Description

Strain Information

Type Congenic; Mutant Strain; Transgenic; Additional information on Genetically Engineered Mutant Mice. Mating System Noncarrier x Hemizygote         (Female x Male) Species laboratory mouse Generation N26+ (21-JUL-08)   Donating Investigator Gillian Bates,   United Medical and Dental Schools

Description
Mice have been generated that are transgenic for the 5' end of the human HD gene carrying approximately 100 CAG repeat expansions. In this founder line (61Gpb), 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. These NII have also been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 15 and 21 weeks for this 61Gpb line. On the BALB/cByJ genetic background, the CAG tract remains somatically stable throughout the life span of the mouse but may contract over generations (even with male transmission). These HDexon1 mice may be useful in Huntington's Disease research.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. Mice with this mutation were originally published on a mixed CBA x C57BL6 genetic background. It should be noted that the phenotype could vary from that originally described. We will modify the strain description as published results become available.

Development
This 1.9 kb transgene was isolated from a phage genomic clone derived from an Huntington's Disease (HD) patient and contained the 5' end of the human huntingtin (Huntington disease) gene. It was composed of approximately 1 kb of 5' UTR sequences, exon 1 (carrying expanded CAG repeats of varying size but of the order of 130 units) and the first 262 bp of intron 1. This construct was microinjected into single cell CBAxC57BL/6 embryos. Male founder R6 was bred to CBA x C57BL/6 females, producing several founder lines. Mice from founder line R6/1 have the transgene integrated as a single intact copy and were originally found to have 116 CAG repeats. At some point, these mice were backcrossed to BALB/cBy mice for at least 25 generations by Dr. Anne Messer at the Wadsworth Center (Univ. of Albany). As of 2007, the donating investigator reports that these mice carry approximately 100 CAG repeats.

Control Information

	Control
	Noncarrier
	001026 BALB/cByJ
Considerations for Choosing Controls

Related Strains

Strains carrying   Tg(HDexon1)61Gpb allele

006471	B6.Cg-Tg(HDexon1)61Gpb/J
002809	B6CBA-Tg(HDexon1)61Gpb/1J

View Strains carrying   Tg(HDexon1)61Gpb     (2 strains)

Strains carrying other alleles of HTT

004360	B6;SJL-Tg(HD)63Aron/J
003627	B6C3-Tg(HD82Gln)81Dbo/J
002810	B6CBA-Tg(HDexon1)62Gpb/1J
006494	B6CBA-Tg(HDexon1)62Gpb/3J
004938	FVB-Tg(YAC128)53Hay/J
008197	FVB/N-Tg(HTT*97Q)IXwy/J
007247	FVB/N-Tg(YAC353G6)W7Hay/J
003640	FVB/NJ-Tg(YAC72)2511Hay/J

View Strains carrying other alleles of HTT     (8 strains)

Additional Web Information

Congenic Nomenclature
Visit the Alzheimer's Disease Mouse Model Resource site for helpful information on Alzheimer's Disease and research resources.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms

Huntington Disease; HD -

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

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

Tg(HDexon1)61Gpb/0

        involves: C57BL/6 * CBA/J * SJL

• vision/eye phenotype
• abnormal eye morphology (MGI Ref ID J:80810)

Tg(HDexon1)61Gpb/?

        involves: C57BL/6 * CBA

• nervous system phenotype
• abnormal neuron morphology (MGI Ref ID J:42085)
  • striatal neurons have prominent and frequent indentations of the nuclear membrane and an apparent increase in the clustering and number of nuclear pores
• neuronal intranuclear inclusions (MGI Ref ID J:42085)
  • 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
  • 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 are granular with occasional filamentous structures around the periphery; they are larger than the nucleolus and occupy 1% of nuclear volume
• abnormal striatum morphology (MGI Ref ID J:42085)
• behavior/neurological phenotype
• abnormal long-term spatial reference memory (MGI Ref ID J:130936)
  • in the last of a series of Barnes circular maze trials, the time required to locate the escape tunnel is increased in 12 week old transgenic mice as compared to wildtype
  • 12 week old transgenic mice raised in an enriched environment perform as well as non-enriched wildtype in circular maze trials
  • transgenic mice use both serial and spatial search strategies in the ultimate trials of the circular maze as compared to wildtype and enriched transgenic mice, which primarily use spatial search strategies
• abnormal short-term spatial reference memory (MGI Ref ID J:130936)
  • beginning at 12 weeks of age, transgenic mice exhibit a deficit in short term memory as evaluated by performance in the Y-maze
• abnormal spatial learning (MGI Ref ID J:130936)
  • in the last of a series of Barnes circular maze trials, the time required to locate the escape tunnel is increased in 12 week old transgenic mice as compred to wildtype
  • 12 week old transgenic mice raised in an enriched environment perform as well as non-enriched wildtype in circular maze trials
• decreased exploration in new environment (MGI Ref ID J:130936)
  • impaired performance in location recognition test is observed by 14 weeks of age
• impaired coordination (MGI Ref ID J:130936)
  • between 8-12 weeks of age, transgenic mice perform on the rotarod as well as wildtype, however, by 14 weeks performance decreases and by 20 weeks performance is significantly impaired

View Research Applications

Research Applications

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

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

Neurobiology Research
Huntington's disease

Research Tools
Neurobiology Research

HTT related

Developmental Biology Research
Neurodevelopmental Defects

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

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

Genes & Alleles

Gene & Allele Information

Allele Symbol		Tg(HDexon1)61Gpb
Allele Name		transgene insertion 61, Gillian Bates
Allele Type		Transgenic (random, expressed)
Common Name(s)		HD R6/1; R6/1; httm;
Mutation Made By		Gillian Bates,   United Medical and Dental Schools
Strain of Origin		CBA x C57BL/6
Expressed Gene		HTT, huntingtin, human
Promoter		HTT, huntingtin, human
General Note		The transgene is ubiquitously expressed. 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 andloss 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). Onset of HD symptoms occurs between 15 and 21 weeks of age.
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 113 CAG repeats, and262 bp of intron 1 followed by a neomycin cassette. Subsequent analysis showed that the number of CAG repeats was prone to increase due to instability in the germline, and a range of 109.5 to 121 was observed. [MGI Ref ID J:36689]

Genotyping

Genotyping Information

Genotyping Protocols

TG(HDexon1), TG(YAC), STD PCR, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

Selected Reference(s)

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):493-506. [PubMed: 8898202]  [MGI Ref ID J:36689]

Additional References

Tg(HDexon1)61Gpb related

Bolivar VJ; Manley K; Messer A. 2004. Early exploratory behavior abnormalities in R6/1 Huntington's disease transgenic mice. Brain Res 1005(1-2):29-35. [PubMed: 15044061]  [MGI Ref ID J:89279]

Canals JM; Pineda JR; Torres-Peraza JF; Bosch M; Martin-Ibanez R; Munoz MT; Mengod G; Ernfors P; Alberch J. 2004. Brain-derived neurotrophic factor regulates the onset and severity of motor dysfunction associated with enkephalinergic neuronal degeneration in Huntington's disease. J Neurosci 24(35):7727-39. [PubMed: 15342740]  [MGI Ref ID J:92634]

Cha JH; Frey AS; Alsdorf SA; Kerner JA; Kosinski CM; Mangiarini L; Penney JB Jr; Davies SW; Bates GP; Young AB. 1999. Altered neurotransmitter receptor expression in transgenic mouse models of Huntington's disease. Philos Trans R Soc Lond B Biol Sci 354(1386):981-9. [PubMed: 10434296]  [MGI Ref ID J:56820]

Cummings DM; Milnerwood AJ; Dallerac GM; Waights V; Brown JY; Vatsavayai SC; Hirst MC; Murphy KP. 2006. Aberrant cortical synaptic plasticity and dopaminergic dysfunction in a mouse model of Huntington's disease. Hum Mol Genet 15(19):2856-68. [PubMed: 16905556]  [MGI Ref ID J:114924]

Cybulska-Klosowicz A; Mazarakis NK; Van Dellen A; Blakemore C; Hannan AJ; Kossut M. 2004. Impaired learning-dependent cortical plasticity in Huntington's disease transgenic mice. Neurobiol Dis 17(3):427-34. [PubMed: 15571978]  [MGI Ref ID J:94576]

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):537-48. [PubMed: 9267033]  [MGI Ref ID J:42085]

Desplats PA; Denny CA; Kass KE; Gilmartin T; Head SR; Sutcliffe JG; Seyfried TN; Thomas EA. 2007. Glycolipid and ganglioside metabolism imbalances in Huntington's disease. Neurobiol Dis 27(3):265-77. [PubMed: 17600724]  [MGI Ref ID J:134905]

Desplats PA; Kass KE; Gilmartin T; Stanwood GD; Woodward EL; Head SR; Sutcliffe JG; Thomas EA. 2006. Selective deficits in the expression of striatal-enriched mRNAs in Huntington's disease. J Neurochem 96(3):743-57. [PubMed: 16405510]  [MGI Ref ID J:108002]

Desplats PA; Lambert JR; Thomas EA. 2008. Functional roles for the striatal-enriched transcription factor, Bcl11b, in the control of striatal gene expression and transcriptional dysregulation in Huntington's disease. Neurobiol Dis 31(3):298-308. [PubMed: 18595722]  [MGI Ref ID J:138707]

Gharami K; Xie Y; An JJ; Tonegawa S; Xu B. 2008. Brain-derived neurotrophic factor over-expression in the forebrain ameliorates Huntington's disease phenotypes in mice. J Neurochem 105(2):369-79. [PubMed: 18086127]  [MGI Ref ID J:135260]

Gines S; Bosch M; Marco S; Gavalda N; Diaz-Hernandez M; Lucas JJ; Canals JM; Alberch J. 2006. Reduced expression of the TrkB receptor in Huntington's disease mouse models and in human brain. Eur J Neurosci 23(3):649-58. [PubMed: 16487146]  [MGI Ref ID J:107146]

Gomez GT; Hu H; McCaw EA; Denovan-Wright EM. 2006. Brain-specific factors in combination with mutant huntingtin induce gene-specific transcriptional dysregulation. Mol Cell Neurosci 31(4):661-75. [PubMed: 16446101]  [MGI Ref ID J:108616]

Gonitel R; Moffitt H; Sathasivam K; Woodman B; Detloff PJ; Faull RL; Bates GP. 2008. DNA instability in postmitotic neurons. Proc Natl Acad Sci U S A 105(9):3467-72. [PubMed: 18299573]  [MGI Ref ID J:132766]

Hansson O; Castilho RF; Korhonen L; Lindholm D; Bates GP; Brundin P. 2001. Partial resistance to malonate-induced striatal cell death in transgenic mouse models of Huntington's disease is dependent on age and CAG repeat length. J Neurochem 78(4):694-703. [PubMed: 11520890]  [MGI Ref ID J:71210]

Hansson O; Guatteo E; Mercuri NB; Bernardi G; Li XJ; Castilho RF; Brundin P. 2001. Resistance to NMDA toxicity correlates with appearance of nuclear inclusions, behavioural deficits and changes in calcium homeostasis in mice transgenic for exon 1 of the huntington gene. Eur J Neurosci 14(9):1492-504. [PubMed: 11722611]  [MGI Ref ID J:128170]

Helmlinger D; Abou-Sleymane G; Yvert G; Rousseau S; Weber C; Trottier Y; Mandel JL; Devys D. 2004. Disease progression despite early loss of polyglutamine protein expression in SCA7 mouse model. J Neurosci 24(8):1881-7. [PubMed: 14985428]  [MGI Ref ID J:90121]

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):3351-9. [PubMed: 12471061]  [MGI Ref ID J:80810]

Kovtun IV; Liu Y; Bjoras M; Klungland A; Wilson SH; McMurray CT. 2007. OGG1 initiates age-dependent CAG trinucleotide expansion in somatic cells. Nature 447(7143):447-52. [PubMed: 17450122]  [MGI Ref ID J:122765]

Kovtun IV; Thornhill AR; McMurray CT. 2004. Somatic deletion events occur during early embryonic development and modify the extent of CAG expansion in subsequent generations. Hum Mol Genet 13(24):3057-68. [PubMed: 15496421]  [MGI Ref ID J:94584]

Lazic SE; Goodman AO; Grote HE; Blakemore C; Morton AJ; Hannan AJ; van Dellen A; Barker RA. 2007. Olfactory abnormalities in Huntington's disease: decreased plasticity in the primary olfactory cortex of R6/1 transgenic mice and reduced olfactory discrimination in patients. Brain Res 1151:219-26. [PubMed: 17400200]  [MGI Ref ID J:122504]

Lazic SE; Grote H; Armstrong RJ; Blakemore C; Hannan AJ; van Dellen A; Barker RA. 2004. Decreased hippocampal cell proliferation in R6/1 Huntington's mice. Neuroreport 15(5):811-3. [PubMed: 15073520]  [MGI Ref ID J:89967]

Lazic SE; Grote HE; Blakemore C; Hannan AJ; van Dellen A; Phillips W; Barker RA. 2006. Neurogenesis in the R6/1 transgenic mouse model of Huntington's disease: effects of environmental enrichment. Eur J Neurosci 23(7):1829-38. [PubMed: 16623840]  [MGI Ref ID J:108068]

Li H; Wyman T; Yu ZX; Li SH; Li XJ. 2003. Abnormal association of mutant huntingtin with synaptic vesicles inhibits glutamate release. Hum Mol Genet 12(16):2021-30. [PubMed: 12913073]  [MGI Ref ID J:85070]

Mangiarini L; Sathasivam K; Mahal A; Mott R; Seller M; Bates GP. 1997. Instability of highly expanded CAG repeats in mice transgenic for the Huntington's disease mutation. Nat Genet 15(2):197-200. [PubMed: 9020849]  [MGI Ref ID J:79042]

Manley K; Pugh J; Messer A. 1999. Instability of the CAG repeat in immortalized fibroblast cell cultures from Huntington's disease transgenic mice. Brain Res 835(1):74-9. [PubMed: 10448198]  [MGI Ref ID J:56438]

Manley K; Shirley TL; Flaherty L; Messer A. 1999. Msh2 deficiency prevents in vivo somatic instability of the CAG repeat in Huntington disease transgenic mice. Nat Genet 23(4):471-3. [PubMed: 10581038]  [MGI Ref ID J:58797]

Mastroberardino PG; Iannicola C; Nardacci R; Bernassola F; De Laurenzi V; Melino G; Moreno S; Pavone F; Oliverio S; Fesus L; Piacentini M. 2002. 'Tissue' transglutaminase ablation reduces neuronal death and prolongs survival in a mouse model of Huntington's disease. Cell Death Differ 9(9):873-80. [PubMed: 12181738]  [MGI Ref ID J:115545]

Mazarakis NK; Cybulska-Klosowicz A; Grote H; Pang T; Van Dellen A; Kossut M; Blakemore C; Hannan AJ. 2005. Deficits in experience-dependent cortical plasticity and sensory-discrimination learning in presymptomatic Huntington's disease mice. J Neurosci 25(12):3059-66. [PubMed: 15788762]  [MGI Ref ID J:98640]

McCaw EA; Hu H; Gomez GT; Hebb AL; Kelly ME; Denovan-Wright EM. 2004. Structure, expression and regulation of the cannabinoid receptor gene (CB1) in Huntington's disease transgenic mice. Eur J Biochem 271(23-24):4909-20. [PubMed: 15606779]  [MGI Ref ID J:98030]

Miller TW; Zhou C; Gines S; MacDonald ME; Mazarakis ND; Bates GP; Huston JS; Messer A. 2005. A human single-chain Fv intrabody preferentially targets amino-terminal Huntingtin's fragments in striatal models of Huntington's disease. Neurobiol Dis 19(1-2):47-56. [PubMed: 15837560]  [MGI Ref ID J:116299]

Milnerwood AJ; Cummings DM; Dallerac GM; Brown JY; Vatsavayai SC; Hirst MC; Rezaie P; Murphy KP. 2006. Early development of aberrant synaptic plasticity in a mouse model of Huntington's disease. Hum Mol Genet 15(10):1690-703. [PubMed: 16600988]  [MGI Ref ID J:109535]

Mishra A; Dikshit P; Purkayastha S; Sharma J; Nukina N; Jana NR. 2008. E6-AP promotes misfolded polyglutamine proteins for proteasomal degradation and suppresses polyglutamine protein aggregation and toxicity. J Biol Chem 283(12):7648-56. [PubMed: 18201976]  [MGI Ref ID J:133935]

Naver B; Stub C; Moller M; Fenger K; Hansen AK; Hasholt L; Sorensen SA. 2003. Molecular and behavioral analysis of the R6/1 Huntington's disease transgenic mouse. Neuroscience 122(4):1049-57. [PubMed: 14643771]  [MGI Ref ID J:128267]

Nicniocaill B; Haraldsson B; Hansson O; O'Connor WT; Brundin P. 2001. Altered striatal amino acid neurotransmitter release monitored using microdialysis in R6/1 Huntington transgenic mice. Eur J Neurosci 13(1):206-10. [PubMed: 11135020]  [MGI Ref ID J:128177]

Nithianantharajah J; Barkus C; Murphy M; Hannan AJ. 2008. Gene-environment interactions modulating cognitive function and molecular correlates of synaptic plasticity in Huntington's disease transgenic mice. Neurobiol Dis 29(3):490-504. [PubMed: 18165017]  [MGI Ref ID J:130936]

Pang TY; Stam NC; Nithianantharajah J; Howard ML; Hannan AJ. 2006. Differential effects of voluntary physical exercise on behavioral and brain-derived neurotrophic factor expression deficits in huntington's disease transgenic mice. Neuroscience 141(2):569-84. [PubMed: 16716524]  [MGI Ref ID J:111765]

Petersen A; Hansson O; Puschban Z; Sapp E; Romero N; Castilho RF; Sulzer D; Rice M; DiFiglia M; Przedborski S; Brundin P. 2001. Mice transgenic for exon 1 of the Huntington's disease gene display reduced striatal sensitivity to neurotoxicity induced by dopamine and 6-hydroxydopamine. Eur J Neurosci 14(9):1425-35. [PubMed: 11722604]  [MGI Ref ID J:128172]

Petersen A; Puschban Z; Lotharius J; NicNiocaill B; Wiekop P; O'Connor WT; Brundin P. 2002. Evidence for dysfunction of the nigrostriatal pathway in the R6/1 line of transgenic Huntington's disease mice. Neurobiol Dis 11(1):134-46. [PubMed: 12460553]  [MGI Ref ID J:130975]

Pineda JR; Canals JM; Bosch M; Adell A; Mengod G; Artigas F; Ernfors P; Alberch J. 2005. Brain-derived neurotrophic factor modulates dopaminergic deficits in a transgenic mouse model of Huntington's disease. J Neurochem 93(5):1057-68. [PubMed: 15934928]  [MGI Ref ID J:99427]

Smith R; Chung H; Rundquist S; Maat-Schieman ML; Colgan L; Englund E; Liu YJ; Roos RA; Faull RL; Brundin P; Li JY. 2006. Cholinergic neuronal defect without cell loss in Huntington's disease. Hum Mol Genet 15(21):3119-31. [PubMed: 16987871]  [MGI Ref ID J:114849]

Smith R; Petersen A; Bates GP; Brundin P; Li JY. 2005. Depletion of rabphilin 3A in a transgenic mouse model (R6/1) of Huntington's disease, a possible culprit in synaptic dysfunction. Neurobiol Dis 20(3):673-84. [PubMed: 15967669]  [MGI Ref ID J:104634]

Spires TL; Grote HE; Garry S; Cordery PM; Van Dellen A; Blakemore C; Hannan AJ. 2004. Dendritic spine pathology and deficits in experience-dependent dendritic plasticity in R6/1 Huntington's disease transgenic mice. Eur J Neurosci 19(10):2799-807. [PubMed: 15147313]  [MGI Ref ID J:90295]

Spires TL; Grote HE; Varshney NK; Cordery PM; van Dellen A; Blakemore C; Hannan AJ. 2004. Environmental enrichment rescues protein deficits in a mouse model of Huntington's disease, indicating a possible disease mechanism. J Neurosci 24(9):2270-6. [PubMed: 14999077]  [MGI Ref ID J:90128]

Teles AV; Rosenstock TR; Okuno CS; Lopes GS; Bertoncini CR; Smaili SS. 2008. Increase in bax expression and apoptosis are associated in Huntington's disease progression. Neurosci Lett 438(1):59-63. [PubMed: 18468793]  [MGI Ref ID J:136970]

Vatsavayai SC; Dallerac GM; Milnerwood AJ; Cummings DM; Rezaie P; Murphy KP; Hirst MC. 2007. Progressive CAG expansion in the brain of a novel R6/1-89Q mouse model of Huntington's disease with delayed phenotypic onset. Brain Res Bull 72(2-3):98-102. [PubMed: 17352932]  [MGI Ref ID J:128652]

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):2193-202. [PubMed: 12657678]  [MGI Ref ID J:82676]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & Husbandry	When maintaining a live colony, hemizygous mice are bred to BALB/cByJ inbred mice or to wildtype siblings.
Mating System	Noncarrier x Hemizygote         (Female x Male)
Diet Information	LabDiet® 5K52/5K67

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

Standard Supply

Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement.

Supply Notes

Usually shipped between four and eight weeks of age. This strain is included in the Induced Mutant Resource Colony collection.

Control Information

	Control
	Noncarrier
	001026 BALB/cByJ
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
International - Control Pricing Information for Genetically Engineered Mutant Strains.

General Terms and Conditions

See Terms of Use

The Jackson Laboratory's Genotype Promise

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.

---

Ordering and Purchasing Information

      Purchasing Information
      JAX^® Mice Orders
      Surgical Services

Contact Information
Orders & Technical Support
Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form

Terms of Use

Terms of Use

General Terms and Conditions

For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries

Contracts Administration

phone:	207-288-6470
fax:	207-288-6655

JAX^® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of MICE, products or services, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.

No Liability

In no event shall The Jackson Laboratory, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, products or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of The Jackson Laboratory, its agents or employees. In purchasing or receiving MICE, products or services from The Jackson Laboratory, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges The Jackson Laboratory from all such causes of action or damages, and further agrees to defend and indemnify The Jackson Laboratory from any costs or damages arising out of any third party claims.

MICE and biological materials are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, products and services by The Jackson Laboratory, and by its licensees and distributors.

Acceptance of delivery of MICE, products or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on The Jackson Laboratory, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, products services by The Jackson Laboratory.