Overview

Also Known As:D2.R6/2 ; D2.R6/2 (CAG ~350) ; R62.280(CHDI-005-7) ; CHDI-81001008

The DBA/2J-congenic R6/2 transgenic mouse line expresses the 5' end of the human huntingtin gene (HTT; HD or Hdh) with ~350 CAG repeat expansions. These D2.R6/2 (CAG ~350) mice may be useful for studying Huntington's disease on a defined congenic background.

Donating Investigator

Gillian P Bates, University College London, Institute of Neurology

Dr. David Howland, CHDI Foundation

Genetic overview

Genetic Background	Generation

Tg(HDexon1)62Gpb

Allele Type
Transgenic (Inserted expressed sequence, Humanized sequence)

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Research Applications

Neurobiology Research
Research Tools

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Stock No. 027425 was formerly associated with CHDI Foundation colony Stock No. 908766 [CHDI-81001008].

Huntington's disease (HD) is an autosomally dominant, fatal neurodegenerative disorder characterized by uncontrolled movements, psychiatric disturbances and cognitive impairment. HD is caused by an unstable trinucleotide (polyglutamine) repeat expansion in the huntingtin gene (HTT; HD or Hdh). For R6/2 transgenic mice, the CAG repeat number is subject to germline/somatic instability and may expand/contract. For additional information on this, see "General Information for R6/2 transgenic mouse lines" below.

Stock No. 027425: The DBA/2J-congenic R6/2 transgenic mouse line with ~350 CAG repeat expansions, called D2.R6/2 (CAG ~350) mice, are not fully characterized to date (April 2014).
However, they may exhibit a similar or delayed phenotype compared to that of R6/2 mice with ~160 CAG repeats on a (C57BL/6 x CBA)F1 genetic background. Those B6CBA.R6/2 (CAG 160) transgenic mice are described and available as Stock No. 002810. Briefly, B6CBA.R6/2 (CAG 160) mice exhibit a progressive neurological phenotype that mimics many of the features of HD. This includes early-onset (9-21 weeks of age), choreiform-like movements, involuntary stereotypic movements, tremor and epileptic seizures, as well as nonmovement disorder components (including unusual vocalization). They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. They develop neuronal intranuclear inclusions (huntingtin and ubiquitin), pancreatic beta cell inclusions (huntingtin) and hyperglycemia. R6/2 mice may exhibit metabolic deficits that prevent them from controlling body temperature as efficiently as their wildtype (noncarrier) littermates. Hemizygous mice have shortened lifespan (median survival may be ~20 weeks or less) with females living slightly longer. Hemizygous females are not fertile. Hemizygous males have a short (3-4 week) breeding window, and only about half are fertile.

This Huntington's disease mouse model is available by way of a collaborative effort between CHDI Foundation, Dr. Gillian P. Bates (United Medical and Dental School, London) and The Jackson Laboratory.

Transgene Insertion Information:
The HDexon1 transgene functions as single copy insertion. Sequence analysis identified its insertion site within an intron of the predicted gene Gm12695 on mouse chromosome 4 (chr4:96,409,585-96,414,930 [assembly NCBI 37/mus musuculus 9)], and the transgene is flanked by two rearranged sequences that do not contain the full exon 1 encoding DNA (Cowin et al. 2011 PLoS ONE 6(12):e28409). Additionally, a segment of Gram-positive bacterial sequence (likely originating from cloning vector contamination) is inserted just upstream of the HTT promoter that drives the expression of the intact copy. Transgene insertion also resulted in a 5.4 kbp deletion of mouse chromosomal DNA near the integration site (Chiang et al. 2012 Nat Genet. 44(4):390-7). As of January 2017, the function of predicted gene Gm12695 is unknown. It is normally expressed at negligible levels in mouse brain. The transgene insertion (in antisense orientation to Gm12695 transcription) results in increased cortical expression of a partial Gm12695 fragment (exons 8-11) - and this transcript is shown to have significant expression among the extensive network of differentially expressed genes associated with the R6/2 model, including those regulating synaptic transmission, cell signaling and transcription (Jacobsen et al. 2017 Sci Rep. 7:41120).

General Information for R6/2 transgenic mouse lines:
The R6/2 transgenic mouse lines express a transgene encoding the 5' end of human HTT with different lengths of CAG repeat expansions. The CAG repeat number is subject to germline and somatic instability, and may expand or contract. The phenotype of R6/2 animals varies greatly as a function of CAG repeat size and, similar to what is observed in humans, R6/2 transgenic mice may exhibit higher incidence of CAG repeat expansion when the transgene is transmitted via paternal inheritance. Interestingly, the copy:phenotype relationship is not linear for R6/2 mice, nor does a large CAG repeat number necessarily lead to an earlier onset and more severe phenotype. Genetic background may also lead to variations in disease severity/progression.
When using lines with unstable CAG repeat length, it is strongly recommended the CAG repeat number be quantified in all the experimental animals - all animals in all experimental groups should carry comparable CAG repeat sizes. CAG repeat sizing of HD mice should be done using high-resolution methods - as assays based on agarose gel electrophoresis typically do not provide sufficient resolution to accurately measure CAG repeat numbers. If labs do not have access to the appropriate equipment for determining CAG repeat length, CAG repeats can be evaluated on a fee-for-service basis by Laragen, Inc.

R6/2 animals on a (C57BL/6 x CBA)F1 genetic background are available with CAG expansion sizes of ~120 and ~160.
B6CBA.R6/2 (CAG 120) mice are Stock No. 006494
B6CBA.R6/2 (CAG 160) mice are Stock No. 002810

R6/2 animals on a C57BL/6J genetic background are available with CAG expansion sizes of ~116, ~168 and ~251.
B6J.R6/2 (CAG 116) mice are Stock No. 027419 [CHDI-81001001]
B6J.R6/2 (CAG 168) mice are Stock No. 027421 [CHDI-81001003]
B6J.R6/2 (CAG 251) mice are Stock No. 027423 [CHDI-81001005]

R6/2 animals on a DBA/2J genetic background are available with the different CAG expansion sizes listed below.
D2.R6/2 (CAG ~180) mice are Stock No. 027422 [CHDI-81001004]
D2.R6/2 (CAG ~380) mice are Stock No. 027424 [CHDI-81001006]
D2.R6/2 (CAG ~350) mice are Stock No. 027425 [CHDI-81001008]

Development

The HDexon1 transgene was isolated from a clone derived from a patient with Huntington's disease by Dr. Gillian P. Bates (while at United Medical and Dental School, London). The ~1.9 kbp transgene originally contained human huntingtin gene (HTT; HD or Hdh) sequences including ~1 kbp 5' UTR region, exon 1 with ~130 CAG repeat expansion and the first 262 bp of intron 1. The transgene was microinjected into single cell CBAxC57BL/6 embryos. This strain was identified as the R6-2 (R6/2) line in the original publication with ~144 CAG repeat expansion. Subsequently, R6/2 mice were backcrossed with DBA/2J inbred mice (Stock No. 000671) for several generations to create the DBA/2J-congenic colony D2.R6/2, called CHDI Foundation colony Stock No. 908766 [CHDI-81001008]. Hemizygous sperm with ~350 CAG repeats was frozen in 2011. In 2015, hemizygous frozen sperm from the CHDI Foundation colony was used by The Jackson Laboratory Repository to fertilize DBA/2J oocytes (Stock No. 000671). The resulting D2.R6/2 hemizygous colony is available as Stock No. 027425.

The HDexon1 transgene functions as single copy insertion. Sequence analysis identified its insertion site within an intron of the predicted gene Gm12695 on mouse chromosome 4 (chr4:96,409,585-96,414,930 [assembly NCBI 37/mus musuculus 9)], and the transgene is flanked by two rearranged sequences that do not contain the full exon 1 encoding DNA (Cowin et al. 2011 PLoS ONE 6(12):e28409). Additionally, a segment of Gram-positive bacterial sequence (likely originating from cloning vector contamination) is inserted just upstream of the HTT promoter that drives the expression of the intact copy. Transgene insertion also resulted in a 5.4 kbp deletion of mouse chromosomal DNA near the integration site (Chiang et al. 2012 Nat Genet. 44(4):390-7).
As of January 2017, the function of predicted gene Gm12695 is unknown. It is normally expressed at negligible levels in mouse brain. The transgene insertion (in antisense orientation to Gm12695 transcription) results in increased cortical expression of a partial Gm12695 fragment (exons 8-11) - and this transcript is shown to have significant expression among the extensive network of differentially expressed genes associated with the R6/2 model, including those regulating synaptic transmission, cell signaling and transcription (Jacobsen et al. 2017 Sci Rep. 7:41120).

Expression Data

Expressed Gene	HTT, huntingtin, human
Site of Expression

Control Suggestions

Noncarrier

Approximate Controls

000671 DBA/2J

Additional Information

Considerations for Choosing Controls

Selected References

Mangiarini L; Sathasivam K; Seller M; Cozens B; Harper A; Hetherington C; Lawton M; Trottier Y; Lehrach H; Davies SW; Bates GP. 1996. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell 87(3):493-506PubMed: 8898202 MGI: J:36689

View All References

Genetics

Tg(HDexon1)62Gpb

Allele Symbol: Tg(HDexon1)62Gpb

Allele Name	transgene insertion 62, Gillian Bates
Allele Type	Transgenic (Inserted expressed sequence, Humanized sequence)
Allele Synonym(s)	R6/2; R6/2B; Tg(HDexon1)62nGpb
Gene Symbol and Name	Tg(HDexon1)62Gpb, transgene insertion 62, Gillian Bates
Gene Synonym(s)
Promoter	HTT, huntingtin, human
Expressed Gene	HTT, huntingtin, human
Strain of Origin	CBA x C57BL/6
Chromosome	4
General Note	Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD. Onset of phenotype is apparent from approximately 8 weeks of age based on home cage behavior. Some functional tests indicate the presence of a motor impairment from 5-6 weeks and cognitive impairment from 3 weeks. Epileptic seizures are seen in a small percentage of transgenic mice. A failure to gain weight is more pronounced in males than females. Immunohistochemistry with antibodies raised against the N-terminus of huntingtin reveals aggregates in the form of intranuclear inclusions and neuropil aggregates. Transgenic mice on a background that involves C57BL/6 and CBA display a progressive neurological phenotype that mimics many of the features of Huntington Disease in humans, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. Frequent urination, loss of body weight and muscle bulk occurs through the course of the disease. Neurological developments include Neuronal Intranuclear Inclusions (NII), which contain both the huntingtin and ubiquitin proteins (NII have subsequently been identified in human HD patients); the onset of HD symptoms occurs between 9 and 11 weeks.
Molecular Note	A human HD fragment containing a polyglutamine-repeat expansion was isolated from a clone derived from a patient with Huntington's disease. The transgene contained approximately 1 kb of 5' UTR region, exon 1 which initially contained 142 CAG repeats, and 262 bp of intron 1. Subsequent analysis showed that the number of CAG repeats was prone to increase when inherited through the male line due to instability in the germline. A range of 141 to 157 was observed. On a background that involves C57BL/6 and CBA, transgenic mice have been observed to carry >(CAG)200 repeat expansions. The insertion site has been localized to a position on mouse chromosome 4 in an intron of predicted gene GM12695. The transgene is ubiquitously expressed.
Mutations Made By	Gillian Bates, University College London, Institute of Neurology

Disease/Phenotype

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Huntington's disease

Research Areas By Phenotype

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

Neurobiology Research
- Huntington's disease
- Ataxia (Movement) Defects
- Behavioral and Learning Defects
- Neurodegeneration
- Neuromuscular defects
Research Tools
- Neurobiology Research

Mammalian Phenotype Terms by Genotype

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

Genotype: Tg(HDexon1)62Gpb/0
involves: C57BL/6 * CBA/J

nervous system phenotype

abnormal photoreceptor inner segment morphology
- inner segment is reduced in thickness at 10 weeks of age

abnormal photoreceptor outer segment morphology
- outer segment is reduced in thickness at 10 weeks of age

abnormal retinal photoreceptor morphology
- misplaced photoreceptor nuclei are seen in the segment layers at 10 weeks of age

disorganized photoreceptor inner segment
- seen at 10 weeks of age

disorganized photoreceptor outer segment
- seen at 10 weeks of age

neuronal intranuclear inclusions
- nuclear inclusions are seen in the retina

retinal photoreceptor degeneration

vision/eye phenotype

abnormal photoreceptor inner segment morphology
- inner segment is reduced in thickness at 10 weeks of age

abnormal photoreceptor outer segment morphology
- outer segment is reduced in thickness at 10 weeks of age

abnormal retina morphology
- retinal dysplasia covers more than 50% of the entire retina

abnormal retinal outer nuclear layer morphology
- outer nuclear layer of the retina exhibits an irregular and wavy shape, disrupted with folds and whorls at 10 weeks of age

abnormal retinal outer plexiform layer morphology
- Normal - however, no inner plexiform layer or ganglion cell layer abnormalities
- misplaced photoreceptor nuclei are seen in the outer plexiform layer at 10 weeks of age

abnormal retinal photoreceptor morphology
- misplaced photoreceptor nuclei are seen in the segment layers at 10 weeks of age

disorganized photoreceptor inner segment
- seen at 10 weeks of age

disorganized photoreceptor outer segment
- seen at 10 weeks of age

retinal photoreceptor degeneration

Genotype: Tg(HDexon1)62Gpb/0
involves: C57BL/6J * CBA/J

behavior/neurological phenotype

abnormal vocalization
- 2 distinct characteristic vocalizations observed

impaired balance
- mice lose balance when sitting on hind limbs, turning and grooming their backs

limb grasping
- dyskinesia of limbs when suspended by the tail

seizures
- handling induced seizures that can be several minutes duration

stereotypic behavior
- onset of motor impairment as early as 4 weeks of age
- stereotypic repetitive stroking of the nose and face, hind limb kicking and scratching movement

tremors
- involuntary jerky shudders
- progressive resting tremor in limbs, trunk and head

growth/size/body region phenotype

decreased body weight
- body weight declines after 10 weeks

weight loss
- body weight is normal at weaning
- overall loss of muscle bulk observed
- with progression of phenotype up to 30% of body weight can be lost

homeostasis/metabolism phenotype

abnormal glucose homeostasis
- abnormal glucose homeostasis

decreased circulating insulin level
- insulin secretion in response to glucose and KCl is decreased 4-fold and 2.5-fold, respectively, by 12 weeks of age

impaired glucose tolerance
- identified at 11.5 weeks of age, insulin response absent

mortality/aging

premature death
- mice can die suddenly
- usually between 10 to 13 weeks of age

nervous system phenotype

decreased brain size
- average of 19% smaller than wildtype

seizures
- handling induced seizures that can be several minutes duration

renal/urinary system phenotype

polyuria

reproductive system phenotype

abnormal female reproductive system morphology
- smaller size ovaries and uteri often observed

female infertility

small ovary

small seminal vesicle
- small seminal ducts and gland size

small testis

small uterus

endocrine/exocrine gland phenotype

abnormal pancreatic alpha cell morphology
- islets exhibit huntingtin inclusions in 24% of cells by 12 weeks of age

abnormal pancreatic beta cell morphology
- islets are hypotrophic by 12 weeks, BrdU incorporation is reduced 6-fold
- islets are smaller in size by 12 weeks
- islets contain few insulin secretory vesicles by 12 weeks
- islets exhibit huntingtin inclusions in 19% of cells by 7 weeks of age, by week 12 frequency is greater than 95%
- significant reduction in insulin and somatostatin content by 12 weeks

abnormal pancreatic delta cell morphology
- islets exhibit huntingtin inclusions in 6% of cells by 12 weeks of age

decreased pancreatic beta cell number
- by 12 weeks, no signs of apoptosis or necrosis are observed

small ovary

small seminal vesicle
- small seminal ducts and gland size

small testis

Genotype: Tg(HDexon1)62Gpb/0
involves: C57BL/6 * CBA

growth/size/body region phenotype

decreased body weight
- progressive loss of body weight

nervous system phenotype

abnormal cerebral cortex morphology
- immunoreactive htt is detected in the cortex beginning at 3.5 weeks

abnormal neuron morphology
- striatal neurons have prominent and frequent indentations of the nuclear membrane and an apparent increase in the clustering and number of nuclear pores by 10-12 weeks of age

abnormal striatum morphology
- immunoreactive htt is detected in the striatum at 4.5 weeks

decreased brain weight
- reduction in brain weight by 5 weeks

neuronal intranuclear inclusions
- htt immunoreactive inclusions are seen in approximately 20% of neurons
- in the striatum, ultrastructural analysis of inclusions reveals a prominent, roughly circular, pale structure
- inclusions appear in the cerebral cortex before they can be detected in the striatum
- inclusions are granular with occasional filamentous structures around the periphery; they are larger than the nucleolus and occupy 1% of nuclear volume
- inclusions are observed within neurons of cerebral cortex, striatum, cerebellum, spinal cord and to a much lesser degree in the hippocampus, thalamus, globus pallidus and substantia nigra
- inclusions are ubiquitinated by 5-6 weeks and can be detected by ultrastructural analysis by 8 weeks

Genotype: Tg(HDexon1)62Gpb/0
involves: C57BL/6 * C57BL/6JOlaHsd * CBA * CBA/CaOlaHsd

behavior/neurological phenotype

decreased grip strength

impaired coordination

nervous system phenotype

decreased brain weight

References

Mangiarini L; Sathasivam K; Seller M; Cozens B; Harper A; Hetherington C; Lawton M; Trottier Y; Lehrach H; Davies SW; Bates GP. 1996. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell 87(3):493-506PubMed: 8898202 MGI: J:36689

Additional - Tg(HDexon1)62Gpb related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Laragen
- Genotyping resources and troubleshooting
Breeding Considerations

For R6/2 transgenic mice, the CAG repeat number is subject to germline/somatic instability and may expand/contract. For additional information, see "General Information for R6/2 transgenic mouse lines" in our Detailed Description section.

When maintaining our live Stock No. 027425 colony, hemizygous males are mated to multiple DBA/2J inbred females (Stock No. 000671). Alternatively, the strain may need to be maintained by breeding ovarian transplant hemizygous females with DBA/2J males (i.e., B6D2F1/J females (Stock No. 100006) transplanted with hemizygous ovaries x DBA/2J males).

In addition, R6/2 transgenic mice may exhibit higher incidence of CAG repeat expansion when the transgene is transmitted via paternal inheritance (similar to what is observed in humans).

Stock No. 027425: The DBA/2J-congenic R6/2 transgenic mouse line with ~350 CAG repeat expansions, called D2.R6/2 (CAG ~350) mice, are not fully characterized to date (April 2014).
However, they may exhibit a similar or delayed phenotype compared to that of R6/2 mice with ~160 CAG repeats on a (C57BL/6 x CBA)F1 genetic background. Those B6CBA.R6/2 (CAG 160) transgenic mice are described and available as Stock No. 002810. Briefly, B6CBA.R6/2 (CAG 160) mice exhibit a progressive neurological phenotype that mimics many of the features of HD (see strain description for more information). Hemizygous mice have shortened lifespan (median survival may be ~20 weeks or less) with females living slightly longer. Hemizygous females are not fertile. Hemizygous males have a short (3-4 week) breeding window, and only about half are fertile.
- Additional Breeding and Husbandry Support
Mating System
- Inbred x Hemizygote
- DBA/2J (000671) x hemizygot
Citation
When using the D2.R6/2 ; D2.R6/2 (CAG ~350) ; R62.280(CHDI-005-7) ; CHDI-81001008 mouse strain in a publication, please cite the originating article(s) and include JAX stock #027425 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
	Hemizygous or non carrier for Tg(HDexon1)62Gpb

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Frozen Mouse Embryo	D2.Cg-Tg(HDexon1)62Gpb/280ChdiJ	$2595.00
Frozen Mouse Embryo	D2.Cg-Tg(HDexon1)62Gpb/280ChdiJ	$2595.00
Frozen Mouse Embryo	D2.Cg-Tg(HDexon1)62Gpb/280ChdiJ	$3373.50
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Also Known As:D2.R6/2 ; D2.R6/2 (CAG ~350) ; R62.280(CHDI-005-7) ; CHDI-81001008

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Expression Data

Control Suggestions

Approximate Controls

Additional Information

Selected References

Tg(HDexon1)62Gpb

Allele Symbol: Tg(HDexon1)62Gpb

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Tg(HDexon1)62Gpb/0involves: C57BL/6 * CBA/J

nervous system phenotype

vision/eye phenotype

Genotype: Tg(HDexon1)62Gpb/0involves: C57BL/6J * CBA/J

behavior/neurological phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

mortality/aging

nervous system phenotype

renal/urinary system phenotype

reproductive system phenotype

endocrine/exocrine gland phenotype

Genotype: Tg(HDexon1)62Gpb/0involves: C57BL/6 * CBA

growth/size/body region phenotype

nervous system phenotype

Genotype: Tg(HDexon1)62Gpb/0involves: C57BL/6 * C57BL/6JOlaHsd * CBA * CBA/CaOlaHsd

behavior/neurological phenotype

nervous system phenotype

References

Additional - Tg(HDexon1)62Gpb related

Genotyping Protocols

Breeding Considerations

Mating System

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

Genotype: Tg(HDexon1)62Gpb/0
involves: C57BL/6 * CBA/J

Genotype: Tg(HDexon1)62Gpb/0
involves: C57BL/6J * CBA/J

Genotype: Tg(HDexon1)62Gpb/0
involves: C57BL/6 * CBA

Genotype: Tg(HDexon1)62Gpb/0
involves: C57BL/6 * C57BL/6JOlaHsd * CBA * CBA/CaOlaHsd