Overview

Also Known As:Swiss Jim Lambert, SJL

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.

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2018-07-27 00:00:00)

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Research Applications

Cardiovascular Research
Cancer Research
Sensorineural Research
Diabetes and Obesity Research
Research Tools
Immunology, Inflammation and Autoimmunity Research
Mouse/Human Gene Homologs
Dermatology Research

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Details

Important Note

This strain is homozygous for the retinal degeneration allele Pde6b^rd1.

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.

Selected References

Bittner RE; Anderson LV; Burkhardt E; Bashir R; Vafiadaki E; Ivanova S; Raffelsberger T; Maerk I; Hoger H; Jung M; Karbasiyan M; Storch M; Lassmann H; Moss JA; Davison K; Harrison R; Bushby KM; Reis A. 1999. Dysferlin deletion in SJL mice (SJL-Dysf) defines a natural model for limb girdle muscular dystrophy 2B [letter] Nat Genet 23(2):141-2PubMed: 10508505 MGI: J:57764
Crispens CG. 1973. Some characteristics of strain SJL-JDg mice. Lab Anim Sci 23(3):408-13PubMed: 4351481 MGI: J:25445
Dal Canto MC; Melvold RW; Kim BS; Miller SD. 1995. Two models of multiple sclerosis: experimental allergic encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus (TMEV) infection. A pathological and immunological comparison. Microsc Res Tech 32(3):215-29PubMed: 8527856 MGI: J:109910
Fischer Lindahl K. 1997. On naming H2 haplotypes: functional significance of MHC class Ib alleles. Immunogenetics 46(1):53-62PubMed: 9148789 MGI: J:41130
Fujinaga S; Poel WE; Williams WC; Dmochowski L. 1970. Biological and morphological studies of SJL-J strain reticulum cell neoplasms induced and transmitted serially in low-leukemia-strain mice. Cancer Res 30(3):729-42PubMed: 4316600 MGI: J:25329
McGeachie JK; Grounds MD. 1995. Retarded myogenic cell replication in regenerating skeletal muscles of old mice: an autoradiographic study in young and old BALBc and SJL/J mice. Cell Tissue Res 280(2):277-82PubMed: 7781025 MGI: J:25692
Murphy ED. 1963. SJL/J, a new inbred strain of mouse with a high, early incidence of reticulum-cell neoplasms Proc Am Assoc Cancer Res 4:46 (Abstr.)MGI: J:2463
Nishina PM; Wang J; Toyofuku W; Kuypers FA; Ishida BY; Paigen B. 1993. Atherosclerosis and plasma and liver lipids in nine inbred strains of mice. Lipids 28(7):599-605PubMed: 8355588 MGI: J:13267
Paigen B; Ishida BY; Verstuyft J; Winters RB; Albee D. 1990. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis 10(2):316-23PubMed: 2317166 MGI: J:22615
Paigen B; Morrow A; Brandon C; Mitchell D; Holmes P. 1985. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis 57(1):65-73PubMed: 3841001 MGI: J:109950
Vafiadaki E; Reis A; Keers S; Harrison R; Anderson LV; Raffelsberger T; Ivanova S; Hoger H; Bittner RE; Bushby K; Bashir R. 2001. Cloning of the mouse dysferlin gene and genomic characterization of the SJL-Dysf mutation. Neuroreport 12(3):625-9PubMed: 11234777 MGI: J:67994
Weller AH; Magliato SA; Bell KP; Rosenberg NL. 1997. Spontaneous myopathy in the SJL/J mouse: pathology and strength loss. Muscle Nerve 20(1):72-82PubMed: 8995586 MGI: J:38007

View All References

Genetics

Oca2^p

Allele Symbol: Oca2^p

Allele Name	pink-eyed dilution
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	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).
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*).

Pde6b^rd1

Allele Symbol: Pde6b^rd1

Allele Name	retinal degeneration 1
Allele Type	Spontaneous
Allele Synonym(s)	Pdeb^rd1; 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: C3H sublines, CBA/J, FVB/NJ, PL/J, SB, SJL/J, and SWR/J.
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.

Dysf^im

Allele Symbol: Dysf^im

Allele Name	inflammatory myopathy
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.

Ahr^d

Allele Symbol: Ahr^d

Allele Name	d variant
Allele Type	Not Applicable
Allele Synonym(s)	ah; Ah^d; Ah^k; 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.

Ceacam1^Hv2-r

Allele Symbol: Ceacam1^Hv2-r

Allele Name	hepatitis virus (MHV-4) resistance
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 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).
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.

Disc1^del

Allele Symbol: Disc1^del

Allele Name	deletion
Allele Type	Spontaneous
Allele Synonym(s)	Disc1^129S6; Disc1^delta6
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.

Rmcf^s

Allele Symbol: Rmcf^s

Allele Name	MCF sensitive
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 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.
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.

Il2^m1

Allele Symbol: Il2^m1

Allele Name	mutation 1
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.

Gpr84^del

Allele Symbol: Gpr84^del

Allele Name	deletion
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.

Ogg1^m1

Allele Symbol: Ogg1^m1

Allele Name	mutation 1
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.

Ogg1^m2

Allele Symbol: Ogg1^m2

Allele Name	mutation 2
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).

Cd5^b

Allele Symbol: Cd5^b

Allele Name	b variant
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.

Mx1^s1

Allele Symbol: Mx1^s1

Allele Name	myxovirus susceptibility 1
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 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).
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.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Cardiovascular Research
- Diet-Induced Atherosclerosis
  - Relatively Resistant
Cancer Research
- Increased Tumor Incidence
  - Other Tissues/Organs: reticulum cell sarcomas, Hodgkin's disease
  - Other Tissues/Organs
Sensorineural Research
- Retinal Degeneration
  - Homozygous for Pde6b^rd1
Diabetes and Obesity Research
- Type 1 Diabetes (IDDM) Analysis Strains
  - Related Inbred Strains
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - NK Cell Deficiency
Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
  - experimental allergic encephalomyelitis (EAE)
Neurobiology Research
- Angelman syndrome
- Muscular Dystrophy
  - Limb-Girdle type
Virology Research
- Hepatitis B Virus

Genotype: Pde6b^rd1 related

Mouse/Human Gene Homologs
- retinitis pigmentosa, autosomal recessive
Sensorineural Research
- Retinal Degeneration

Genotype: Ahr^d related

Research Tools
- Toxicology Research
Metabolism Research

Genotype: Dysf^im related

Mouse/Human Gene Homologs
- muscular dystrophy, limb-girdle
  - type 2B

Genotype: Oca2^p related

Dermatology Research
- Color and White Spotting Defects
Mouse/Human Gene Homologs
- albinism, oculocutaneous type II, OCA2
Neurobiology Research
- Angelman syndrome

Mammalian Phenotype Terms by Genotype

The following phenotype relates to a compound genotype created using this strain

Genotype: Ceacam1^Hv2-r/Ceacam1^Hv2-r
SJL/J

immune system phenotype

decreased susceptibility to viral infection
- Background Sensitivity - resistance to infection by the A59 strains of mouse hepatitis virus MHV-4, and is found only in the SJL/J strain

decreased susceptibility to Coronaviridae infection
- Background Sensitivity - resistance to infection by the A59 strains of mouse hepatitis virus MHV-4 , and is found only in the SJL/J strain

decreased susceptibility to Hepadnaviridae infection
- Background Sensitivity - resistance to infection by the A59 strains of mouse hepatitis virus MHV-4, and is found only in the SJL/J strain

Genotype: Dysf^im/Dysf^im
involves: SJL

muscle phenotype

progressive muscle weakness
- detectable by 3 weeks of age

dystrophic muscle
- changes apparent from 3 weeks of age

Phenotype Information

Body Weight Information - JAX^® Mice Strain SJL/J (000686)
Festing Inbred Strain Characteristics: SJL
JAX^® Physiological Data Summary [pdf]

References

Bittner RE; Anderson LV; Burkhardt E; Bashir R; Vafiadaki E; Ivanova S; Raffelsberger T; Maerk I; Hoger H; Jung M; Karbasiyan M; Storch M; Lassmann H; Moss JA; Davison K; Harrison R; Bushby KM; Reis A. 1999. Dysferlin deletion in SJL mice (SJL-Dysf) defines a natural model for limb girdle muscular dystrophy 2B [letter] Nat Genet 23(2):141-2PubMed: 10508505 MGI: J:57764
Crispens CG. 1973. Some characteristics of strain SJL-JDg mice. Lab Anim Sci 23(3):408-13PubMed: 4351481 MGI: J:25445
Dal Canto MC; Melvold RW; Kim BS; Miller SD. 1995. Two models of multiple sclerosis: experimental allergic encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus (TMEV) infection. A pathological and immunological comparison. Microsc Res Tech 32(3):215-29PubMed: 8527856 MGI: J:109910
Fischer Lindahl K. 1997. On naming H2 haplotypes: functional significance of MHC class Ib alleles. Immunogenetics 46(1):53-62PubMed: 9148789 MGI: J:41130
Fujinaga S; Poel WE; Williams WC; Dmochowski L. 1970. Biological and morphological studies of SJL-J strain reticulum cell neoplasms induced and transmitted serially in low-leukemia-strain mice. Cancer Res 30(3):729-42PubMed: 4316600 MGI: J:25329
McGeachie JK; Grounds MD. 1995. Retarded myogenic cell replication in regenerating skeletal muscles of old mice: an autoradiographic study in young and old BALBc and SJL/J mice. Cell Tissue Res 280(2):277-82PubMed: 7781025 MGI: J:25692
Murphy ED. 1963. SJL/J, a new inbred strain of mouse with a high, early incidence of reticulum-cell neoplasms Proc Am Assoc Cancer Res 4:46 (Abstr.)MGI: J:2463
Nishina PM; Wang J; Toyofuku W; Kuypers FA; Ishida BY; Paigen B. 1993. Atherosclerosis and plasma and liver lipids in nine inbred strains of mice. Lipids 28(7):599-605PubMed: 8355588 MGI: J:13267
Paigen B; Ishida BY; Verstuyft J; Winters RB; Albee D. 1990. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis 10(2):316-23PubMed: 2317166 MGI: J:22615
Paigen B; Morrow A; Brandon C; Mitchell D; Holmes P. 1985. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis 57(1):65-73PubMed: 3841001 MGI: J:109950
Vafiadaki E; Reis A; Keers S; Harrison R; Anderson LV; Raffelsberger T; Ivanova S; Hoger H; Bittner RE; Bushby K; Bashir R. 2001. Cloning of the mouse dysferlin gene and genomic characterization of the SJL-Dysf mutation. Neuroreport 12(3):625-9PubMed: 11234777 MGI: J:67994
Weller AH; Magliato SA; Bell KP; Rosenberg NL. 1997. Spontaneous myopathy in the SJL/J mouse: pathology and strength loss. Muscle Nerve 20(1):72-82PubMed: 8995586 MGI: J:38007

Additional References

Dveksler GS; Dieffenbach CW; Cardellichio CB; McCuaig K; Pensiero MN; Jiang GS; Beauchemin N; Holmes KV. 1993. Several members of the mouse carcinoembryonic antigen-related glycoprotein family are functional receptors for the coronavirus mouse hepatitis virus-A59. J Virol 67(1):1-8PubMed: 8380065 MGI: J:92495
Kumar RK. 1983. Hodgkin's disease. SJL/J murine lymphoma. Am J Pathol 110(3):393-6PubMed: 6829714 MGI: J:35739
Mitchell CA; McGeachie JK; Grounds MD. 1992. Cellular differences in the regeneration of murine skeletal muscle: a quantitative histological study in SJL/J and BALB/c mice. Cell Tissue Res 269(1):159-66PubMed: 1423478 MGI: J:2981
Moy SS; Nadler JJ; Young NB; Nonneman RJ; Segall SK; Andrade GM; Crawley JN; Magnuson TR. 2008. Social approach and repetitive behavior in eleven inbred mouse strains. Behav Brain Res 191(1):118-29PubMed: 18440079 MGI: J:138681
Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11PubMed: 15081119 MGI: J:89298
Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12PubMed: 2169579 MGI: J:34840
Rohan RM; Fernandez A; Udagawa T; Yuan J; D'Amato RJ. 2000. Genetic heterogeneity of angiogenesis in mice. FASEB J 14(7):871-6PubMed: 10783140 MGI: J:61808
Shen FW; Chorney MJ; Boyse EA. 1982. Further polymorphism of the Tla locus defined by monoclonal TL antibodies. Immunogenetics 15(6):573-8PubMed: 7106865 MGI: J:6828
Smith BK; Andrews PK; West DB. 2000. Macronutrient diet selection in thirteen mouse strains. Am J Physiol Regul Integr Comp Physiol 278(4):R797-805PubMed: 10749765 MGI: J:61602
Tsunoda I; Kuang LQ; Theil DJ; Fujinami RS. 2000. Antibody association with a novel model for primary progressive multiple sclerosis: induction of relapsing-remitting and progressive forms of EAE in H2s mouse strains. Brain Pathol 10(3):402-18PubMed: 10885659 MGI: J:137818
Tsunoda I; Libbey JE; Kuang LQ; Terry EJ; Fujinami RS. 2005. Massive apoptosis in lymphoid organs in animal models for primary and secondary progressive multiple sclerosis. Am J Pathol 167(6):1631-46PubMed: 16314476 MGI: J:137817
West DB; Boozer CN; Moody DL; Atkinson RL. 1992. Dietary obesity in nine inbred mouse strains. Am J Physiol 262(6 Pt 2):R1025-32PubMed: 1621856 MGI: J:1348
Xie C; Sharma R; Wang H; Zhou XJ; Mohan C. 2004. Strain distribution pattern of susceptibility to immune-mediated nephritis. J Immunol 172(8):5047-55PubMed: 15067087 MGI: J:122988
Yokomori K; Lai MM. 1992. The receptor for mouse hepatitis virus in the resistant mouse strain SJL is functional: implications for the requirement of a second factor for viral infection. J Virol 66(12):6931-8PubMed: 1279194 MGI: J:3241

Additional - Ahr^d related

Additional - Cd5^b related

Additional - Ceacam1^Hv2-r related

Additional - Disc1^del related

Additional - Dysf^im related

Additional - Gpr84^del related

Additional - Il2^m1 related

Additional - Mx1^s1 related

Additional - Oca2^p related

Additional - Ogg1^m1 related

Additional - Ogg1^m2 related

Additional - Pde6b^rd1 related

Additional - Rmcf^s related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Genotyping resources and troubleshooting
Inbred mouse strains are maintained through sibling (sister x brother) matings; no genotyping required.
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is a good breeder.
- Additional Breeding and Husbandry Support
Mating System
- Sibling x Sibling
Appearance
- albino
  Related Genotype: Oca2^p Tyr^c/Oca2^p Tyr^c A/A
Citation
When using the SJL mouse strain in a publication, please include JAX stock #000686 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

MP16 (Standard)

MP13 (Maximum)

RB04 (Maximum)

Pricing & Availability

Readily Available

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Volume Pricing Details

QUANTITY	Volume Pricing

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.

Cryorecovery - Pricing

Service/Product	Description	Price
	Please inquire

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

The Jackson Laboratory's Genotype Promise

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.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:Swiss Jim Lambert, SJL

Genetic overview

Research Applications

Base Price

Volume Pricing Available!

Important Note

Detailed Description

Development

Selected References

Oca2p

Allele Symbol: Oca2p

Pde6brd1

Allele Symbol: Pde6brd1

Dysfim

Allele Symbol: Dysfim

Ahrd

Allele Symbol: Ahrd

Ceacam1Hv2-r

Allele Symbol: Ceacam1Hv2-r

Disc1del

Allele Symbol: Disc1del

Rmcfs

Allele Symbol: Rmcfs

Il2m1

Allele Symbol: Il2m1

Gpr84del

Allele Symbol: Gpr84del

Ogg1m1

Allele Symbol: Ogg1m1

Ogg1m2

Allele Symbol: Ogg1m2

Cd5b

Allele Symbol: Cd5b

Mx1s1

Allele Symbol: Mx1s1

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Pde6brd1 related

Genotype: Ahrd related

Genotype: Dysfim related

Genotype: Oca2p related

Mammalian Phenotype Terms by Genotype

Genotype: Ceacam1Hv2-r/Ceacam1Hv2-rSJL/J

immune system phenotype

Genotype: Dysfim/Dysfiminvolves: SJL

muscle phenotype

Phenotype Information

References

Additional References

Additional - Ahrd related

Additional - Cd5b related

Additional - Ceacam1Hv2-r related

Additional - Disc1del related

Additional - Dysfim related

Additional - Gpr84del related

Additional - Il2m1 related

Additional - Mx1s1 related

Additional - Oca2p related

Additional - Ogg1m1 related

Additional - Ogg1m2 related

Additional - Pde6brd1 related

Additional - Rmcfs related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

Live Mouse

Volume Pricing Details

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Oca2^p

Allele Symbol: Oca2^p

Pde6b^rd1

Allele Symbol: Pde6b^rd1

Dysf^im

Allele Symbol: Dysf^im

Ahr^d

Allele Symbol: Ahr^d

Ceacam1^Hv2-r

Allele Symbol: Ceacam1^Hv2-r

Disc1^del

Allele Symbol: Disc1^del

Rmcf^s

Allele Symbol: Rmcf^s

Il2^m1

Allele Symbol: Il2^m1

Gpr84^del

Allele Symbol: Gpr84^del

Ogg1^m1

Allele Symbol: Ogg1^m1

Ogg1^m2

Allele Symbol: Ogg1^m2

Cd5^b

Allele Symbol: Cd5^b

Mx1^s1

Allele Symbol: Mx1^s1

Genotype: Pde6b^rd1 related

Genotype: Ahr^d related

Genotype: Dysf^im related

Genotype: Oca2^p related

Genotype: Ceacam1^Hv2-r/Ceacam1^Hv2-r
SJL/J

Genotype: Dysf^im/Dysf^im
involves: SJL

Additional - Ahr^d related

Additional - Cd5^b related

Additional - Ceacam1^Hv2-r related

Additional - Disc1^del related

Additional - Dysf^im related

Additional - Gpr84^del related

Additional - Il2^m1 related

Additional - Mx1^s1 related

Additional - Oca2^p related

Additional - Ogg1^m1 related

Additional - Ogg1^m2 related

Additional - Pde6b^rd1 related

Additional - Rmcf^s related