|These G85R-SOD1 transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease).|
Type Congenic; Transgenic; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Generation N14+N5pN1
Donating Investigator Dr. Don Cleveland, Ludwig Institute for Cancer Res. (UCSD)
Mice hemizygous for this G85R-SOD1 transgene are viable and fertile, with transgenic expression of a G85R mutant form of human SOD1 associated with human familial Amyotrophic Lateral Sclerosis (ALS). Mice from this founder line (line 148) exhibit unaltered endogenous SOD1 activity; the G85R mutation is characterized as an "enzymatically inactive" mutation. Like wildtype SOD1, the G85R mutant SOD1 protein also forms monomer-misfolded oligomers associated with degenerating motor neurons.
Hemizygotes develop symptoms and pathology resembling human ALS; becoming paralyzed in one or more limbs due to loss of motor neurons from the spinal cord. On the C57BL/6 genetic background, hemizygous mice have a longer lifespan (median lifespan of 361 days). After the first initial phenotype observation, the disease progresses rapidly with death around 12-13 months of age. The onset and progression of motor dysfunction is accompanied by weight loss. For more detailed information, please view graph of B6.Cg-Tg(SOD1*G85R)148Dwc/J survival and weight data 2009-2010. [pdf]
These G85R-SOD1 transgenic mice may be useful in studying neuromuscular disorders, including Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig's Disease).
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 G85R-SOD1 transgenic mice were originally created on a mixed genetic background, it should be noted that the phenotype of these transgenic mice on a C57BL/6-congenic background may vary greatly from that originally described. We will modify the strain description if necessary as published results become available.
The G85R-SOD1 (or SOD1-G85R) transgene was designed with a mutant human SOD1 gene (harboring a single amino acid substitution of glycine to arginine at codon 85) driven by its endogenous human promoter. This 12 kb transgene was microinjected into hybrid (C57BL/6J x C3H/HeJ)F2 mouse embryos and transgenic G85R-SOD1 mice (founder line 148) were established. These mice were then backcrossed to C57BL/6J inbred mice for many generations prior to arrival at The Jackson Laboratory.
|Considerations for Choosing Controls|
Amyotrophic Lateral Sclerosis (ALS)
009680 B6.B-Vps54wr/J 010700 B6.Cg-Tg(Prnp-TARDBP*A315T)95Balo/J 002298 B6.Cg-Tg(SOD1)2Gur/J 016149 B6.Cg-Tg(SOD1*G37R)1Dwc/J 008229 B6.Cg-Tg(SOD1*G37R)29Dpr/J 008342 B6.Cg-Tg(SOD1*G37R)42Dpr/J 004435 B6.Cg-Tg(SOD1*G93A)1Gur/J 002299 B6.Cg-Tg(SOD1*G93A)dl1Gur/J 018917 B6;SJL-Tg(Prnp-CCS)17Jlel/J 017907 B6N.Cg-Tg(Prnp-TARDBP)96Dwc/J 017933 B6N.Cg-Tg(Prnp-TARDBP*Q331K)103Dwc/J 017930 B6N.Cg-Tg(Prnp-TARDBP*Q331K)109Dwc/J 016201 B6SJL-Tg(Prnp-TARDBP)4Jlel/J 002297 B6SJL-Tg(SOD1)2Gur/J 002726 B6SJL-Tg(SOD1*G93A)1Gur/J 002300 B6SJL-Tg(SOD1*G93A)dl1Gur/J 016608 C57BL/6-Tg(Prnp-TARDBP)3cPtrc/J 017604 C57BL/6-Tg(Prnp-TARDBP*M337V)4Ptrc/J 002628 C57BL/6-Tg(SOD1)10Cje/J 002629 C57BL/6-Tg(SOD1)3Cje/J 005706 C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J 008230 FVB(Cg)-Tg(Thy1-SOD1*G93A)T3Hgrd/J 005110 FVB-Tg(Sod1*G86R)M1Jwg/J 013199 FVB.Cg-Tg(SOD1*G93A)1Gur/J 013574 FVB/N-Tg(149m19)M141Kunst/J 017919 STOCK Tg(CAG-EGFP,-dsRed2/RNAi:Tardbp)6Zxu/J 017934 STOCK Tg(CAG-dsRed2/RNAi:Tardbp)6Zxu/J 017916 STOCK Tg(Prnp-FUS)WT3Cshw/J 016144 STOCK Tg(Prnp-TARDBP)4Jlel/J 016143 STOCK Tg(Prnp-TARDBP*A315T)23Jlel/JView Amyotrophic Lateral Sclerosis (ALS) (30 strains)Strains carrying other alleles of SOD1
017458 B6(C)-Tg(UAS-EGFP,-SOD1*G37R)135Gsn/J 017460 B6(C)-Tg(UAS-EGFP,-SOD1*G37R)677Gsn/J 002298 B6.Cg-Tg(SOD1)2Gur/J 016149 B6.Cg-Tg(SOD1*G37R)1Dwc/J 008229 B6.Cg-Tg(SOD1*G37R)29Dpr/J 008342 B6.Cg-Tg(SOD1*G37R)42Dpr/J 004435 B6.Cg-Tg(SOD1*G93A)1Gur/J 002299 B6.Cg-Tg(SOD1*G93A)dl1Gur/J 025402 B6SJL-Tg(Prnp-Immt/SOD1)1Gmnf/J 025403 B6SJL-Tg(Prnp-Immt/SOD1*G93A)7Gmnf/J 002297 B6SJL-Tg(SOD1)2Gur/J 002726 B6SJL-Tg(SOD1*G93A)1Gur/J 002300 B6SJL-Tg(SOD1*G93A)dl1Gur/J 002628 C57BL/6-Tg(SOD1)10Cje/J 002629 C57BL/6-Tg(SOD1)3Cje/J 008230 FVB(Cg)-Tg(Thy1-SOD1*G93A)T3Hgrd/J 013199 FVB.Cg-Tg(SOD1*G93A)1Gur/JView Strains carrying other alleles of SOD1 (17 strains)
View Related Disease (OMIM) TermsRelated Disease (OMIM) Terms provided by MGI
- Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.View Mammalian Phenotype TermsMammalian Phenotype Terms provided by MGIassigned by genotype
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.
Tg(SOD1*G85R)148Dwc/?Background Not Specified
- nervous system phenotype
- abnormal astrocyte morphology
- at 6 months of age round Lewy body-like inclusions are visible in astrocytes (MGI Ref ID J:77600)
- number of inclusions increases with age (MGI Ref ID J:77600)
- inclusions have a dense core and a clear peripheral halo (MGI Ref ID J:77600)
- core consists of heterogeneous mass of short filamentous material covered with small granules (MGI Ref ID J:77600)
- periphery has a less dense and, in some cases, linear array of filaments (MGI Ref ID J:77600)
- astrocytosis (MGI Ref ID J:77600)
- abnormal neuron morphology
- abnormalities are evident in ventral motor neurons, small neurons of the central canal and interneurons of the dorsal horns, however, no abnormalities are observed in cortical or subcortical structures (MGI Ref ID J:77600)
- abnormal motor neuron morphology
- prior to onset of disease a small number of motor neurons exhibit a few diffuse aggregates that are immunoreactive for SOD1 and ubiquitin (MGI Ref ID J:77600)
- aggregates progress to rounded Lewy body-like or irregular inclusions in cell bodies (MGI Ref ID J:77600)
- end-stage transgenics exhibit large inclusions in a few neurons in cell bodies and axonal processes (MGI Ref ID J:77600)
- decreased motor neuron number
- loss of motor neurons in ventral horn of spinal cord (MGI Ref ID J:77600)
- axon degeneration
- at 6.5 months a small number of large ventral motor neuron axons exhibit degeneration, although the loss is not significant (MGI Ref ID J:77600)
- at 8 months (disease onset) 25% of large motor axons are absent , of the remaining axons, 10% are undergoing degeneration and within another two weeks 66% are absent small caliber axons are not affected (MGI Ref ID J:77600)
- at 8 months 2.5% of large sensory axons are absent (MGI Ref ID J:77600)
- among large axons, 7.5% of dorsal root axons are absent at end stage (MGI Ref ID J:77600)
- behavior/neurological phenotype
- decreased grip strength
- weakened grip strength, the first indication of phenotype, is observed by 8 months and spreads rapidly to other limbs (MGI Ref ID J:77600)
- complete paralysis occurs two weeks after onset of weakened grip strength (MGI Ref ID J:77600)
- muscle phenotype
- muscular atrophy (MGI Ref ID J:77600)
- progressive muscle weakness (MGI Ref ID J:77600)
View Research ApplicationsResearch ApplicationsThis mouse can be used to support research in many areas including:
Amyotrophic Lateral Sclerosis (ALS)
|Allele Name||transgene insertion 148, Don W Cleveland|
|Allele Type||Transgenic (Inserted expressed sequence)|
|Common Name(s)||148-G85R; G85R; G85R SOD1 line148; G85R line 148; SOD1 G85R line 148; Tg(SOD1-G85R)148Dwc;|
|Mutation Made By||Dr. Don Cleveland, Ludwig Institute for Cancer Res. (UCSD)|
|Expressed Gene||SOD1, superoxide dismutase 1, soluble, human|
|Promoter||SOD1, superoxide dismutase 1, soluble, human|
|General Note||Transgenic animals initially exhibit hindlimb weakness that spreads with rapid progression to forelimbs and results in muscle atrophy and complete paralysis within 2 weeks. Founders 148-G85R and 74-G85R are the highest and lowest expressing transgenic lines, respectively, and differ in onset of clinical symptoms, presumably due to gene dosage. Founder 148-G85R exhibits muscle weakness at 8-10 months of age whereas founder 74-G85R exhibits the phenotype 12-14 months of age. Despite the difference in disease onset both founders show the same rate of disease progression after appearance of initial symptoms.|
|Molecular Note||A 12 kb genomic fragment of human SOD1 carrying a glycine to arginine substitution at amino acid 85 (G85R), a mutation associated with familial amyotrophic lateral sclerosis (ALS), was used as the transgene. [MGI Ref ID J:77600]|
Bruijn LI; Becher MW; Lee MK; Anderson KL; Jenkins NA; Copeland NG; Sisodia SS; Rothstein JD; Borchelt DR; Price DL; Cleveland DW. 1997. ALS-linked SOD1 mutant G85R mediates damage to astrocytes and promotes rapidly progressive disease with SOD1-containing inclusions. Neuron 18(2):327-38. [PubMed: 9052802] [MGI Ref ID J:77600]
Amendola J; Verrier B; Roubertoux P; Durand J. 2004. Altered sensorimotor development in a transgenic mouse model of amyotrophic lateral sclerosis. Eur J Neurosci 20(10):2822-6. [PubMed: 15548226] [MGI Ref ID J:101282]
Bernard-Marissal N; Moumen A; Sunyach C; Pellegrino C; Dudley K; Henderson CE; Raoul C; Pettmann B. 2012. Reduced calreticulin levels link endoplasmic reticulum stress and Fas-triggered cell death in motoneurons vulnerable to ALS. J Neurosci 32(14):4901-12. [PubMed: 22492046] [MGI Ref ID J:184132]
Borchelt DR; Lee MK; Slunt HS; Guarnieri M; Xu ZS; Wong PC; Brown RH Jr; Price DL; Sisodia SS; Cleveland DW. 1994. Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity. Proc Natl Acad Sci U S A 91(17):8292-6. [PubMed: 8058797] [MGI Ref ID J:133801]
Bories C; Amendola J; Lamotte d'Incamps B; Durand J. 2007. Early electrophysiological abnormalities in lumbar motoneurons in a transgenic mouse model of amyotrophic lateral sclerosis. Eur J Neurosci 25(2):451-9. [PubMed: 17284186] [MGI Ref ID J:118629]
Bruijn LI; Houseweart MK; Kato S; Anderson KL; Anderson SD; Ohama E; Reaume AG; Scott RW; Cleveland DW. 1998. Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1. Science 281(5384):1851-4. [PubMed: 9743498] [MGI Ref ID J:50039]
Chang Y; Kong Q; Shan X; Tian G; Ilieva H; Cleveland DW; Rothstein JD; Borchelt DR; Wong PC; Lin CL. 2008. Messenger RNA oxidation occurs early in disease pathogenesis and promotes motor neuron degeneration in ALS. PLoS ONE 3(8):e2849. [PubMed: 18682740] [MGI Ref ID J:140123]
Damiano M; Starkov AA; Petri S; Kipiani K; Kiaei M; Mattiazzi M; Flint Beal M; Manfredi G. 2006. Neural mitochondrial Ca capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn-superoxide dismutase mutant mice. J Neurochem 96(5):1349-61. [PubMed: 16478527] [MGI Ref ID J:106152]
Duplan L; Bernard N; Casseron W; Dudley K; Thouvenot E; Honnorat J; Rogemond V; De Bovis B; Aebischer P; Marin P; Raoul C; Henderson CE; Pettmann B. 2010. Collapsin response mediator protein 4a (CRMP4a) is upregulated in motoneurons of mutant SOD1 mice and can trigger motoneuron axonal degeneration and cell death. J Neurosci 30(2):785-96. [PubMed: 20071543] [MGI Ref ID J:157705]
Filipchuk AA; Durand J. 2012. Postnatal dendritic development in lumbar motoneurons in mutant superoxide dismutase 1 mouse model of amyotrophic lateral sclerosis. Neuroscience 209:144-54. [PubMed: 22387111] [MGI Ref ID J:184723]
Graffmo KS; Forsberg K; Bergh J; Birve A; Zetterstrom P; Andersen PM; Marklund SL; Brannstrom T. 2013. Expression of wild-type human superoxide dismutase-1 in mice causes amyotrophic lateral sclerosis. Hum Mol Genet 22(1):51-60. [PubMed: 23026746] [MGI Ref ID J:191143]
Kikuchi H; Almer G; Yamashita S; Guegan C; Nagai M; Xu Z; Sosunov AA; McKhann GM 2nd; Przedborski S. 2006. Spinal cord endoplasmic reticulum stress associated with a microsomal accumulation of mutant superoxide dismutase-1 in an ALS model. Proc Natl Acad Sci U S A 103(15):6025-30. [PubMed: 16595634] [MGI Ref ID J:108290]
Liebl MP; Kaya AM; Tenzer S; Mittenzwei R; Koziollek-Drechsler I; Schild H; Moosmann B; Behl C; Clement AM. 2014. Dimerization of visinin-like protein 1 is regulated by oxidative stress and calcium and is a pathological hallmark of amyotrophic lateral sclerosis. Free Radic Biol Med 72:41-54. [PubMed: 24742816] [MGI Ref ID J:212114]
Liu J; Shinobu LA; Ward CM; Young D; Cleveland DW. 2005. Elevation of the Hsp70 chaperone does not effect toxicity in mouse models of familial amyotrophic lateral sclerosis. J Neurochem 93(4):875-82. [PubMed: 15857390] [MGI Ref ID J:98232]
Lobsiger CS; Boillee S; Cleveland DW. 2007. Toxicity from different SOD1 mutants dysregulates the complement system and the neuronal regenerative response in ALS motor neurons. Proc Natl Acad Sci U S A 104(18):7319-26. [PubMed: 17463094] [MGI Ref ID J:133802]
Lobsiger CS; Boillee S; McAlonis-Downes M; Khan AM; Feltri ML; Yamanaka K; Cleveland DW. 2009. Schwann cells expressing dismutase active mutant SOD1 unexpectedly slow disease progression in ALS mice. Proc Natl Acad Sci U S A 106(11):4465-70. [PubMed: 19251638] [MGI Ref ID J:146766]
Marinkovic P; Reuter MS; Brill MS; Godinho L; Kerschensteiner M; Misgeld T. 2012. Axonal transport deficits and degeneration can evolve independently in mouse models of amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A 109(11):4296-301. [PubMed: 22371592] [MGI Ref ID J:182236]
Nguyen KT; Barrett JN; Garcia-Chacon L; David G; Barrett EF. 2011. Repetitive nerve stimulation transiently opens the mitochondrial permeability transition pore in motor nerve terminals of symptomatic mutant SOD1 mice. Neurobiol Dis 42(3):381-90. [PubMed: 21310237] [MGI Ref ID J:172765]
Nguyen KT; Zhang Z; Barrett EF; David G. 2012. Morphological and functional changes in innervation of a fast forelimb muscle in SOD1-G85R mice. Neurobiol Dis 48(3):399-408. [PubMed: 22813866] [MGI Ref ID J:197508]
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]
Raoul C; Buhler E; Sadeghi C; Jacquier A; Aebischer P; Pettmann B; Henderson CE; Haase G. 2006. Chronic activation in presymptomatic amyotrophic lateral sclerosis (ALS) mice of a feedback loop involving Fas, Daxx, and FasL. Proc Natl Acad Sci U S A 103(15):6007-12. [PubMed: 16581901] [MGI Ref ID J:108289]
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]
Tokuda E; Okawa E; Watanabe S; Ono S; Marklund SL. 2013. Dysregulation of intracellular copper homeostasis is common to transgenic mice expressing human mutant superoxide dismutase-1s regardless of their copper-binding abilities. Neurobiol Dis 54:308-19. [PubMed: 23321002] [MGI Ref ID J:197756]
Tummala H; Jung C; Tiwari A; Higgins CM; Hayward LJ; Xu Z. 2005. Inhibition of chaperone activity is a shared property of several Cu,Zn-superoxide dismutase mutants that cause amyotrophic lateral sclerosis. J Biol Chem 280(18):17725-31. [PubMed: 15753080] [MGI Ref ID J:99092]
Vargas MR; Burton NC; Kutzke J; Gan L; Johnson DA; Schafer M; Werner S; Johnson JA. 2013. Absence of Nrf2 or its selective overexpression in neurons and muscle does not affect survival in ALS-linked mutant hSOD1 mouse models. PLoS One 8(2):e56625. [PubMed: 23418589] [MGI Ref ID J:199339]
Vijayvergiya C; Beal MF; Buck J; Manfredi G. 2005. Mutant superoxide dismutase 1 forms aggregates in the brain mitochondrial matrix of amyotrophic lateral sclerosis mice. J Neurosci 25(10):2463-70. [PubMed: 15758154] [MGI Ref ID J:134416]
Watanabe M; Dykes-Hoberg M; Culotta VC; Price DL; Wong PC; Rothstein JD. 2001. Histological evidence of protein aggregation in mutant SOD1 transgenic mice and in amyotrophic lateral sclerosis neural tissues. Neurobiol Dis 8(6):933-41. [PubMed: 11741389] [MGI Ref ID J:119899]
Watanabe S; Nagano S; Duce J; Kiaei M; Li QX; Tucker SM; Tiwari A; Brown RH Jr; Beal MF; Hayward LJ; Culotta VC; Yoshihara S; Sakoda S; Bush AI. 2007. Increased affinity for copper mediated by cysteine 111 in forms of mutant superoxide dismutase 1 linked to amyotrophic lateral sclerosis. Free Radic Biol Med 42(10):1534-42. [PubMed: 17448900] [MGI Ref ID J:121596]
Williamson TL; Bruijn LI; Zhu Q; Anderson KL; Anderson SD; Julien JP; Cleveland DW. 1998. Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant. Proc Natl Acad Sci U S A 95(16):9631-6. [PubMed: 9689132] [MGI Ref ID J:76716]
Williamson TL; Cleveland DW. 1999. Slowing of axonal transport is a very early event in the toxicity of ALS-linked SOD1 mutants to motor neurons. Nat Neurosci 2(1):50-6. [PubMed: 10195180] [MGI Ref ID J:55584]
Zhai J; Zhou W; Li J; Hayworth CR; Zhang L; Misawa H; Klein R; Scherer SS; Balice-Gordon RJ; Kalb RG. 2011. The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease. Hum Mol Genet 20(21):4116-31. [PubMed: 21816949] [MGI Ref ID J:176684]
Zhong Z; Deane R; Ali Z; Parisi M; Shapovalov Y; O'Banion MK; Stojanovic K; Sagare A; Boillee S; Cleveland DW; Zlokovic BV. 2008. ALS-causing SOD1 mutants generate vascular changes prior to motor neuron degeneration. Nat Neurosci 11(4):420-2. [PubMed: 18344992] [MGI Ref ID J:136100]
Animal Health ReportsProduction of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.
Breeding & Husbandry Mutant mice were bred to C57BL/6J mice to generate this congenic strain. When maintaining the live congenic colony, hemizygous carriers may be bred with wildtype siblings or C57BL/6J inbred mice.
|Pricing for USA, Canada and Mexico shipping destinations|
Cryopreserved Mice - Ready for Recovery
Price (US dollars $) Cryorecovery* $2140.00
At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.
Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
|Pricing for International shipping destinations|
Cryopreserved Mice - Ready for Recovery
Price (US dollars $) Cryorecovery* $2782.00
Cryorecovery - Standard.
Progeny testing is not required.
|Considerations for Choosing Controls|
|Control Pricing Information for Genetically Engineered Mutant Strains.|
For Licensing and Use Restrictions view the link(s) below:
- Strain(s) not available to companies or for-profit entities.
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