Overview

These huntingtin knock-in mice (originally termed HdhQ200) carry a mutant allele with a 200 CAG/polyQ repeat mutation, and exhibit a more aggressive and earlier onset of the behavioral and neurological phenotype as compared to the HdhQ150 strain (STOCK no. 4595) with progressive motor deficits starting at 50 weeks of age. This mutant strain may be useful in studies related to Huntington's disease.

Donating Investigator

Dr. Peter J Detloff, University of Alabama at Birmingham

Genetic overview

Genetic Background	Generation

Htt^tm2Detl

Allele Type	Gene Symbol	Gene Name
Targeted	Htt	huntingtin

View Genetics

Research Applications

Mouse/Human Gene Homologs
Neurobiology Research
Research Tools

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

As early as 9 weeks of age heterozygous mice exhibit cytoplasmic aggregation foci of HTT (huntingtin) protein, and by 20 weeks of age exhibit striatal neuronal intranuclear inclusions (NIIs). By 40 weeks of age, the striatal aggregation foci are perinuclear and exhibit increased immunoreactivity for ubiquitin and autophagosome marker LC3. Heterozygotes exhibit impaired balance and diminished motor coordination by 50 weeks of age, and abnormal gait by 60 weeks. By 80 weeks of age, heterozygotes display loss of grip strength, striatal and cortical astrogliosis, and a loss of approximately 50% of striatal dopamine receptor binding with increased glial fibrillary acidic protein immunoreactivity. Increased glial fibrillary acidic protein immunoreactivity is present in the striatum and ubiquititin- and huntingtin-positive neuronal intranuclear inclusions (NIIs) are detected throughout the dorsal striatum, nucleus accumbens and to a lesser extent other regions of the brain. Mutant CAG/polyQ repeat expression is slightly lower than wildtype levels as detected by Western blot analysis and qRTPCR of brain tissue. Mutant mice may be noticeably smaller than wild-type littermates. Mice homozygous for the targeted allele are viable and fertile. Onset of symptoms occurs earlier for homozygotes than for heterozygotes. Motor deficits are detected in homozygotes as early as 20 weeks of age. After 30 weeks of age mutant mice may become infertile.

This strain is one of a set of different CAG/polyQ repeat length mutants derived from HdhQ150 (STOCK no. 004595 ). The set includes, STOCK numbers: 016521, 016522, 016523, 016524, 016525.

Development

In the first step of a two step procedure, exon 1 was replaced with the selectable marker Hprt in 129P2/OlaHsd-derived HM1 embryonic stem (ES) cells. A second round of targeting was performed to replace Hprt with exon 1 sequence including a 150 CAG repeat segment. Correctly targeted ES cells were injected into C57BL/6J blastocysts. Before being donated to the Repository, the mice were backcrossed to C57BL/6J for 12 generations while being selectively bred for the 200 CAG repeat segment which arose due to repeat instability. Upon arrival at The Jackson Laboratory, the mice were crossed to C57BL/6J (Stock No. 000664) at least once to establish the colony. The mice must be monitored for CAG repeat length due to the instability of the repeat segment.

Control Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Heng MY; Duong DK; Albin RL; Tallaksen-Greene SJ; Hunter JM; Lesort MJ; Osmand A; Paulson HL; Detloff PJ. 2010. Early autophagic response in a novel knock-in model of Huntington disease. Hum Mol Genet 19(19):3702-20PubMed: 20616151 MGI: J:163641
Kumar A; Zhang J; Tallaksen-Greene S; Crowley MR; Crossman DK; Morton AJ; Van Groen T; Kadish I; Albin RL; Lesort M; Detloff PJ. 2016. Allelic series of Huntington's disease knock-in mice reveals expression discorrelates. Hum Mol Genet 25(8):1619-36PubMed: 26908599 MGI: J:229738
Lin CH; Tallaksen-Greene S; Chien WM; Cearley JA; Jackson WS; Crouse AB; Ren S; Li XJ; Albin RL; Detloff PJ. 2001. Neurological abnormalities in a knock-in mouse model of Huntington's disease. Hum Mol Genet 10(2):137-44PubMed: 11152661 MGI: J:67074

View All References

Genetics

Htt^tm2Detl

Allele Symbol: Htt^tm2Detl

Allele Name	targeted mutation 2, Peter J Detloff
Allele Type	Targeted
Allele Synonym(s)	CHL2; Hdh^(CAG)150; Hdh^Q150; Hdh150Q; Hdh200Q; HdhCAG150; HdhQ150; HdhQ200
Gene Symbol and Name	Htt, huntingtin
Gene Synonym(s)
Promoter	Htt, huntingtin, mouse, laboratory
Strain of Origin	129P2/OlaHsd-Hprt^b-m3
Chromosome	5
Molecular Note	This allele carries 150 CAG repeat units in the first exon of the endogenous gene. CAG repeat numbers in this gene are highly unstable. Mice carrying this allele may have more or fewer repeats than stated in the original description.

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).

Huntington's disease

Research Areas By Phenotype

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

Genotype: Htt^tm2Detl related

Mouse/Human Gene Homologs
- Huntington's disease (chorea)
Neurobiology Research
- Huntington's disease
- Cortical Defects
- Neurodegeneration

Research Tools
- Neurobiology Research
Neurobiology Research
- Huntington's disease
- Astrocyte Defects
  - astrocytosis
Mouse/Human Gene Homologs
- Huntington's disease (chorea)

Mammalian Phenotype Terms by Genotype

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

Genotype: Htt^tm2Detl/Htt^tm2Detl
involves: 129P2/OlaHsd * C57BL/6J

behavior/neurological phenotype

abnormal behavior
- the discrepancy between onset age of behavioral and neurological phenotypes is believed to reflect the percentage of C57BL/6 in the strain background (50-75% C57BL/6 - early onset (J:67074), 75-90% C57BL/6 - late onset (J:123681))

abnormal gait
- 9 out of 10 homozygotes with severe gait disturbance display either clasping or open cage inactivity
- staggering gait/loss of gait pattern is observed in homozygotes at 100 weeks of age
- young homozygotes (15-40 weeks) exhibit a more severe gait abnormality than age-matched heterozygotes

abnormal motor capabilities/coordination/movement
- at 20 weeks of age mice performed better in motor learning and motor performance on the accelerated rotarod than wild-type controls
- homozygotes are viable and developmentally normal but present symptoms of motor deficits with an onset of ~25 weeks; symptom presentation is variable among individual mutants
- muscle power as assessed by latency to fall in the hanging wire test is not impaired in 100 week old mice

abnormal motor coordination/balance
- at 5.0 rpm., homozygotes (15-40 weeks) stay for a significantly shorter time on a slowly rotating rod than age-matched heterozygotes

hypoactivity
- homozygotes younger than 40 weeks of age tend to exhibit open cage inactivity, suggesting that an increase in mutant allele dose causes an earlier onset of this abnormality
- reduced activity first observed in animals at 70 weeks of age as measured by automated activity cages, by 100 weeks activity is significantly reduced

impaired balance
- 80% of 100 week old mice fail to traverse the 5 mm beam
- 90% of 100 week old mice exhibit a hindlimb drag while traversing beam
- as early as 40 weeks of age, homozygotes exhibit a hindlimb drag while traversing beam
- beginning at 70 weeks of age time to traverse 11 mm round and 5 mm square balance beams is increased as compared to wild-type

impaired coordination
- significant increase in number of falls on the accelerated rotarod at 100 weeks of age in comparison to wild-type and heterozygotes, however, motor learning is not impaired

impaired limb coordination
- at >40 weeks of age, homozygotes exhibit an early-onset increase in the distance between front and hind paws ('overlap' distance) relative to age-matched heterozygotes

limb grasping
- clasping behavior produced by tail suspension test is observed in a small number of homozygotes at 20 weeks of age; by 70 - 100 weeks of age clasping behavior is common
- during tail suspension, >60% of young homozygotes (15-40 weeks) versus only <20% of wild-type or Hdh^tm1Detl homozygotes (carrying a 80 unit CAG repeat) tend to clasp
- homozygotes with a 150 unit CAG repeat exhibit an earlier onset of limb clasping relative to heterozygotes

short stride length
- hindpaw and forepaw stride lengths are reduced in homozygotes at 100 weeks of age as compared to wild-type

tonic-clonic seizures
- 4 out of 25 mutant mice (250 trials; 25-60 weeks of age) exhibit a convulsive spell consistent with a tonic-clonic seizure; more than one occurrences are noted in two mice during a 10 trial period
- seizures are not observed in mice with higher percentage of C57BL/6 in genetic background

tremors
- resting tremor observed in animals at 100 weeks of age

growth/size/body region phenotype

decreased body size
- at >25 weeks of age, ~1 in 10 mutants appears significantly smaller than its wild-type littermate; this size difference progresses slowly with age

weight loss
- most significant loss observed between 70 and 100 weeks of age as compared to wild-type
- progressive weight loss with age

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - homozygotes display normal blood glucose levels relative to wild-type mice

nervous system phenotype
- Normal - homozygotes display no extreme reductions in major brain regions up to 52 weeks of age

nervous system phenotype

abnormal dorsal striatum morphology
- striatal dopamine D1 receptor sites are decreased by 79% as compared to wild-type at 100 weeks of age
- striatal dopamine D2 receptor sites are decreased by 42% as compared to wild-type at 100 weeks of age

abnormal neuron morphology
- striatal neurons appear atrophic and irregularly shaped

abnormal striatum morphology
- homozygotes exhibit a 42.8% reduction in striatal neuron number
- mean striatal volume is reduced to 40.4% as compared to wild-type at 100 weeks of age

abnormal ventral striatum morphology
- striatal dopamine D1 receptor sites are decreased by 86% as compared to wild-type at 100 weeks of age
- striatal dopamine D2 receptor sites are decreased by 32% as compared to wild-type at 100 weeks of age

gliosis
- mutant mice exhibit significant reactive gliosis in the striatum; notably, neuronal number remains relatively unaffected

neuron degeneration
- starting at ~40 weeks, mutants exhibit neuronal intranuclear inclusions (NIIs) predominantly in the striatum; no dystrophic neurites are observed

neuronal intranuclear inclusions
- starting at ~40 weeks, mutants exhibit neuronal intranuclear inclusions (NIIs) predominantly in the striatum

tonic-clonic seizures
- 4 out of 25 mutant mice (250 trials; 25-60 weeks of age) exhibit a convulsive spell consistent with a tonic-clonic seizure; more than one occurrences are noted in two mice during a 10 trial period
- seizures are not observed in mice with higher percentage of C57BL/6 in genetic background

Genotype: Htt^tm2Detl/Htt⁺
involves: 129P2/OlaHsd * C57BL/6J

behavior/neurological phenotype

abnormal behavior
- the discrepancy between onset age of behavioral and neurological phenotypes is believed to reflect the percentage of C57BL/6 in the strain background (50-75% C57BL/6 - early onset (J:67074), 75-90% C57BL/6 - late onset (J:123681))

abnormal gait
- old (but not young) heterozygotes display a 2-fold increase in stride and base length variation relative to wild-type mice, suggesting that the mutation causes a late-onset variability in gait
- old heterozygotes (greater than 40 weeks) exhibit an abnormal gait relative to wild-type mice
- staggering gait observed in animals at 100 weeks of age

abnormal motor capabilities/coordination/movement
- heterozygotes are viable and developmentally normal but present symptoms of motor deficits with an onset of ~60 weeks; symptom presentation is variable among individual mutants

abnormal motor coordination/balance
- at 5.0 rpm., heterozygotes (15-40 weeks) stay for a significantly shorter time on a slowly rotating rod relative to age-matched wild-type mice

enhanced coordination
- at 20 weeks of age mice performed better in motor performance on the accelerated rotarod than wild-type controls
- heterozygotes outperform homozygotes on the rotarod up to 40 weeks of age

hypoactivity
- at 15-40 weeks of age, a few heterozygotes remain inactive upon removal of the cage lid whereas all wild-type mice show exploratory activity by walking around the cage
- the proportion of heterozygotes tending to remain inactive increases significantly with age (>40 weeks), indicating that the tendency to be inactive is a late-onset trait conferred by the mutant allele

impaired balance
- 50% of 100 week old mice fail to traverse the 5 mm beam
- 63% of 100 week old mice exhibit a hindlimb drag while traversing beam
- beginning at 70 weeks of age time to traverse 11 mm round and 5 mm square balance beam is increased as compared to wild-type

impaired limb coordination
- at >40 weeks of age, heterozygotes show a late-onset increase in the average distance between front and hind paws ('overlap' distance) relative to age-matched wild-type mice or Hdh^tm1Detl heterozygotes (carrying a 80 unit CAG repeat)

limb grasping
- during tail suspension, >60% of old heterozygotes (>40 weeks) versus only <20% of wild-type or Hdh^tm1Detl homozygotes (carrying a 80 unit CAG repeat) tend to clasp
- the tendency to clasp is a late-onset trait conferred by the Hdh^tm2Detl allele

short stride length
- hindpaw and forepaw stride lengths are reduced in heterozygotes at 100 weeks of age as compared to wild-type

growth/size/body region phenotype

decreased body size
- at 52 weeks of age, some heterozygotes are significantly smaller than wild-type littermates

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - heterozygotes display normal blood glucose levels relative to wild-type mice

nervous system phenotype
- Normal - heterozygotes display no extreme reductions in major brain regions up to 52 weeks of age

mortality/aging

premature death
- only 3 of 45 heterozygotes die prior to 1 year of age; heterozygotes typically survive for >1 year

nervous system phenotype

abnormal dorsal striatum morphology
- striatal dopamine D1 receptor sites are decreased by 42% as compared to wild-type at 100 weeks of age
- striatal dopamine D2 receptor sites are decreased by 17% as compared to wild-type at 100 weeks of age

abnormal ventral striatum morphology
- striatal dopamine D1 receptor sites are decreased by 50% as compared to wild-type at 100 weeks of ag
- striatal dopamine D2 receptor sites are decreased by 17% as compared to wild-type at 100 weeks of age

gliosis
- mutant mice exhibit significant reactive gliosis in the striatum; notably, neuronal number remains relatively unaffected

neuron degeneration
- starting at ~40 weeks, mutants exhibit neuronal intranuclear inclusions (NIIs) predominantly in the striatum; however, no dystrophic neurites are observed

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

Genotype: Htt^tm2Detl/Htt⁺
B6J.129P2-Htt

behavior/neurological phenotype

impaired coordination
- mice with about 250 CAG repeats exhibit a motor deficit on the balance beam at 6 months of age, spending more time to cross the beam; motor deficits progress with age

growth/size/body region phenotype

weight loss
- mice with about 250 CAG repeats exhibit lower body weight; they gain body weight normally up to 4 months, stop gaining weight and then lose weight

hematopoietic system phenotype

microgliosis
- mice with about 250 CAG repeats exhibit increased proliferation of microglia in the striatum

homeostasis/metabolism phenotype

increased taurine level
- mice with about 250 CAG repeats show increased levels of taurine in the striatum at 12 months of age

immune system phenotype

microgliosis
- mice with about 250 CAG repeats exhibit increased proliferation of microglia in the striatum

nervous system phenotype

abnormal myelination
- mice with about 250 CAG repeats show developmental delay of myelination, with lower levels of all isoforms of myelin basic protein and myelin oligodendrocyte glycoprotein in the striatum at P14

abnormal oligodendrocyte physiology
- Normal - however, the number of oligodendrocyte precursor cells is normal
- mice with about 250 CAG repeats exhibit enhanced proliferation of oligodendrocyte precursor cells in the corpus callosum and striatum at 9 and 12 months of age
- primary oligodendrocyte precursor cells from P6 mice with about 250 CAG repeats exhibit an extended S-phase

abnormal striatum morphology
- e and taurine at 12 months of age
- mice with about 250 CAG repeats show a reduction in the striatum volume by 6 months of age but not at 3 months
- striatal metabolites are altered by 9 months of age in mice with about 250 CAG repeats, with lower levels of N-acetylaspartate at 9 months, and lower levels of gamma-aminobutyric acid (GABA), glutamate, NAA, creatine + PCr and increased levels of glutamine and taurine at 12 months of age

brain atrophy
- mice backcrossed to C57BL/6J for 8 generations yields mice with about 250 CAG repeats which show acceleration of brain atrophy (striatum and neocortex) compared to mice with 150 or 200 CAG repeats that is most robust between 2 and 6 months of age

decreased myelin sheath thickness
- mice with about 250 CAG repeats exhibit numerous smaller axons that are hypomyelinated with increased G-ratios (diameter of axon/outer diameter of the myelinaged fiber) in the corpus callosum at 12 months of age, indicating thinner myelin sheaths

decreased neocortex volume
- mice with about 250 CAG repeats show a reduction in the neocortex volume by 6 months of age but not at 3 months

decreased oligodendrocyte number
- mice with about 250 CAG repeats have decreased numbers of mature oligodendrocytes in the brain at P14

dysmyelination
- mice with about 250 CAG repeats show fewer myelinated axons in the corpus callosum at P14

microgliosis
- mice with about 250 CAG repeats exhibit increased proliferation of microglia in the striatum

neuronal intranuclear inclusions
- mice with about 250 CAG repeats show nuclear progressive accumulation of mutant HTT aggregates from 6 to 12 months of age

References

Heng MY; Duong DK; Albin RL; Tallaksen-Greene SJ; Hunter JM; Lesort MJ; Osmand A; Paulson HL; Detloff PJ. 2010. Early autophagic response in a novel knock-in model of Huntington disease. Hum Mol Genet 19(19):3702-20PubMed: 20616151 MGI: J:163641
Kumar A; Zhang J; Tallaksen-Greene S; Crowley MR; Crossman DK; Morton AJ; Van Groen T; Kadish I; Albin RL; Lesort M; Detloff PJ. 2016. Allelic series of Huntington's disease knock-in mice reveals expression discorrelates. Hum Mol Genet 25(8):1619-36PubMed: 26908599 MGI: J:229738
Lin CH; Tallaksen-Greene S; Chien WM; Cearley JA; Jackson WS; Crouse AB; Ren S; Li XJ; Albin RL; Detloff PJ. 2001. Neurological abnormalities in a knock-in mouse model of Huntington's disease. Hum Mol Genet 10(2):137-44PubMed: 11152661 MGI: J:67074

Additional - Htt^tm2Detl related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Htt repeat assay
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, breeding C57BL/6J females with heterozygous males is suggested to help stabilize the CAG/polyQ repeat segment length. After 30 weeks of age mutant mice may become infertile. Onset of symptoms occurs earlier for homozygotes than for heterozygotes. The mice must be monitored for CAG/polyQ repeat length due to the instability of the repeat segment.
- Additional Breeding and Husbandry Support
Citation
When using the B6.129P2-Htt^tm2Detl/200J mouse strain in a publication, please cite the originating article(s) and include JAX stock #016523 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or wildtype for Htt<tm2Detl>

Related Products and Services

Frozen Mouse Embryo	B6.129P2-Htt<tm2Detl>/200J Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.129P2-Htt<tm2Detl>/200J Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.129P2-Htt<tm2Detl>/200J Frozen Embryo	$3373.50
Frozen Mouse Embryo	B6.129P2-Htt<tm2Detl>/200J Frozen Embryo	$3373.50

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Htttm2Detl

Allele Symbol: Htttm2Detl

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: Htttm2Detl related

Mammalian Phenotype Terms by Genotype

Genotype: Htttm2Detl/Htttm2Detlinvolves: 129P2/OlaHsd * C57BL/6J

behavior/neurological phenotype

growth/size/body region phenotype

mammalian phenotype

nervous system phenotype

Genotype: Htttm2Detl/Htt+involves: 129P2/OlaHsd * C57BL/6J

behavior/neurological phenotype

growth/size/body region phenotype

mammalian phenotype

mortality/aging

nervous system phenotype

Genotype: Htttm2Detl/Htt+B6J.129P2-Htt

behavior/neurological phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

nervous system phenotype

References

Additional - Htttm2Detl related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Htt^tm2Detl

Allele Symbol: Htt^tm2Detl

Genotype: Htt^tm2Detl related

Genotype: Htt^tm2Detl/Htt^tm2Detl
involves: 129P2/OlaHsd * C57BL/6J

Genotype: Htt^tm2Detl/Htt⁺
involves: 129P2/OlaHsd * C57BL/6J

Genotype: Htt^tm2Detl/Htt⁺
B6J.129P2-Htt

Additional - Htt^tm2Detl related