Strain Name:

B6.Cg-Tg(SOD1*G37R)29Dpr/J

Stock Number:

008229

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These transgenic mice develop symptoms and pathology resembling human Amyotrophic Lateral Sclerosis (ALS) with paralysis in one or more limbs attributable to the loss of motor neurons from the spinal cord and a moderate increase in SOD1 activity in the spinal cord. These G37R-SOD1 transgenic mice may be useful in studying neuromuscular disorders, including ALS.

Description

Strain Information

Type Congenic; Mutant Strain; Transgenic;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Mating SystemNoncarrier x Hemizygote         (Female x Male)   23-OCT-09
Specieslaboratory mouse
GenerationN6+F8 (10-DEC-13)
Generation Definitions
 
Donating InvestigatorDr. Don Cleveland,   Ludwig Institute for Cancer Res. (UCSD)

Description
Mice hemizygous for this G37R-SOD1 transgene are viable and fertile. The expressed G37R mutant form of human SOD1 is characterized as an enzymatically active, "gain of adverse function" mutation. Transgenic mice from this founder line (line 29) express a moderate (7-fold) increase in SOD1 activity in spinal cord, with pathology restricted to motor neurons in the spinal cord and brainstem. Like wild-type SOD1, the G37R mutant SOD1 protein also forms monomer-misfolded oligomers associated with degenerating motor neurons. Hemizygous mice develop symptoms and pathology resembling human Amyotrophic Lateral Sclerosis (ALS), with paralyzation in one or more limbs attributable to the loss of motor neurons from the spinal cord.

On a mixed genetic background, G37R-SOD1 transgenic mice die around six to eight months of age. While original publications of G37R-SOD1 transgenic mice on a C57BL/6-congenic background described mice surviving more than one year (median lifespan 376 days, Ezzi et al. 2010 J Neurochem 115(5):1102-11), the C57BL/6-congenic G37R-SOD1 mice available from The Jackson Laboratory Repository in 2013 survive up to 500 days of age. In 2013, the donating investigator confirmed that their mouse colony also exhibits an extended lifespan up to 500 days of age.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. As the G37R-SOD1 transgenic mice were originally created on a mixed genetic background, it should be noted that the phenotype of the congenic mice could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
The G37R-SOD1 (or SOD1-G37R) transgene was designed with a mutant human SOD1 gene (harboring a single amino acid substitution of glycine to arginine at codon 37) driven by its endogenous human promoter. This 12 kbp transgene was microinjected into hybrid (C57BL/6J x C3H/HeJ)F2 mouse embryos and transgenic G37R-SOD1 mice (founder line 29) were established. The donating investigator reports the mice were then backcrossed to C57BL/6J inbred mice for many generations prior to sending to The Jackson Laboratory Repository (see SNP note below).

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background.

Control Information

  Control
   Noncarrier
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

View Amyotrophic Lateral Sclerosis (ALS)     (30 strains)

View Strains carrying other alleles of SOD1     (17 strains)

Additional Web Information

Working with ALS Mice manual [.pdf]
This resource was prepared by scientists with Prize4Life and The Jackson Laboratory.

Visit the Amyotrophic Lateral Sclerosis (ALS) Mouse Model Resource site for helpful information on ALS Disease and research resources.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.
Amyotrophic Lateral Sclerosis 1; ALS1
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Tg(SOD1*G37R)29Dpr/0

        involves: C3H/HeJ * C57BL/6J
  • nervous system phenotype
  • abnormal neuron morphology
    • numerous ubiquitin-immunoreactive, Thioflavin-S positive fibrillar protein aggregates resembling hyaline inclusions are seen in the spinal cord, ventral midbrain, and the brain stem, with fewer in the cerebellum   (MGI Ref ID J:119631)
    • decreased motor neuron number
      • at late stages   (MGI Ref ID J:69178)
    • motor neuron degeneration
      • motor neuron degeneration is observed in the ventral horns of the lumbar, thoracic, and cervical spinal cord as well as the brain stem   (MGI Ref ID J:69178)
      • degeneration is associated with vacuole formation in both dendrites and axons of motor neurons   (MGI Ref ID J:69178)
  • behavior/neurological phenotype
  • hindlimb paralysis
    • eventually mice develop hindlimb paralysis   (MGI Ref ID J:69178)
  • hypoactivity
    • at 6 to 8 months of age, mice exhibit decreased spontaneous movement compared to wild-type mice   (MGI Ref ID J:69178)
  • tremors
    • at 6 to 8 months of age, mice exhibit axial tremors   (MGI Ref ID J:69178)
  • weakness
    • at 6 to 8 months of age, mice exhibit asymmetric weakness of the limbs and when suspended by their tail exhibit difficulties extending and moving hindlimbs   (MGI Ref ID J:69178)
  • muscle phenotype
  • abnormal muscle electrophysiology
    • mice exhibit spontaneous, positive sharp waves associated with denervation atrophy   (MGI Ref ID J:69178)
  • muscular atrophy
    • at 6 to 8 months of age, mice exhibit muscle wasting particularly along the flanks   (MGI Ref ID J:69178)
  • cellular phenotype
  • abnormal mitochondrion morphology
    • motor neurons exhibit mitochondrial degradation   (MGI Ref ID J:69178)
  • growth/size/body phenotype
  • weight loss
    • progressive   (MGI Ref ID J:69178)
  • integument phenotype
  • rough coat
    • at 6 to 8 months of age   (MGI Ref ID J:69178)

Tg(SOD1*G37R)29Dpr/0

        involves: C3H/HeJ * C57BL/6 * C57BL/6J
  • mortality/aging
  • premature death
    • mean life expectancy is 9.5 months   (MGI Ref ID J:69179)
    • most of the mice (75%) die before 1 year old   (MGI Ref ID J:69179)
    • mean life span is 50.5 +/- 2.6 weeks   (MGI Ref ID J:144848)
    • increased mean life span and more surviving neurons after injection of lipophilic iron chelator SIH intraperitoneally   (MGI Ref ID J:144848)
  • nervous system phenotype
  • decreased sensory neuron number
    • massive axonal loss and cell death in the sensory axons in one-year old mice   (MGI Ref ID J:69179)
  • motor neuron degeneration
    • massive axonal loss and cell death in the motor axons in one-year old mice   (MGI Ref ID J:69179)
  • growth/size/body phenotype
  • weight loss
    • body weight drop between 47.5 and 50 weeks of age   (MGI Ref ID J:144848)
    • no changes in body weight when treated twice a week with SIH during this period   (MGI Ref ID J:144848)
  • homeostasis/metabolism phenotype
  • abnormal iron homeostasis
    • increased mitochondrial ferritin in the ventral horn motor neurons and astrocytes in the spinal cord at 12 months of age   (MGI Ref ID J:144848)
    • abnormal iron level
      • iron accumulation (56% increase) in the spinal cord at 12 months of age   (MGI Ref ID J:144848)
      • small, round cytoplasmic inclusions in the cell bodies of the large ventral horn motor neurons   (MGI Ref ID J:144848)
      • a more diffuse accumulation in the entire cell body in some glial cells in the gray and white matter   (MGI Ref ID J:144848)
View Research Applications

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

Neurobiology Research
Amyotrophic Lateral Sclerosis (ALS)
Neurodegeneration

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tg(SOD1*G37R)29Dpr
Allele Name transgene insertion 29, Donald L Price
Allele Type Transgenic (Inserted expressed sequence)
Common Name(s) G37R SOD1 (line 29); Tg(SOD1-G37R)29Dpr;
Mutation Made ByDr. Donald Price,   Johns Hopkins University School of Med
Strain of Origin(C57BL/6J x C3H/HeJ)F2
Expressed Gene SOD1, superoxide dismutase 1, soluble, human
Promoter SOD1, superoxide dismutase 1, soluble, human
Molecular Note A 12 kb genomic DNA fragment containing a mutated form of human SOD1 with a glycine to arginine substitution at amino acid 37 (G37R) was used for the transgene. The G37R mutation is found in some cases of familial amyotrophic lateral sclerosis (FALS). [MGI Ref ID J:69178]
 

Genotyping

Genotyping Information

Genotyping Protocols

Sod TgN Copy Number, QPCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Ezzi SA; Lariviere R; Urushitani M; Julien JP. 2010. Neuronal over-expression of chromogranin A accelerates disease onset in a mouse model of ALS. J Neurochem 115(5):1102-11. [PubMed: 20807312]  [MGI Ref ID J:168609]

Wong PC; Pardo CA; Borchelt DR; Lee MK; Copeland NG; Jenkins NA; Sisodia SS; Cleveland DW; Price DL. 1995. An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria. Neuron 14(6):1105-16. [PubMed: 7605627]  [MGI Ref ID J:69178]

Additional References

Tg(SOD1*G37R)29Dpr related

Beaulieu JM; Nguyen MD; Julien JP. 1999. Late onset death of motor neurons in mice overexpressing wild-type peripherin J Cell Biol 147(3):531-44. [PubMed: 15132161]  [MGI Ref ID J:58388]

Couillard-Despres S; Meier J; Julien JP. 2000. Extra axonal neurofilaments do not exacerbate disease caused by mutant Cu,Zn superoxide dismutase. Neurobiol Dis 7(4):462-70. [PubMed: 10964615]  [MGI Ref ID J:64581]

Couillard-Despres S; Zhu Q; Wong PC; Price DL; Cleveland DW; Julien JP. 1998. Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase. Proc Natl Acad Sci U S A 95(16):9626-30. [PubMed: 9689131]  [MGI Ref ID J:69179]

Eyer J; Cleveland DW; Wong PC; Peterson AC. 1998. Pathogenesis of two axonopathies does not require axonal neurofilaments. Nature 391(6667):584-7. [PubMed: 9468135]  [MGI Ref ID J:91502]

Filali M; Lalonde R; Rivest S. 2011. Sensorimotor and cognitive functions in a SOD1(G37R) transgenic mouse model of amyotrophic lateral sclerosis. Behav Brain Res 225(1):215-21. [PubMed: 21816178]  [MGI Ref ID J:175860]

Gowing G; Dequen F; Soucy G; Julien JP. 2006. Absence of tumor necrosis factor-alpha does not affect motor neuron disease caused by superoxide dismutase 1 mutations. J Neurosci 26(44):11397-402. [PubMed: 17079668]  [MGI Ref ID J:114680]

Gowing G; Lalancette-Hebert M; Audet JN; Dequen F; Julien JP. 2009. Macrophage colony stimulating factor (M-CSF) exacerbates ALS disease in a mouse model through altered responses of microglia expressing mutant superoxide dismutase. Exp Neurol 220(2):267-275. [PubMed: 19733170]  [MGI Ref ID J:154464]

Jeong SY; Rathore KI; Schulz K; Ponka P; Arosio P; David S. 2009. Dysregulation of iron homeostasis in the CNS contributes to disease progression in a mouse model of amyotrophic lateral sclerosis. J Neurosci 29(3):610-9. [PubMed: 19158288]  [MGI Ref ID J:144848]

Karch CM; Borchelt DR. 2010. An examination of alpha B-crystallin as a modifier of SOD1 aggregate pathology and toxicity in models of familial amyotrophic lateral sclerosis. J Neurochem 113(5):1092-100. [PubMed: 20067574]  [MGI Ref ID J:161425]

Karch CM; Prudencio M; Winkler DD; Hart PJ; Borchelt DR. 2009. Role of mutant SOD1 disulfide oxidation and aggregation in the pathogenesis of familial ALS. Proc Natl Acad Sci U S A 106(19):7774-9. [PubMed: 19416874]  [MGI Ref ID J:148399]

Kim D; Nguyen MD; Dobbin MM; Fischer A; Sananbenesi F; Rodgers JT; Delalle I; Baur JA; Sui G; Armour SM; Puigserver P; Sinclair DA; Tsai LH. 2007. SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis. EMBO J 26(13):3169-79. [PubMed: 17581637]  [MGI Ref ID J:133121]

Lariviere RC; Beaulieu JM; Nguyen MD; Julien JP. 2003. Peripherin is not a contributing factor to motor neuron disease in a mouse model of amyotrophic lateral sclerosis caused by mutant superoxide dismutase. Neurobiol Dis 13(2):158-66. [PubMed: 12828939]  [MGI Ref ID J:126210]

Nguyen MD; Boudreau M; Kriz J; Couillard-Despres S; Kaplan DR; Julien JP. 2003. Cell cycle regulators in the neuronal death pathway of amyotrophic lateral sclerosis caused by mutant superoxide dismutase 1. J Neurosci 23(6):2131-40. [PubMed: 12657672]  [MGI Ref ID J:82675]

Nguyen MD; D'Aigle T; Gowing G; Julien JP; Rivest S. 2004. Exacerbation of motor neuron disease by chronic stimulation of innate immunity in a mouse model of amyotrophic lateral sclerosis. J Neurosci 24(6):1340-9. [PubMed: 14960605]  [MGI Ref ID J:96812]

Nguyen MD; Lariviere RC; Julien JP. 2001. Deregulation of Cdk5 in a mouse model of ALS: toxicity alleviated by perikaryal neurofilament inclusions. Neuron 30(1):135-47. [PubMed: 11343650]  [MGI Ref ID J:69136]

Nguyen MD; Lariviere RC; Julien JP. 2000. Reduction of axonal caliber does not alleviate motor neuron disease caused by mutant superoxide dismutase 1. Proc Natl Acad Sci U S A 97(22):12306-11. [PubMed: 11050249]  [MGI Ref ID J:125477]

Proescher JB; Son M; Elliott JL; Culotta VC. 2008. Biological effects of CCS in the absence of SOD1 enzyme activation: implications for disease in a mouse model for ALS. Hum Mol Genet 17(12):1728-37. [PubMed: 18337307]  [MGI Ref ID J:135987]

Rakhit R; Robertson J; Vande Velde C; Horne P; Ruth DM; Griffin J; Cleveland DW; Cashman NR; Chakrabartty A. 2007. An immunological epitope selective for pathological monomer-misfolded SOD1 in ALS. Nat Med 13(6):754-9. [PubMed: 17486090]  [MGI Ref ID J:133800]

Robertson J; Sanelli T; Xiao S; Yang W; Horne P; Hammond R; Pioro EP; Strong MJ. 2007. Lack of TDP-43 abnormalities in mutant SOD1 transgenic mice shows disparity with ALS. Neurosci Lett 420(2):128-32. [PubMed: 17543992]  [MGI Ref ID J:143016]

Shaw BF; Lelie HL; Durazo A; Nersissian AM; Xu G; Chan PK; Gralla EB; Tiwari A; Hayward LJ; Borchelt DR; Valentine JS; Whitelegge JP. 2008. Detergent-insoluble aggregates associated with amyotrophic lateral sclerosis in transgenic mice contain primarily full-length, unmodified superoxide dismutase-1. J Biol Chem 283(13):8340-50. [PubMed: 18192269]  [MGI Ref ID J:135231]

Urushitani M; Sik A; Sakurai T; Nukina N; Takahashi R; Julien JP. 2006. Chromogranin-mediated secretion of mutant superoxide dismutase proteins linked to amyotrophic lateral sclerosis. Nat Neurosci 9(1):108-18. [PubMed: 16369483]  [MGI Ref ID J:105360]

Veglianese P; Lo Coco D; Bao Cutrona M; Magnoni R; Pennacchini D; Pozzi B; Gowing G; Julien JP; Tortarolo M; Bendotti C. 2006. Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS. Mol Cell Neurosci 31(2):218-31. [PubMed: 16219474]  [MGI Ref ID J:106424]

Wang J; Martin E; Gonzales V; Borchelt DR; Lee MK. 2008. Differential regulation of small heat shock proteins in transgenic mouse models of neurodegenerative diseases. Neurobiol Aging 29(4):586-97. [PubMed: 17316906]  [MGI Ref ID J:135061]

Wang J; Slunt H; Gonzales V; Fromholt D; Coonfield M; Copeland NG; Jenkins NA; Borchelt DR. 2003. Copper-binding-site-null SOD1 causes ALS in transgenic mice: aggregates of non-native SOD1 delineate a common feature. Hum Mol Genet 12(21):2753-64. [PubMed: 12966034]  [MGI Ref ID J:86421]

Wang J; Xu G; Gonzales V; Coonfield M; Fromholt D; Copeland NG; Jenkins NA; Borchelt DR. 2002. Fibrillar inclusions and motor neuron degeneration in transgenic mice expressing superoxide dismutase 1 with a disrupted copper-binding site. Neurobiol Dis 10(2):128-38. [PubMed: 12127151]  [MGI Ref ID J:119631]

Wang J; Xu G; Slunt HH; Gonzales V; Coonfield M; Fromholt D; Copeland NG; Jenkins NA; Borchelt DR. 2005. Coincident thresholds of mutant protein for paralytic disease and protein aggregation caused by restrictively expressed superoxide dismutase cDNA. Neurobiol Dis 20(3):943-52. [PubMed: 16046140]  [MGI Ref ID J:104655]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryMutant mice were bred to C57BL/6J mice to generate this congenic strain. When maintaining the live congenic colony, hemizygous carriers may be bred to wildtype (noncarrier) mice from the colony or to C57BL/6J inbred mice. The C57BL/6-congenic G37R-SOD1 transgenic mice available from The Jackson Laboratory Repository in 2013 survive up to 500 days of age.
Mating SystemNoncarrier x Hemizygote         (Female x Male)   23-OCT-09
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $239.00Female or MaleHemizygous for Tg(SOD1*G37R)29Dpr  
Price per Pair (US dollars $)Pair Genotype
$311.00Hemizygous for Tg(SOD1*G37R)29Dpr x Noncarrier  
$311.00Noncarrier x Hemizygous for Tg(SOD1*G37R)29Dpr  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $310.70Female or MaleHemizygous for Tg(SOD1*G37R)29Dpr  
Price per Pair (US dollars $)Pair Genotype
$404.30Hemizygous for Tg(SOD1*G37R)29Dpr x Noncarrier  
$404.30Noncarrier x Hemizygous for Tg(SOD1*G37R)29Dpr  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   Noncarrier
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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