Overview

JAXTag™

Also Known As:B6CBA-R6/2 (CAG 120 +/- 5)

These transgenic mice display a progressive neurological phenotype that mimics many of the features of Huntington Disease (HD) in humans, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. Frequent urination and loss of body weight and muscle bulk occurs through the course of the disease. Neurological developments include Neuronal Intranuclear Inclusions, which contain both the huntingtin and ubiquitin proteins. This line is transgenic for the 5' end of the human HD gene carrying approximately 120 +/- 5 (CAG)repeat expansions.

Donating Investigator

Gillian P Bates, University College London, Institute of Neurology

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2018-07-27 00:00:00)

Tg(HDexon1)62Gpb

Allele Type
Transgenic (Inserted expressed sequence, Humanized sequence)

View Genetics

Research Applications

Diabetes and Obesity Research
Cardiovascular Research

View All Research Applications

Base Price

Starting at:

$329.53 Domestic price for male 3-week

437.13 Domestic price for breeder pair

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Details

Important Note

January 2007: alteration in strain name and phenotype. Please see Strain Development for additional information.

Detailed Description

This line is transgenic for the 5' end of the human HD gene carrying approximately 120 +/- 5 (CAG) repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including 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. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 9 and 11 weeks. Commonly known as the "R6/2" strain.

Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cells develop huntingtin inclusions as early as 7 weeks of age, by 12 weeks more than 95% of beta cells have inclusions. Pancreatic alpha and delta cells also exhibit some inclusions (24% and 6% of cells, respectively) by 12 weeks. Pancreatic islets become hypotonic and beta cells are dramatically reduced in number by 12 weeks. Beta cells contain very few insulin secretory vesicles. (Bjorkquvist M., et al. 2005)

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).

This strain ships with a JAXTag^TM affixed. Learn more about JAXTag^TM.

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.

Development

The transgene is about 1 kb of the human HD gene and includes the promoter region, exon 1 with 120 +/- 5 CAG repeats. This strain was identified as the R6-2 line in the original publication.

In fall 2006, the B6CBA-Tg(HDexon1)62Gpb/1J colony was shown to have a reduction in the number of CAG repeat units in the transgene (approximately 100-105 CAG repeats), and to exhibit a concomitant decrease in severity and delayed onset in the expected neurological phenotype. The Repository recovered frozen embryos from the HDexon1 line during the winter of 2006/7. The cryo-recovered line has approximately 160 +/- 10 CAG repeats, and onset of HD symptoms occurs between 9 and 11 weeks of age, as originally reported for this strain.

The cryo-recovered line continues as B6CBA-Tg(HDexon1)62Gpb/1J (Stock No. 002810). The phenotypically changed line formerly distributed as Stock No. 002810 is now named B6CBA-Tg(HDexon1)62Gpb/3J (Stock No. 006494) and is maintained with a CAG repeat of 120 +/- 5 repeat units.

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

Additional Information

Considerations for Choosing Controls

Selected References

Cummings DM; Alaghband Y; Hickey MA; Joshi PR; Hong SC; Zhu C; Ando TK; Andre VM; Cepeda C; Watson JB; Levine MS. 2012. A critical window of CAG repeat-length correlates with phenotype severity in the R6/2 mouse model of Huntington's disease. J Neurophysiol 107(2):677-91PubMed: 22072510 MGI: J:229736
Grima JC; Daigle JG; Arbez N; Cunningham KC; Zhang K; Ochaba J; Geater C; Morozko E; Stocksdale J; Glatzer JC; Pham JT; Ahmed I; Peng Q; Wadhwa H; Pletnikova O; Troncoso JC; Duan W; Snyder SH; Ranum LP; Thompson LM; Lloyd TE; Ross CA; Rothstein JD. 2017. Mutant Huntingtin Disrupts the Nuclear Pore Complex. Neuron 94(1):93-107.e6PubMed: 28384479 MGI: J:240166
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
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):319-36PubMed: 19464370 MGI: J:185262

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:

Diabetes and Obesity Research
- Type 2 Diabetes (NIDDM)
  - adult onset
- Hypoinsulinemia
  - adult onset
- Hyperglycemia
  - adult onset
Cardiovascular 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
B6.Cg-Tg(HDexon1)62Gpb/240

behavior/neurological phenotype

abnormal gait
- narrower base (separation between legs) than controls

decreased grip strength
- progressive deterioration of grip strength especially in males at 14 weeks of age

decreased startle reflex
- observed at 6 and 14 weeks of age in both genders

decreased vertical activity
- mice rear less in the center of the open field test than controls starting at 12 weeks of age in the light phase
- rearing is similar to controls in dark phase

hypoactivity
- in dark phase, hypoactivity is significant at 6 weeks of age in both genders
- mice cover less distance in center starting at 12 weeks in light phase and 6 weeks in dark phase
- mice cover less total distance in light phase of open field test starting at 6 weeks of age in females and 8 weeks of age in males

impaired coordination
- mice exhibit a progressive impairment on the rotarod test beginning at 8 weeks of age

increased anxiety-related response
- increased preference for dark in dark/light choice test at 14 weeks of age

short stride length
- shorter splay length (contralateral) than controls at 14 weeks of age
- stride length (ipsilateral) is similar to controls

growth/size/body region phenotype

decreased body weight
- body weight decreases by 10 weeks of age in females and 9 weeks in males

mortality/aging

premature death
- all mice die within 9 weeks of the first death
- median survival of 141 days for females and 179 days for males

nervous system phenotype

decreased prepulse inhibition
- observed at 14 weeks of age, especially in females

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

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

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
B6CBA-Tg(HDexon1)62Gpb/3J

behavior/neurological phenotype

abnormal gait
- wider base (separation between legs) than controls; females exhibit difference earlier than males

decreased grip strength
- progressive deterioration of grip strength especially in males between 10-14 weeks of age

decreased startle reflex
- beginning at 4 weeks of age

decreased vertical activity
- mice exhibit a progressive decrease in climbing activity starting at 4 weeks of age
- mice rear less in the center of the open field test than controls at all ages in the light phase and by 6 weeks of age in the dark phase

hypoactivity
- in the dark phase both sexes are hypoactive beginning at 12 weeks of age
- in the light phase females are less active at 8 and 14 weeks of age
- in the light phase males are less active starting at 6 weeks of age
- mice are hypoactive in the open field test in both the light and dark phases of the light cycle
- progressive hypoactivity is observed in the center of the open field beginning at 4 weeks of age

impaired coordination
- latency time decreases with age
- mice exhibit a reduced latency to fall on rotarod test beginning at 4 weeks of age as compared to wild-type

increased anxiety-related response
- increased preference for dark in dark/light choice test at 12 and 14 weeks of age

short stride length
- decreased stride length (ipsilateral) observed at 8 weeks of age
- shorter splay length (contralateral) than controls

growth/size/body region phenotype

decreased body weight
- decrease in body weight is observed by 7 weeks in both genders

mortality/aging

premature death
- all mice die within 12 weeks of the first death
- median survival of 113 days

nervous system phenotype

decreased prepulse inhibition
- observed after 8 weeks of age

References

Cummings DM; Alaghband Y; Hickey MA; Joshi PR; Hong SC; Zhu C; Ando TK; Andre VM; Cepeda C; Watson JB; Levine MS. 2012. A critical window of CAG repeat-length correlates with phenotype severity in the R6/2 mouse model of Huntington's disease. J Neurophysiol 107(2):677-91PubMed: 22072510 MGI: J:229736
Grima JC; Daigle JG; Arbez N; Cunningham KC; Zhang K; Ochaba J; Geater C; Morozko E; Stocksdale J; Glatzer JC; Pham JT; Ahmed I; Peng Q; Wadhwa H; Pletnikova O; Troncoso JC; Duan W; Snyder SH; Ranum LP; Thompson LM; Lloyd TE; Ross CA; Rothstein JD. 2017. Mutant Huntingtin Disrupts the Nuclear Pore Complex. Neuron 94(1):93-107.e6PubMed: 28384479 MGI: J:240166
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
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):319-36PubMed: 19464370 MGI: J:185262

Additional References

Dargaei Z; Liang X; Serranilla M; Santos J; Woodin MA. 2019. Alterations in Hippocampal Inhibitory Synaptic Transmission in the R6/2 Mouse Model of Huntington's Disease. Neuroscience 404:130-140PubMed: 30797895 MGI: J:276159
Joshi AU; Minhas PS; Liddelow SA; Haileselassie B; Andreasson KI; Dorn GW 2nd; Mochly-Rosen D. 2019. Fragmented mitochondria released from microglia trigger A1 astrocytic response and propagate inflammatory neurodegeneration. Nat Neurosci 22(10):1635-1648PubMed: 31551592 MGI: J:281497
Lin MS; Liao PY; Chen HM; Chang CP; Chen SK; Chern Y. 2019. Degeneration of ipRGCs in Mouse Models of Huntington's Disease Disrupts Non-Image-Forming Behaviors Before Motor Impairment. J Neurosci 39(8):1505-1524PubMed: 30587542 MGI: J:271675

Additional - Tg(HDexon1)62Gpb related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Laragen
- Standard PCR:Laragen
- Standard PCR:Laragen
- Standard PCR:TG(HDexon1), TG(YAC)
- Probe:Tg(HDexon1)62Gpb-EP3
- Standard PCR:Tg(HDexon1)62Gpb CAG Sizing
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is a good breeder.

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.

Hemizygous females are not fertile. Hemizygous males have a 3-4 week breeding window so mating scheme should be via multiple females. Also, only about half of the male hemizygotes are fertile. The breeding scheme was: B6CBAF1 females X hemizygous HD62 males, preferably a trio (2 B6CBAF1 females and one hemizygous male). Strain is now maintained by ovarian transplant hemizygote females x B6CBAF1/J males. Both mating schemes are available to the customer, but OT hemi female x B6CBAF1/J is recommended mating scheme. The expected coat color from breeding is Black, Agouti.
- Additional Breeding and Husbandry Support
Appearance
- black
  Related Genotype: a/a
  
  agouti, ataxic, tremors
  Related Genotype: A/? HTT/-
  
  agouti
  Related Genotype: A/?
  
  black, ataxic,tremors
  Related Genotype: a/a HTT/-
Citation
When using the B6CBA-R6/2 (CAG 120 +/- 5) mouse strain in a publication, please cite the originating article(s) and include JAX stock #006494 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

MP13 (Maximum)

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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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Also Known As:B6CBA-R6/2 (CAG 120 +/- 5)

Donating Investigator

Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Development

Expression Data

Control Suggestions

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/0B6.Cg-Tg(HDexon1)62Gpb/240

behavior/neurological phenotype

growth/size/body region phenotype

mortality/aging

nervous system phenotype

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

behavior/neurological phenotype

nervous system 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/0B6CBA-Tg(HDexon1)62Gpb/3J

behavior/neurological phenotype

growth/size/body region phenotype

mortality/aging

nervous system phenotype

References

Additional References

Additional - Tg(HDexon1)62Gpb related

Genotyping Protocols

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Breeder Pair

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

Genotype: Tg(HDexon1)62Gpb/0
B6.Cg-Tg(HDexon1)62Gpb/240

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

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

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

Genotype: Tg(HDexon1)62Gpb/0
B6CBA-Tg(HDexon1)62Gpb/3J