Strain Name:

FVB-Tg(YAC128)53Hay/J

Stock Number:

004938

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These transgenic mice express the human huntingtin protein. Hyperkinesis begins at 3 months of age with progressive motor impairment appearing at 6 months of age. This is followed by progressive neurodegeneration, starting at 9 months of age, and hypokinesis at 12 months. Mutants exhibit decreased brain weight and reduced striatal and cortical volumes. This mutant mouse strain represents a model that may be useful in studies of Huntington's disease.

Description

Strain Information

Type Mutant Strain; Transgenic;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemInbred x Hemizygote         (Female x Male)   01-MAR-06
Specieslaboratory mouse
GenerationN12+N14 (17-DEC-12)
Generation Definitions
 
Donating Investigator Michael Hayden,   University of British Columbia

Description
These transgenic mice express the human huntingtin protein containing a 128 CAG repeat expansion. Human huntingtin mRNA and protein is detected. Hyperkinesis begins at 3 months of age with progressive motor impairment appearing at 6 months of age. This is followed by progressive neurodegeneration, starting at 9 months of age, and hypokinesis at 12 months. The motor dysfunction, Rotorod deficit, is correlated with neuronal loss. Mutants exhibit decreased brain weight and reduced striatal and cortical volumes. 18% shrinkage of striatal neurons is observed in 12 month old mutants. A significant decrease (15%) in the number of striatal neurons occurs by 12 months of age. Nuclear huntingtin aggregate inclusions of striatal neurons from 18 month old mutant mice are detected at the light microscopy level. This mutant mouse strain represents a model that may be useful in studies of Huntington's disease.

Development
A YAC containing a full-length human huntingtin gene was modified with a 128 CAG repeat expansion in exon 1. The resulting construct (YAC128) was injected into FVB/N pronuclei.

Control Information

  Control
   Noncarrier
 
  Considerations for Choosing Controls

Related Strains

View Huntington's Disease Models     (28 strains)

View Strains carrying other alleles of HTT     (14 strains)

Additional Web Information

Visit the Huntington's Diease Resource site for helpful information on Huntington's 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.
Huntington Disease; HD
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tg(YAC128)53Hay/0

        FVB/N-Tg(YAC128)53Hay
  • nervous system phenotype
  • abnormal basal ganglion morphology
    • mean area of striatal neurons is decreased by 18% in 12 month old mice   (MGI Ref ID J:84453)
    • striatal volume is decreased by 15% by 9 months of age   (MGI Ref ID J:84453)
    • abnormal striatum morphology
      • the levels of both the endogenous excitotoxin quinolinic acid (QUIN) and its bioprecursor, 3-hydroxykynurenine (3-HK) are increased in the striatum beginning at 8 months of age, similarly to that seen in Huntington disease patients   (MGI Ref ID J:111237)
      • reduced compared to wild-type controls at 18 months (10.9 mm3 vs 12.3 mm3)   (MGI Ref ID J:120991)
      • significant volume loss is detected at 12 months compared to wild-type controls   (MGI Ref ID J:120991)
      • neuronal loss is observed at 12 months relative to controls   (MGI Ref ID J:120991)
      • diffuse huntingtin (htt) fragments showing nuclear localization in striatum at 3 months, and this increases with age such that at 12 months, most striatal neurons are positive for htt   (MGI Ref ID J:120991)
      • loss of striatal neurons   (MGI Ref ID J:105723)
      • decrease in striatal volume at 12 months of age   (MGI Ref ID J:105723)
      • abnormal medium spiny neuron morphology
        • medium spiny neurons (MSN) are decreased 8% by 9 months of age   (MGI Ref ID J:84453)
    • loss of basal ganglia neurons
      • transgenic mice exhibit a 9% decrease in striatal neurons by 9 months, progressing to a 15-18% loss by 12 months   (MGI Ref ID J:84453)
      • medium spiny neurons (MSN), the major neuronal cell type of the straitum, are decreased 8% by 9 months of age   (MGI Ref ID J:84453)
  • abnormal cerebral cortex morphology
    • cortex volume decreased by 7% by 12 months of age   (MGI Ref ID J:84453)
    • QUIN and 3-HK levels are elevated in the cerebral cortex, similarly to that seen in Huntington disease patients   (MGI Ref ID J:111237)
  • decreased brain weight
    • total brain weight decreases by 5% at 9 months, progressing to a 10% decrease by 1 year   (MGI Ref ID J:84453)
    • cerebellum weight is unchanged   (MGI Ref ID J:84453)
    • reduced compared to wild-type controls at 18 months (0.35 grams vs 0.38 grams)   (MGI Ref ID J:120991)
  • increased susceptibility to neuronal excitotoxicity
    • in medium spiny neurons in response to NMDA (500 um) exposure compared to wild-type mice or mice carrying Tg(YAC128)55Hay   (MGI Ref ID J:105723)
  • neuronal intranuclear inclusions
    • neuronal inclusions observed throughout nucleoplasm of all striatal cells by 18 months of age   (MGI Ref ID J:84453)
    • at 18 months of age in the striatum and cortex   (MGI Ref ID J:105723)
  • behavior/neurological phenotype
  • abnormal learning/memory/conditioning
    • cognitive deficits including difficulties in changing strategies and delayed platform finding beginning at 2 months of age   (MGI Ref ID J:105723)
    • abnormal motor learning
      • impaired in a rotarod assay beginning at 2 months of age   (MGI Ref ID J:105723)
  • abnormal motor capabilities/coordination/movement
    • motor abnormalities similar to those seen in the clinical course of Huntington disease   (MGI Ref ID J:105723)
    • disease progression is accelerated compared to mice hemizygous for Tg(YAC128)55Hay   (MGI Ref ID J:105723)
    • bradykinesia
      • starting at 4 months of age, a hypokinetic phenotype is displayed compared to wild-type controls in open field test   (MGI Ref ID J:120991)
    • hyperactivity
      • hyperkinetic phenotype observed at 3 months in open field apparatus   (MGI Ref ID J:84453)
      • at 2 months of age   (MGI Ref ID J:105723)
    • hypoactivity
      • hypokinetic phenotype observed beginning at 6 months of age and becoming significant by 12 months of age in open field apparatus   (MGI Ref ID J:84453)
      • beginning after 3 months of age as measured by decrease in spontaneous ambulation in open-field testing   (MGI Ref ID J:105723)
    • impaired coordination
      • progressive decrease in fixed speed rotarod performance beginning at 6 months of age   (MGI Ref ID J:84453)
      • significant deficit in rotarod tests at 2 months of age   (MGI Ref ID J:120991)
      • in a rotarod assay beginning after 3 months of age and becoming worse with age   (MGI Ref ID J:105723)
  • growth/size phenotype
  • increased body weight   (MGI Ref ID J:84453)
  • cellular phenotype
  • increased susceptibility to neuronal excitotoxicity
    • in medium spiny neurons in response to NMDA (500 um) exposure compared to wild-type mice or mice carrying Tg(YAC128)55Hay   (MGI Ref ID J:105723)
  • homeostasis/metabolism phenotype
  • increased susceptibility to neuronal excitotoxicity
    • in medium spiny neurons in response to NMDA (500 um) exposure compared to wild-type mice or mice carrying Tg(YAC128)55Hay   (MGI Ref ID J:105723)

Tg(YAC128)53Hay/0

        FVB-Tg(YAC128)53Hay/J
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mice do not exhibit a deterioration in grip strength as compared to controls   (MGI Ref ID J:185262)
    • stride length, splay length and base are similar to controls   (MGI Ref ID J:185262)
    • decreased vertical activity
      • mice exhibit a decrease in climbing activity at 16 weeks of age   (MGI Ref ID J:185262)
    • hyperactivity
      • in the light phase of the open field test, females are hyperactive as compared to controls only at 52 weeks of age   (MGI Ref ID J:185262)
      • in the dark phase, mice cover more distance in center than controls   (MGI Ref ID J:185262)
    • hypoactivity
      • mice are hypoactive (total distance covered) in dark phase of open field test starting at 36 and 52 weeks of age in females and 16 weeks of age in males   (MGI Ref ID J:185262)
      • hypoactivity is not observed in light phase   (MGI Ref ID J:185262)
    • impaired coordination
      • mice do not perform as well on rotarod test as controls, but performance does not worsen with age   (MGI Ref ID J:185262)
    • increased anxiety-related response
      • increased preference for dark in males in dark/light choice test starting at 52 weeks of age   (MGI Ref ID J:185262)
    • increased vertical activity
      • mice rear more at 36 and 52 weeks in the light phase of the open field test   (MGI Ref ID J:185262)
      • in the dark phase males rear more only at 52 weeks of age   (MGI Ref ID J:185262)
  • growth/size phenotype
  • increased body weight
    • body weight is significantly increased in males at 32 weeks   (MGI Ref ID J:185262)
    • females are not consistently heavier, exhibiting heavier weights between 48 and 76 weeks   (MGI Ref ID J:185262)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • mice do not exhibit alterations in startle reflex or in prepulse inhibition   (MGI Ref ID J:185262)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Tg(YAC128)53Hay/0

        B6.FVB-Tg(YAC128)53Hay
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mice do not exhibit a deterioration in grip strength as compared to controls   (MGI Ref ID J:185262)
    • stride length, splay length and base are similar to controls   (MGI Ref ID J:185262)
    • rearing activity is similar to controls   (MGI Ref ID J:185262)
    • mice do not behave differently from controls in the light/dark choice test   (MGI Ref ID J:185262)
    • hypoactivity
      • mice are hypoactive (total distance covered) in the open field test starting at 12 weeks of age in the light phase and 8,16 and 34 weeks in the dark phase   (MGI Ref ID J:185262)
      • hypoactivity in the center is only observed in the dark phase at 16 and 34 weeks   (MGI Ref ID J:185262)
    • impaired coordination
      • mice do not perform as well on rotarod test as controls, but performance does not worsen with age   (MGI Ref ID J:185262)
      • females perform worse than males   (MGI Ref ID J:185262)
  • growth/size phenotype
  • increased body weight
    • body weight is significantly increased in males at 8 weeks and females at 16 weeks, although male weight does not reach significance at 56 weeks   (MGI Ref ID J:185262)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • mice do not exhibit alterations in startle reflex although there is significant variability across age and gender   (MGI Ref ID J:185262)
    • decreased prepulse inhibition
      • observed at 56 weeks of age   (MGI Ref ID J:185262)
View Research Applications

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

HTT related

Developmental Biology Research
Neurodevelopmental Defects

Mouse/Human Gene Homologs
Huntington's disease (chorea)

Neurobiology Research
Ataxia (Movement) Defects
Behavioral and Learning Defects
Cortical Defects
Huntington's disease
Neurodegeneration
Neurodevelopmental Defects
Neurotransmitter Receptor and Synaptic Vesicle Defects
Tremor Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tg(YAC128)53Hay
Allele Name transgene insertion 53, Michael Hayden
Allele Type Transgenic (random, expressed)
Common Name(s) HD53; YAC 128; YAC128;
Mutation Made By Elizabeth Slow,   University of British Columbia
Strain of OriginFVB/N
Expressed Gene HTT, huntingtin, human
Promoter HTT, huntingtin, human
Molecular Note A YAC containing a full-length human huntingtin gene under the control of the endogenous human HDH promoter was modified with a 128 CAG repeat expansion. The resulting construct (YAC128) was used to generate transgenic mice. Founder line 53 integrated the most copies of the transgene and had the highest levels of protein expression (75% of endogenous levels) as determined by densitometric analysis. [MGI Ref ID J:84453]
 

Genotyping

Genotyping Information

Genotyping Protocols

HDexon K2G CAG repeat, Fluorescent PCR
TG(HDexon1), TG(YAC), Standard PCR
(YAC128)53Hay, Standard PCR
HDexon Hi T CAG, Fluorescent PCR
TG(HDexon1), TG(YAC), Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Menalled L; El-Khodor BF; Patry M; Suarez-Farinas M; Orenstein SJ; Zahasky B; Leahy C; Wheeler V; Yang XW; MacDonald M; Morton AJ; Bates G; Leeds J; Park L; Howland D; Signer E; Tobin A; Brunner D. 2009. Systematic behavioral evaluation of Huntington's disease transgenic and knock-in mouse models. Neurobiol Dis 35(3):319-36. [PubMed: 19464370]  [MGI Ref ID J:185262]

Slow EJ; van Raamsdonk J; Rogers D; Coleman SH; Graham RK; Deng Y; Oh R; Bissada N; Hossain SM; Yang YZ; Li XJ; Simpson EM; Gutekunst CA; Leavitt BR; Hayden MR. 2003. Selective striatal neuronal loss in a YAC128 mouse model of Huntington disease. Hum Mol Genet 12(13):1555-67. [PubMed: 12812983]  [MGI Ref ID J:84453]

Additional References

Tg(YAC128)53Hay related

Bjorkqvist M; Wild EJ; Thiele J; Silvestroni A; Andre R; Lahiri N; Raibon E; Lee RV; Benn CL; Soulet D; Magnusson A; Woodman B; Landles C; Pouladi MA; Hayden MR; Khalili-Shirazi A; Lowdell MW; Brundin P; Bates GP; Leavitt BR; Moller T; Tabrizi SJ. 2008. A novel pathogenic pathway of immune activation detectable before clinical onset in Huntington's disease. J Exp Med 205(8):1869-77. [PubMed: 18625748]  [MGI Ref ID J:138558]

Crook ZR; Housman D. 2011. Huntington's disease: can mice lead the way to treatment? Neuron 69(3):423-35. [PubMed: 21315254]  [MGI Ref ID J:174750]

Cummings DM; Andre VM; Uzgil BO; Gee SM; Fisher YE; Cepeda C; Levine MS. 2009. Alterations in cortical excitation and inhibition in genetic mouse models of Huntington's disease. J Neurosci 29(33):10371-86. [PubMed: 19692612]  [MGI Ref ID J:151920]

Dey ND; Bombard MC; Roland BP; Davidson S; Lu M; Rossignol J; Sandstrom MI; Skeel RL; Lescaudron L; Dunbar GL. 2010. Genetically engineered mesenchymal stem cells reduce behavioral deficits in the YAC 128 mouse model of Huntington's disease. Behav Brain Res 214(2):193-200. [PubMed: 20493905]  [MGI Ref ID J:162156]

Graham RK; Deng Y; Slow EJ; Haigh B; Bissada N; Lu G; Pearson J; Shehadeh J; Bertram L; Murphy Z; Warby SC; Doty CN; Roy S; Wellington CL; Leavitt BR; Raymond LA; Nicholson DW; Hayden MR. 2006. Cleavage at the caspase-6 site is required for neuronal dysfunction and degeneration due to mutant huntingtin. Cell 125(6):1179-91. [PubMed: 16777606]  [MGI Ref ID J:120991]

Graham RK; Pouladi MA; Joshi P; Lu G; Deng Y; Wu NP; Figueroa BE; Metzler M; Andre VM; Slow EJ; Raymond L; Friedlander R; Levine MS; Leavitt BR; Hayden MR. 2009. Differential susceptibility to excitotoxic stress in YAC128 mouse models of Huntington disease between initiation and progression of disease. J Neurosci 29(7):2193-204. [PubMed: 19228972]  [MGI Ref ID J:146832]

Graham RK; Slow EJ; Deng Y; Bissada N; Lu G; Pearson J; Shehadeh J; Leavitt BR; Raymond LA; Hayden MR. 2006. Levels of mutant huntingtin influence the phenotypic severity of Huntington disease in YAC128 mouse models. Neurobiol Dis 21(2):444-55. [PubMed: 16230019]  [MGI Ref ID J:105723]

Guidetti P; Bates GP; Graham RK; Hayden MR; Leavitt BR; MacDonald ME; Slow EJ; Wheeler VC; Woodman B; Schwarcz R. 2006. Elevated brain 3-hydroxykynurenine and quinolinate levels in Huntington disease mice. Neurobiol Dis 23(1):190-7. [PubMed: 16697652]  [MGI Ref ID J:111237]

Gupta S; Jie S; Colby DW. 2012. Protein misfolding detected early in pathogenesis of transgenic mouse model of Huntington disease using amyloid seeding assay. J Biol Chem 287(13):9982-9. [PubMed: 22187438]  [MGI Ref ID J:184100]

Lawhorn C; Smith DM; Brown LL. 2008. Striosome-matrix pathology and motor deficits in the YAC128 mouse model of Huntington's disease. Neurobiol Dis 32(3):471-8. [PubMed: 18809498]  [MGI Ref ID J:142829]

Milnerwood AJ; Gladding CM; Pouladi MA; Kaufman AM; Hines RM; Boyd JD; Ko RW; Vasuta OC; Graham RK; Hayden MR; Murphy TH; Raymond LA. 2010. Early increase in extrasynaptic NMDA receptor signaling and expression contributes to phenotype onset in Huntington's disease mice. Neuron 65(2):178-90. [PubMed: 20152125]  [MGI Ref ID J:167657]

Milnerwood AJ; Raymond LA. 2007. Corticostriatal synaptic function in mouse models of Huntington's disease: early effects of huntingtin repeat length and protein load. J Physiol 585(Pt 3):817-31. [PubMed: 17947312]  [MGI Ref ID J:144266]

Oliveira JM; Jekabsons MB; Chen S; Lin A; Rego AC; Goncalves J; Ellerby LM; Nicholls DG. 2007. Mitochondrial dysfunction in Huntington's disease: the bioenergetics of isolated and in situ mitochondria from transgenic mice. J Neurochem 101(1):241-9. [PubMed: 17394466]  [MGI Ref ID J:144268]

Pouladi MA; Xie Y; Skotte NH; Ehrnhoefer DE; Graham RK; Kim JE; Bissada N; Yang XW; Paganetti P; Friedlander RM; Leavitt BR; Hayden MR. 2010. Full-length huntingtin levels modulate body weight by influencing insulin-like growth factor 1 expression. Hum Mol Genet 19(8):1528-38. [PubMed: 20097678]  [MGI Ref ID J:158346]

Song W; Chen J; Petrilli A; Liot G; Klinglmayr E; Zhou Y; Poquiz P; Tjong J; Pouladi MA; Hayden MR; Masliah E; Ellisman M; Rouiller I; Schwarzenbacher R; Bossy B; Perkins G; Bossy-Wetzel E. 2011. Mutant huntingtin binds the mitochondrial fission GTPase dynamin-related protein-1 and increases its enzymatic activity. Nat Med 17(3):377-82. [PubMed: 21336284]  [MGI Ref ID J:171134]

Valenza M; Carroll JB; Leoni V; Bertram LN; Bjorkhem I; Singaraja RR; Di Donato S; Lutjohann D; Hayden MR; Cattaneo E. 2007. Cholesterol biosynthesis pathway is disturbed in YAC128 mice and is modulated by huntingtin mutation. Hum Mol Genet 16(18):2187-98. [PubMed: 17613541]  [MGI Ref ID J:143144]

Williams BB; Li D; Wegrzynowicz M; Vadodaria BK; Anderson JG; Kwakye GF; Aschner M; Erikson KM; Bowman AB. 2010. Disease-toxicant screen reveals a neuroprotective interaction between Huntington's disease and manganese exposure. J Neurochem 112(1):227-37. [PubMed: 19845833]  [MGI Ref ID J:157032]

Zhang H; Li Q; Graham RK; Slow E; Hayden MR; Bezprozvanny I. 2008. Full length mutant huntingtin is required for altered Ca2+ signaling and apoptosis of striatal neurons in the YAC mouse model of Huntington's disease. Neurobiol Dis 31(1):80-8. [PubMed: 18502655]  [MGI Ref ID J:144442]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX12

Colony Maintenance

Breeding & HusbandryThis strain originated on an FVB/N background, was backcrossed for 12 generations on the same (October 2003). The strain is maintained as a hemizygote.
Mating SystemInbred x Hemizygote         (Female x Male)   01-MAR-06
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(YAC128)53Hay  
Price per Pair (US dollars $)Pair Genotype
$296.00Hemizygous for Tg(YAC128)53Hay x Noncarrier  
$296.00Noncarrier x Hemizygous for Tg(YAC128)53Hay  

Standard Supply

Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.

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(YAC128)53Hay  
Price per Pair (US dollars $)Pair Genotype
$384.80Hemizygous for Tg(YAC128)53Hay x Noncarrier  
$384.80Noncarrier x Hemizygous for Tg(YAC128)53Hay  

Standard Supply

Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live. Repository-Live represents an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. Repository-live orders are treated as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.

General Supply Notes

Control Information

  Control
   Noncarrier
 
  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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