Overview

This strain is discontinued, please refer to strains:
002810 B6CBA-Tg(HDexon1)62Gpb/1J
006494 B6CBA-Tg(HDexon1)62Gpb/3J

Donating Investigator

Gillian P Bates, University College London, Institute of Neurology

Genetic overview

Genetic Background	Generation

Tg(HDexon1)62Gpb

Allele Type
Transgenic (Inserted expressed sequence, Humanized sequence)

View Genetics

Research Applications

View All Research Applications

Details

Detailed Description

This line is transgenic for the 5' end of the human HD gene carrying >(CAG)200 repeat expansions. The CAG repeat is unstable on transmission with a tendency to increase when inherited through the male line. The transgene is ubiquitously expressed. 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. However, the use of appropriate functional tests indicates 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 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. Commonly known as the "R6/2" strain.

Expression Data

Expressed Gene	HTT, huntingtin, human
Site of Expression

Control Suggestions

Noncarrier

Approximate Controls

100011 B6CBAF1/J

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
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:

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
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 References

Bogdanov MB; Andreassen OA; Dedeoglu A; Ferrante RJ; Beal MF. 2001. Increased oxidative damage to DNA in a transgenic mouse model of Huntington's disease. J Neurochem 79(6):1246-9PubMed: 11752065 MGI: J:73480
Davies SW; Turmaine M; Cozens BA; DiFiglia M; Sharp AH; Ross CA ; Scherzinger E ; Wanker EE ; Mangiarini L ; Bates GP. 1997. Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation. Cell 90(3):537-48PubMed: 9267033 MGI: J:42085
Dedeoglu A; Kubilus JK; Jeitner TM; Matson SA; Bogdanov M; Kowall NW; Matson WR; Cooper AJ; Ratan RR; Beal MF; Hersch SM; Ferrante RJ. 2002. Therapeutic effects of cystamine in a murine model of Huntington's disease. J Neurosci 22(20):8942-50PubMed: 12388601 MGI: J:79781
Dedeoglu A; Kubilus JK; Yang L; Ferrante KL; Hersch SM; Beal MF; Ferrante RJ. 2003. Creatine therapy provides neuroprotection after onset of clinical symptoms in Huntington's disease transgenic mice. J Neurochem 85(6):1359-67PubMed: 12787055 MGI: J:83796
Fain JN; Del Mar NA; Meade CA; Reiner A; Goldowitz D. 2001. Abnormalities in the functioning of adipocytes from R6/2 mice that are transgenic for the Huntington's disease mutation. Hum Mol Genet 10(2):145-52PubMed: 11152662 MGI: J:67073
Ferrante RJ; Kubilus JK; Lee J; Ryu H; Beesen A; Zucker B; Smith K; Kowall NW; Ratan RR; Luthi-Carter R; Hersch SM. 2003. Histone deacetylase inhibition by sodium butyrate chemotherapy ameliorates the neurodegenerative phenotype in Huntington's disease mice. J Neurosci 23(28):9418-27PubMed: 14561870 MGI: J:88202
Hay DG; Sathasivam K; Tobaben S; Stahl B; Marber M; Mestril R; Mahal A; Smith DL; Woodman B; Bates GP. 2004. Progressive decrease in chaperone protein levels in a mouse model of Huntington's disease and induction of stress proteins as a therapeutic approach. Hum Mol Genet 13(13):1389-405PubMed: 15115766 MGI: J:91194
Helmlinger D; Yvert G; Picaud S; Merienne K; Sahel J; Mandel JL; Devys D. 2002. Progressive retinal degeneration and dysfunction in R6 Huntington's disease mice. Hum Mol Genet 11(26):3351-9PubMed: 12471061 MGI: J:80810
Karpuj MV; Becher MW; Springer JE; Chabas D; Youssef S; Pedotti R; Mitchell D; Steinman L. 2002. Prolonged survival and decreased abnormal movements in transgenic model of Huntington disease, with administration of the transglutaminase inhibitor cystamine. Nat Med 8(2):143-9PubMed: 11821898 MGI: J:74541
Li H; Li SH; Yu ZX; Shelbourne P; Li XJ. 2001. Huntingtin aggregate-associated axonal degeneration is an early pathological event in Huntington's disease mice. J Neurosci 21(21):8473-81PubMed: 11606636 MGI: J:72357
Lievens JC; Woodman B; Mahal A; Spasic-Boscovic O; Samuel D; Kerkerian-Le Goff L; Bates GP. 2001. Impaired glutamate uptake in the r6 huntington's disease transgenic mice. Neurobiol Dis 8(5):807-21PubMed: 11592850 MGI: J:72696
Luthi-Carter R; Hanson SA; Strand AD; Bergstrom DA; Chun W; Peters NL; Woods AM; Chan EY; Kooperberg C; Krainc D; Young AB; Tapscott SJ; Olson JM. 2002. Dysregulation of gene expression in the R6/2 model of polyglutamine disease: parallel changes in muscle and brain. Hum Mol Genet 11(17):1911-26PubMed: 12165554 MGI: J:78591
Luthi-Carter R; Strand A; Peters NL; Solano SM; Hollingsworth ZR; Menon AS; Frey AS; Spektor BS; Penney EB; Schilling G; Ross CA; Borchelt DR; Tapscott SJ; Young AB; Cha JH; Olson JM. 2000. Decreased expression of striatal signaling genes in a mouse model of Huntington's disease. Hum Mol Genet 9(9):1259-71PubMed: 10814708 MGI: J:62544
Meade CA; Deng YP; Fusco FR; Del Mar N; Hersch S; Goldowitz D; Reiner A. 2002. Cellular localization and development of neuronal intranuclear inclusions in striatal and cortical neurons in R6/2 transgenic mice. J Comp Neurol 449(3):241-69PubMed: 12115678 MGI: J:77468
Menalled L; Zanjani H; MacKenzie L; Koppel A; Carpenter E; Zeitlin S; Chesselet MF. 2000. Decrease in striatal enkephalin mRNA in mouse models of Huntington's disease. Exp Neurol 162(2):328-42PubMed: 10739639 MGI: J:61687
Mihm MJ; Amann DM; Schanbacher BL; Altschuld RA; Bauer JA; Hoyt KR. 2007. Cardiac dysfunction in the R6/2 mousse model of Huntington's disease Neurobiol Dis 25(2):297-308PubMed: 17126554 MGI: J:116660
Rebec GV; Barton SJ; Ennis MD. 2002. Dysregulation of ascorbate release in the striatum of behaving mice expressing the Huntington's disease gene. J Neurosci 22(2):RC202PubMed: 11784814 MGI: J:79994
Yu ZX; Li SH; Evans J; Pillarisetti A; Li H; Li XJ. 2003. Mutant huntingtin causes context-dependent neurodegeneration in mice with Huntington's disease. J Neurosci 23(6):2193-202PubMed: 12657678 MGI: J:82676
Zhang Y; Ona VO; Li M; Drozda M; Dubois-Dauphin M; Przedborski S; Ferrante RJ; Friedlander RM. 2003. Sequential activation of individual caspases, and of alterations in Bcl-2 proapoptotic signals in a mouse model of Huntington's disease. J Neurochem 87(5):1184-92PubMed: 14622098 MGI: J:86809

Additional - Tg(HDexon1)62Gpb related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:TG(HDexon1), TG(YAC)
- Standard PCR:Tg(HDexon1)62Gpb
- Genotyping resources and troubleshooting
Mating System
- F1 x Hemizygote

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General Terms and Conditions

Questions about Terms of Use

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Licensing Information

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Donating Investigator

Genetic overview

Research Applications

Detailed Description

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/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

Mating System

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
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