Strain Name:

B6.Cg-Tg(Prnp-SNCA*A53T)23Mkle/J

Stock Number:

006823

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Availability:

Repository- Live

Use Restrictions Apply, see Terms of Use
These Hualpha-Syn(A53T) transgenic mice display an age-dependent phenotype including progressive motor deficits, intraneuronal inclusion bodies and neuronal loss. This line may be useful for studying Parkinson's disease and other synucleinopathies associated with motor neuron loss and ubiquitinated inclusions in the brain stem and the spinal cord, Lewy bodies, and synaptic plasticity.

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.
Specieslaboratory mouse
GenerationN20+N2F1 (20-AUG-14)
Generation Definitions
 
Donating Investigator Michael K. Lee,   University of Minnesota

Description
The donating investigator reports that homozygous mice are not viable. Mice hemizygous for the MoPrP-Hualpha-Syn(A53T) transgene are viable and fertile, but the donating investigator reports that female carriers do not breed well. These Hualpha-Syn(A53T) mice (also called G2-3(A53T), Hualpha-Syn(A53T), PrPsynA53T, or A53TαS Tg mice [line G2-3(A53T)]) express the familial Parkinson's disease-associated A53T missense mutant form of human alpha-synuclein (alpha-Syn or αS). Northern blot analysis shows high transgene expression in brain tissues is directed primarily to the hindbrain by the mouse prion protein promoter. Transgenic mice from line G2-3(A53T) express the A53T mutant alpha-Syn protein at approximately six times the level of endogenous mouse alpha-Syn. Hemizygous mice spontaneously develop adult-onset neurodegenerative disease between 9-16 months of age (mean age of onset is approximately 13 months, approximately 90% penetrant), with a progressive motoric dysfunction leading to death within 14-21 days of onset. Approximately 10% of the transgenic animals do not develop locomotor phenotype by 16-18 months of age. Affected mice exhibit neuronal abnormalities (in perikarya and neurites) including pathological accumulations of alpha-Syn and ubiquitin. Brain regions also show alpha-Syn-dependent neurodegeneration associated with increased/abnormal detergent-insoluble alpha-Syn and alpha-Syn aggregation. In neurons exhibiting alpha-Syn pathology, disease onset is coincident with induction of endoplasmic reticulum chaperones. Hemizygous mice also have adult onset hyperactivity associated with D1 receptor and dopamine transporter-mediated alterations in dopamine neurotransmission. These A53T mutant alpha-Syn expressing mice have significantly greater in vivo neurotoxicity when compared with A30P mutant or wildtype alpha-Syn expressing mice on the same genetic background.
This model is being used to screen for neuroprotective agents in the NINDS-funded CINAPS project.

Development
A 436 bp human alpha-synuclein cDNA bearing a familial Parkinson's disease-linked A53T missense mutation was inserted downstream of a mouse prion protein promoter. This MoPrP-Hualpha-Syn(A53T) transgene was used for pronuclear injection into one-cell (C3H/HeJ x C57BL/6J) hybrid mouse embryos. The resulting Hualpha-Syn(A53T) transgenic mice (founder line G2-3) were subsequently backcrossed to C57BL/6J mice for at least 20 generations prior to arrival at The Jackson Laboratory. Upon arrival, transgenic mice were additionally bred to C57BL/6J mice to establish the colony.

Control Information

  Control
   Noncarrier
   000664 C57BL/6J
 
  Considerations for Choosing Controls

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View Strains carrying other alleles of Prnp     (39 strains)

View Strains carrying other alleles of SNCA     (29 strains)

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.
Parkinson Disease 1, Autosomal Dominant; PARK1
- Potential model based on transgenic expression of an ortholog of a human gene that is associated with this disease. Phenotypic similarity to the human disease has not been tested.
Dementia, Lewy Body; DLB   (SNCA)
Parkinson Disease 4, Autosomal Dominant; PARK4   (SNCA)
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(Prnp-SNCA*A53T)23Mkle/0

        involves: C3H/HeJ * C57BL/6J
  • mortality/aging
  • premature death
    • within 14-21 days of onset of motor problems and disease onset, mutants rapidly progress to death most likely due to inability to feed and drink   (MGI Ref ID J:77344)
  • nervous system phenotype
  • abnormal nervous system morphology
    • average age of onset of clinical abnormalities is 10.1 +/- 1.2 months   (MGI Ref ID J:77344)
    • neuropathological abnormalities develop before motor dysfunction is visible   (MGI Ref ID J:77344)
    • abnormal neuron morphology
      • mutants exhibit accumulation of ubiquitin and phosphorylated Nefh (NF-H) in perikarya and neurites   (MGI Ref ID J:77344)
      • affected neurons contain fibrillar inclusions   (MGI Ref ID J:77344)
      • abnormal neuronal accumulations are not seen in mutants younger than 4 months of age   (MGI Ref ID J:77344)
      • neuronal intranuclear inclusions
        • mutants exhibit accumulation of alpha-synuclein in neuronal cell bodies and neurites of the midbrain, cerebellum, brainstem and spinal cord   (MGI Ref ID J:77344)
    • abnormal spinal cord morphology
      • spinal cord exhibits astrocytic response and ubiquitin and alpha- synuclein accumulation in ventral horn motor neurons   (MGI Ref ID J:77344)
    • astrocytosis
      • astroglial reaction is seen in the midbrain, deep cerebellar nuclei, brainstem and spinal cord, indicating neurodegeneration, but not in the cortex, hippocampus, thalamus, and caudate/putamen   (MGI Ref ID J:77344)
    • neurodegeneration
      • mutants develop adult-onset neurodegenerative disease   (MGI Ref ID J:77344)
      • astroglial reaction is seen in the midbrain, deep cerebellar nuclei, brainstem and spinal cord, indicating neurodegeneration   (MGI Ref ID J:77344)
  • behavior/neurological phenotype
  • abnormal motor capabilities/coordination/movement
    • mutants develop motor signs characterized by sustained posturing, reduced amplitude, and abundance of spontaneous activity with age   (MGI Ref ID J:77344)
    • ataxia   (MGI Ref ID J:77344)
    • bradykinesia   (MGI Ref ID J:77344)
    • dystonia   (MGI Ref ID J:77344)
    • impaired righting response
      • mutants eventually develop progressive loss of righting reflex   (MGI Ref ID J:77344)
    • paralysis
      • mutants eventually develop paralysis   (MGI Ref ID J:77344)
  • muscle phenotype
  • dystonia   (MGI Ref ID J:77344)
View Research Applications

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

Neurobiology Research
Ataxia (Movement) Defects
Neurodegeneration
Neurotransmitter Receptor and Synaptic Vesicle Defects
Parkinson's Disease
      synuclein mutants

Research Tools
Neurobiology Research

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tg(Prnp-SNCA*A53T)23Mkle
Allele Name transgene insertion 23, Michael K Lee
Allele Type Transgenic (Inserted expressed sequence)
Common Name(s) A53T-syn; G2-3; Hualpha-Syn(A53T); MoPrP-Hualpha-Syn(A53T); PrPsynA53T; Tg(Prnp-SNCA*A53T)23Dpr;
Mutation Made By Michael Lee,   University of Minnesota
Strain of Origin(C3H/HeJ x C57BL/6J)F1
Expressed Gene SNCA, synuclein, alpha (non A4 component of amyloid precursor), human
Promoter Prnp, prion protein, mouse, laboratory
General Note This line was originally designated G2-3. Lines H5 and N2-5 were also generated. Mice transgenic for lines H5 and N2-5 display a phenotype similar to that displayed by mice carrying line 23. A fourth line of transgenic mice (L5) which did not develop disease, expressed a low level of the mutant human protein.

Transgenic mice express high levels of mutant human Ala53Thr alpha synuclein in brain and develop an adult onset neurodegenerative disease characterized by progressive motoric dysfunction that rapidly progresses to death in most animals. Expression of the mutant protein is associated with significantly enhanced in vivo neurotoxicity. Transgenic mice develop motor signs characterized by sustained posturing, reduced amplitude, and abundance of spontaneous activity. In many instances, the affected mice seem to exhibit bradykinesia, mild ataxia, and dystonia. These mice eventually develop progressive loss of righting reflex and paralysis.

Although the abundance of alpha-synuclein transcriptin both human and mouse substantia nigra (SN) decreases with age, levels of alpha-synuclein protein remain at high levels, resulting in an elevated level of alpha-synuclein relative to other synucleins. The level of A53T mutant human alpha-synuclein (SNCA) protein in brains of mice of lines N2-5 and H5, adjusted for transgene copy number, becomes significantly elevated as the mice age in comparison with the brain levels of human alpha-synuclein in mice bearing similar transgenes encoding A30P mutant [Tg(Prnp-SNCA*A30P)2Dpr] and wild-type [Tg(Prnp-SNCA)22Dpr] human SNCA, which do not change with age. (The present A53T mutant line, G2-3, was not analyzed in these studies because the severity of its brain pathology might interfere with the results.) (J:137012)

Molecular Note The transgene contains a human alpha synuclein cDNA encoding the Ala53Thr amino acid substitution, and the murine prion promoter. [MGI Ref ID J:77344]
 
 

Genotyping

Genotyping Information

Genotyping Protocols

** human SNCA*A53T, Pyrosequencing
Tg(Prnp-SNCA*A53T)23Mkle, Melt Curve Analysis
Tg(Prnp-SNCA*A53T)23Mkle, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Tg(Prnp-SNCA*A53T)23Mkle related

Colla E; Coune P; Liu Y; Pletnikova O; Troncoso JC; Iwatsubo T; Schneider BL; Lee MK. 2012. Endoplasmic reticulum stress is important for the manifestations of alpha-synucleinopathy in vivo. J Neurosci 32(10):3306-20. [PubMed: 22399753]  [MGI Ref ID J:182734]

Daher JP; Pletnikova O; Biskup S; Musso A; Gellhaar S; Galter D; Troncoso JC; Lee MK; Dawson TM; Dawson VL; Moore DJ. 2012. Neurodegenerative phenotypes in an A53T alpha-synuclein transgenic mouse model are independent of LRRK2. Hum Mol Genet 21(11):2420-31. [PubMed: 22357653]  [MGI Ref ID J:183780]

Larson ME; Sherman MA; Greimel S; Kuskowski M; Schneider JA; Bennett DA; Lesne SE. 2012. Soluble alpha-Synuclein Is a Novel Modulator of Alzheimer's Disease Pathophysiology. J Neurosci 32(30):10253-66. [PubMed: 22836259]  [MGI Ref ID J:186543]

Lee MK; Stirling W; Xu Y; Xu X; Qui D; Mandir AS; Dawson TM; Copeland NG; Jenkins NA; Price DL. 2002. Human alpha-synuclein-harboring familial Parkinson's disease-linked Ala-53 --> Thr mutation causes neurodegenerative disease with alpha-synuclein aggregation in transgenic mice. Proc Natl Acad Sci U S A 99(13):8968-73. [PubMed: 12084935]  [MGI Ref ID J:77344]

Li W; Lesuisse C; Xu Y; Troncoso JC; Price DL; Lee MK. 2004. Stabilization of alpha-synuclein protein with aging and familial parkinson's disease-linked A53T mutation. J Neurosci 24(33):7400-9. [PubMed: 15317865]  [MGI Ref ID J:137012]

Li W; West N; Colla E; Pletnikova O; Troncoso JC; Marsh L; Dawson TM; Jakala P; Hartmann T; Price DL; Lee MK. 2005. Aggregation promoting C-terminal truncation of alpha-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations. Proc Natl Acad Sci U S A 102(6):2162-7. [PubMed: 15684072]  [MGI Ref ID J:96471]

Liu CW; Giasson BI; Lewis KA; Lee VM; Demartino GN; Thomas PJ. 2005. A precipitating role for truncated alpha-synuclein and the proteasome in alpha-synuclein aggregation: implications for pathogenesis of Parkinson disease. J Biol Chem 280(24):22670-8. [PubMed: 15840579]  [MGI Ref ID J:100267]

Martin LJ; Pan Y; Price AC; Sterling W; Copeland NG; Jenkins NA; Price DL; Lee MK. 2006. Parkinson's disease alpha-synuclein transgenic mice develop neuronal mitochondrial degeneration and cell death. J Neurosci 26(1):41-50. [PubMed: 16399671]  [MGI Ref ID J:104170]

Miller RM; Kiser GL; Kaysser-Kranich T; Casaceli C; Colla E; Lee MK; Palaniappan C; Federoff HJ. 2007. Wild-type and mutant alpha-synuclein induce a multi-component gene expression profile consistent with shared pathophysiology in different transgenic mouse models of PD. Exp Neurol 204(1):421-32. [PubMed: 17254569]  [MGI Ref ID J:119487]

Smith WW; Liu Z; Liang Y; Masuda N; Swing DA; Jenkins NA; Copeland NG; Troncoso JC; Pletnikov M; Dawson TM; Martin LJ; Moran TH; Lee MK; Borchelt DR; Ross CA. 2010. Synphilin-1 attenuates neuronal degeneration in the A53T alpha-synuclein transgenic mouse model. Hum Mol Genet 19(11):2087-98. [PubMed: 20185556]  [MGI Ref ID J:159700]

Thomas B; Mandir AS; West N; Liu Y; Andrabi SA; Stirling W; Dawson VL; Dawson TM; Lee MK. 2011. Resistance to MPTP-neurotoxicity in alpha-synuclein knockout mice is complemented by human alpha-synuclein and associated with increased beta-synuclein and Akt activation. PLoS One 6(1):e16706. [PubMed: 21304957]  [MGI Ref ID J:169549]

Unger EL; Eve DJ; Perez XA; Reichenbach DK; Xu Y; Lee MK; Andrews AM. 2006. Locomotor hyperactivity and alterations in dopamine neurotransmission are associated with overexpression of A53T mutant human alpha-synuclein in mice. Neurobiol Dis 21(2):431-43. [PubMed: 16230020]  [MGI Ref ID J:105725]

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]

Yang Q; She H; Gearing M; Colla E; Lee M; Shacka JJ; Mao Z. 2009. Regulation of neuronal survival factor MEF2D by chaperone-mediated autophagy. Science 323(5910):124-7. [PubMed: 19119233]  [MGI Ref ID J:143024]

von Coelln R; Thomas B; Andrabi SA; Lim KL; Savitt JM; Saffary R; Stirling W; Bruno K; Hess EJ; Lee MK; Dawson VL; Dawson TM. 2006. Inclusion body formation and neurodegeneration are parkin independent in a mouse model of alpha-synucleinopathy. J Neurosci 26(14):3685-96. [PubMed: 16597723]  [MGI Ref ID J:107254]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX12

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, hemizygous males are bred to wildtype female siblings or to inbred C57BL/6J females. The donating investigator reports that female carriers do not breed well and homozygotes are not viable.
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 $232.00Female or MaleHemizygous for Tg(Prnp-SNCA*A53T)23Mkle  
Price per Pair (US dollars $)Pair Genotype
$304.00Noncarrier x Hemizygous for Tg(Prnp-SNCA*A53T)23Mkle  

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 $301.60Female or MaleHemizygous for Tg(Prnp-SNCA*A53T)23Mkle  
Price per Pair (US dollars $)Pair Genotype
$395.20Noncarrier x Hemizygous for Tg(Prnp-SNCA*A53T)23Mkle  

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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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.
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