accession ID: MGI:3715154
Generation method: Spontaneous
Attributes: Null/Knockout
Marker symbol: Mx1
Marker name: MX dynamin-like GTPase 1
Chromosome: 16
Strain of origin: multiple strains
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.
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 Mx1^r.

The Mx1^r 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 Mx1^s1 allele which produces mRNA lacking exons 9, 10, and 11 of the Mx1^r 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 Mx1^s2 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).

Allele

Symbol: Oca2^p
Name: pink-eyed dilution
MGI accession ID: MGI:1856114
Generation method: Spontaneous
Marker symbol: Oca2
Marker name: oculocutaneous albinism II
Chromosome: 7
Strain of origin: Asiatic fancy mice
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*).
General note:

Oca2^p 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).

Allele

Symbol: Hbb^s
Name: single
MGI accession ID: MGI:2677684
Generation method: Not Applicable
Marker symbol: Hbb
Marker name: hemoglobin beta chain complex
Chromosome: 7
Strain of origin: C57BL/6
Molecular note: This natural variant identified by protein sequencing, produces a single beta globin with one reactive cysteine (betaCyst13). Two structurally identical beta globins migrate during electrophoresis in a dimer with alpha globin as a single band, therefore the s designation.

Allele

Symbol: B2m^a
Name: a variant
MGI accession ID: MGI:6357680
Generation method: Spontaneous
Attributes: Not Applicable
Marker symbol: B2m
Marker name: beta-2 microglobulin
Chromosome: 2
Strain of origin: multiple strains
Molecular note: The a variant is slightly slower running on SDS PAGE and was found to have an aspartic acid at amino acid position 85. This allele is found in A, BALB/c, LP and most other strains.