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| Dopamine-deficient (DA-deficient, DA-/-, or DD) mice are homozygous for the TH mutant allele and heterozygous for the DBH-TH mutant allele (Th-/-;DbhTh/+). While no expression from the TH mutant allele is observed in any tissues (resulting in deficiency of both dopamine (DA) and norepinephrine (NE)), the DBH-TH mutant allele contains the TH coding sequence under the control of the endogenous DBH promoter region and restores TH expression in noradrenergic neurons. These DD mice may be useful in studying dopaminergic neurobiology (including neurotransmitters, addiction, feeding, learning and memory, catecholamines, and Parkinsonian phenotypes). | |||||||||||||||||||
- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
- Health & care
- References
- Pricing & purchasing
- Terms of use
Description
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Strain Information
Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation ?+N1F1pN1
Generation DefinitionsDonating Investigator Claire Cannon, Marquette University Important Note
Dopamine-deficient (DA-deficient, DA-/-, or DD) mice are homozygous for the TH mutant allele and heterozygous for the DBH-TH mutant allele (Th-/-; DbhTh/+). When maintained as congenic on a C57BL/6 genetic background, Th-/-; DbhTh/+ mice may exhibit declining birth rates and increased mortality (Hnasko et al 2007 J Neurosci 27:12484-8). Therefore, the colony at The Jackson Laboratory is maintained as heterozygous for both mutant alleles.Description
Mice heterozygous for both targeted mutations are viable and fertile. Dopamine-deficient (DA-deficient, DA-/-, or DD) mice are homozygous for the TH mutant allele and heterozygous for the DBH-TH mutant allele (Th-/-; DbhTh/+). While no expression from the TH mutant allele is observed in any tissues (resulting in deficiency of both dopamine (DA) and norepinephrine (NE)), the DBH-TH mutant allele contains the TH coding sequence under the control of the endogenous DBH promoter region and restores TH expression in noradrenergic neurons. DD mice become hypoactive and hypophagic around two weeks of age and usually die before four weeks of age. Treatment with L-DOPA, the product of TH enzymatic activity, rescues size, feeding, and life span. These DD mice may be useful in studying dopaminergic neurobiology (including neurotransmitters, addiction, feeding, learning and memory, catecholamines, and Parkinsonian phenotypes).NOTE: Th-/-; DbhTh/+ mice congenic on a C57BL/6 genetic background may exhibit declining birth rates and increased mortality (Hnasko et al 2007 J Neurosci 27:12484-8).
Development
To generate the TH knockout allele , the pTH4 targeting vector was designed to replace the proximal promoter and first two exons of the Th locus with a PGK-neomycin resistance cassette. The construct was electroporated into 129S7/SvEvBrd-Hprt1+ derived AB1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts and the resulting heterozygous mice were maintained on a C57BL/6/129S hybrid background.
To generate the DBH-TH mutant allele (DbhTh), the pDBH-TH vector was designed to insert the entire mouse Th coding region (including 1 kb sequence after the polyA site) and a neo cassette between exons 1 and 2 of the Dbh locus. The construct was electroporated into unspecified embryonic stem (ES) cells and heterozygous animals were obtained.
Next, mice heterozygous for the TH mutant allele (Th-/+) were bred with mice heterozygous for the DBH-TH mutant allele (DbhTh/+). The donating investigator reports that double mutant mice were subsequently backcrossed to C57BL/6J mice for several (9-14) generations prior to arrival at The Jackson Laboratory. Upon arrival, mutant mice were bred with C57BL/6J inbred mice (Stock No. 000664) for at least one generation to establish the colony.A 27 SNP (single nucleotide polymorphism) panel analysis performed by The Jackson Laboratory revealed the mice to be ~85% C57BL/6 genetic background; 4 of 27 markers were segregating for C57BL/6 or 129S allele-type markers (on chromosomes 2, 3, 8 and 11). These data suggest that, prior to arrival at the Jackson Laboratory, the mice were not backcrossed to C57BL/6 for as many generations as originally reported.
Control Information
| Control | ||
|---|---|---|
| 101043 B6129SF1/J | (approximate) | |
| 101045 B6129SF2/J | (approximate) | |
| 000664 C57BL/6J | (approximate) | |
| Considerations for Choosing Controls | ||
Related Strains
Parkinson's Disease Models
View Parkinson's Disease Models (109 strains)
008532 B6;129-Thtm1(cre/Esr1)Nat/J 008779 STOCK Thtm1Srt/J
Additional Web Information
Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.
Phenotype
Phenotype Information
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Dopamine Beta-Hydroxylase Deficiency, Congenital (DBH)
Segawa Syndrome, Autosomal Recessive (TH)
assigned by genotype
Dbhtm2(Th)Rpa/Dbh+ Thtm1Rpa/Thtm1Rpa
involves: 129S7/SvEvBrd * C57BL/6J
- mortality/aging
- premature death
- can be maintained for at least 1.5 years with daily treatment of 50 mg/kg L-DOPA and feeding with breeder chow (4.35 kcal/g) (MGI Ref ID J:58125)
- behavior/neurological phenotype
- abnormal gait
- 24 or more hours after L-DOPA treatment the gait is awkward (MGI Ref ID J:58125)
- akinesia
- 24 hours after L-DOPA treatment 1- and 4-limb akinesia is increased compared to controls (MGI Ref ID J:58125)
- catalepsy
- 24 hours after L-DOPA treatment forelimb catalepsy is increased compared to controls (MGI Ref ID J:58125)
- decreased food intake
- decreased compensatory feeding amount
- if food is with held for 3 or 6 hours after L-DOPA treatment mice compensate by consuming more food in the next 3 hours to consume about the same amount of food as when food is continually available; however no compensation if food is with held for 9 hours (MGI Ref ID J:58125)
- after a 30 hour fast when presented with a high sucrose, high-fat diet mice begin to consume food but cease eating sooner and consume only about 25% of the amount eaten by wild-type mice (MGI Ref ID J:58125)
- hunched posture (MGI Ref ID J:58125)
- hyperactivity
- for 6 - 9 hours after L-DOPA treatment activity level is higher than in wild-type (MGI Ref ID J:58125)
- treatment with L-DOPA and carbidopa induces a biphasic increase in activity that is more prolonged than when L-DOPA is given alone; however, in wild-type mice L-DOPA and carbidopa treatment induces inactivity (MGI Ref ID J:58125)
- hypoactivity
- hyporesponsive to tactile stimuli
- 1 hour after L-DOPA treatment a decrease in response in the paw pinch assay is seen (MGI Ref ID J:58125)
- impaired behavioral response to addictive substance
- 19 hours after L-DOPA treatment a single dose of amphetamine (5mg/kg) induces a shorter increase in activity (1 hour compared to 2 hours in controls) and a second dose of amphetamine fails to alter activity unlike in controls (MGI Ref ID J:58125)
- impaired coordination
- 24 or more hours after L-DOPA treatment rotarod and pole test performance are poor (MGI Ref ID J:58125)
- increased stereotypic behavior
- treatment with L-DOPA and carbidopa induces intense stereotypic behavior (licking and chewing of paws) between 1 and 5 hours after treatment, no such behavior is seen in controls (MGI Ref ID J:58125)
- integument phenotype
- hyporesponsive to tactile stimuli
- 1 hour after L-DOPA treatment a decrease in response in the paw pinch assay is seen (MGI Ref ID J:58125)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Dbhtm2(Th)Rpa/Dbh+ Thtm1Rpa/Thtm1Rpa
involves: 129S7/SvEvBrd
- mortality/aging
- premature death
- growth/size phenotype
- decreased body size
- at P10 - P15 (MGI Ref ID J:30404)
- behavior/neurological phenotype
- adipsia
- injection with L-DOPA restores drinking behavior (MGI Ref ID J:30404)
- aphagia
- injection with L-DOPA restores eating behavior with maximal intake during the first 2 hours after injection and cessation of eating by about 6 hours post injection (MGI Ref ID J:30404)
- decreased stereotypic behavior
- make about 280 stereotypical beam breaks per hour compared to about 700 per hour for controls (MGI Ref ID J:30404)
- hunched posture
- at P10 - P15 (MGI Ref ID J:30404)
- hypoactivity
- at P10 - P15, travel only about 3m/hr compared to 23 m/hr in controls (MGI Ref ID J:30404)
- however at P16, reflexion, corneal, startle, righting, grasping, and placing reflexes are all similar to controls, balance is not impaired, and no tremors are seen (MGI Ref ID J:30404)
- within 15 minutes of injection of L-DOPA activity levels increase peaking at about 1 hour post injection and then decreasing so that by 12 hours post injection mice are hypoactive (MGI Ref ID J:30404)
- poor grooming
- at P10 - P15 (MGI Ref ID J:30404)
- nervous system phenotype
- abnormal nervous system physiology
- expression levels of tachykinin 1 and dynorphin are decreased in the striatum (MGI Ref ID J:30404)
- decreased dopamine level
- dopamine levels in the brain are low; however, levels of norepinephrine in the brain, heart, salivary glands, and adrenal glands are similar to controls (MGI Ref ID J:30404)
- decreased brain size
- brain size is reduced and neurons are slightly more compact; however, dopaminergic neuron and striatum morphology are similar to controls (MGI Ref ID J:30404)
- homeostasis/metabolism phenotype
- decreased dopamine level
- dopamine levels in the brain are low; however, levels of norepinephrine in the brain, heart, salivary glands, and adrenal glands are similar to controls (MGI Ref ID J:30404)
This mouse can be used to support research in many areas including:
Developmental Biology Research
Perinatal Lethality
Neurobiology Research
Behavioral and Learning Defects
Neurotransmitter Receptor and Synaptic Vesicle Defects
Parkinson's Disease
Response to Catecholamines
Research Tools
Toxicology Research
drug metabolism
drug/compound testing
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Dbhtm2(Th)Rpa | ||
|---|---|---|---|
| Allele Name | targeted mutation 2, Richard D Palmiter | ||
| Allele Type | Targeted (knock-in) | ||
| Common Name(s) | DBH-TH-; DbhTh; | ||
| Expressed Gene | Th, tyrosine hydroxylase, mouse, laboratory | ||
| Molecular Note | The entire Th coding region, including 1kb sequence after the polyadenylation site and a neomycin resistance cassette, was inserted between exons 1 and 2 of the Dbh gene. [MGI Ref ID J:30404] | ||
| Gene Symbol and Name | Dbh, dopamine beta hydroxylase | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | DBM; DOPBHY; | ||
| Allele Symbol | Thtm1Rpa | ||
| Allele Name | targeted mutation 1, Richard D Palmiter | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | DA-; TH-; pTH4; | ||
| Strain of Origin | 129S7/SvEvBrd-Hprt<+> | ||
| ES Cell Line Name | AB1 | ||
| ES Cell Line Strain | 129S7/SvEvBrd-Hprt<+> | ||
| Molecular Note | A neomycin selection cassette replaced the proximal promoter and exons 1 and 2. [MGI Ref ID J:24347] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Dbhtm2(Th)Rpa MCA, Melt Curve Analysis
THtm1Rpa MCA, Melt Curve Analysis
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Cannon CM; Palmiter RD. 2003. Reward without dopamine. J Neurosci 23(34):10827-31. [PubMed: 14645475] [MGI Ref ID J:86847]
Hnasko TS; Sotak BN; Palmiter RD. 2007. Cocaine-conditioned place preference by dopamine-deficient mice is mediated by serotonin. J Neurosci 27(46):12484-8. [PubMed: 18003826] [MGI Ref ID J:127594]
Szczypka MS; Rainey MA; Kim DS; Alaynick WA; Marck BT; Matsumoto AM; Palmiter RD. 1999. Feeding behavior in dopamine-deficient mice. Proc Natl Acad Sci U S A 96(21):12138-43. [PubMed: 10518589] [MGI Ref ID J:58125]
Zhou QY; Palmiter RD. 1995. Dopamine-deficient mice are severely hypoactive, adipsic, and aphagic. Cell 83(7):1197-209. [PubMed: 8548806] [MGI Ref ID J:30404]
Additional References
Dbhtm2(Th)Rpa relatedThtm1Rpa relatedChartoff EH; Marck BT; Matsumoto AM; Dorsa DM; Palmiter RD. 2001. Induction of stereotypy in dopamine-deficient mice requires striatal D1 receptor activation. Proc Natl Acad Sci U S A 98(18):10451-6. [PubMed: 11517332] [MGI Ref ID J:126668]
Chartoff EH; Szczypka MS; Palmiter RD; Dorsa DM. 2004. Endogenous neurotensin attenuates dopamine-dependent locomotion and stereotypy. Brain Res 1022(1-2):71-80. [PubMed: 15353215] [MGI Ref ID J:92531]
Denenberg VH; Kim DS; Palmiter RD. 2004. The role of dopamine in learning, memory, and performance of a water escape task. Behav Brain Res 148(1-2):73-8. [PubMed: 14684249] [MGI Ref ID J:87763]
Fadok JP; Dickerson TM; Palmiter RD. 2009. Dopamine is necessary for cue-dependent fear conditioning. J Neurosci 29(36):11089-97. [PubMed: 19741115] [MGI Ref ID J:152679]
Hasbani DM; Perez FA; Palmiter RD; O'Malley KL. 2005. Dopamine depletion does not protect against acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxicity in vivo. J Neurosci 25(41):9428-33. [PubMed: 16221852] [MGI Ref ID J:123449]
Hnasko TS; Perez FA; Scouras AD; Stoll EA; Gale SD; Luquet S; Phillips PE; Kremer EJ; Palmiter RD. 2006. Cre recombinase-mediated restoration of nigrostriatal dopamine in dopamine-deficient mice reverses hypophagia and bradykinesia. Proc Natl Acad Sci U S A 103(23):8858-63. [PubMed: 16723393] [MGI Ref ID J:110806]
Hnasko TS; Sotak BN; Palmiter RD. 2005. Morphine reward in dopamine-deficient mice. Nature 438(7069):854-7. [PubMed: 16341013] [MGI Ref ID J:103809]
Hnasko TS; Szczypka MS; Alaynick WA; During MJ; Palmiter RD. 2004. A role for dopamine in feeding responses produced by orexigenic agents. Brain Res 1023(2):309-18. [PubMed: 15374756] [MGI Ref ID J:92829]
Kim DS; Palmiter RD. 2003. Adenosine receptor blockade reverses hypophagia and enhances locomotor activity of dopamine-deficient mice. Proc Natl Acad Sci U S A 100(3):1346-51. [PubMed: 12538862] [MGI Ref ID J:81841]
Kim DS; Palmiter RD; Cummins A; Gerfen CR. 2006. Reversal of supersensitive striatal dopamine D(1) receptor signaling and extracellular signal-regulated kinase activity in dopamine-deficient mice. Neuroscience 137(4):1381-8. [PubMed: 16388913] [MGI Ref ID J:105583]
Land BB; Bruchas MR; Schattauer S; Giardino WJ; Aita M; Messinger D; Hnasko TS; Palmiter RD; Chavkin C. 2009. Activation of the kappa opioid receptor in the dorsal raphe nucleus mediates the aversive effects of stress and reinstates drug seeking. Proc Natl Acad Sci U S A 106(45):19168-73. [PubMed: 19864633] [MGI Ref ID J:154773]
Lemos JC; Wanat MJ; Smith JS; Reyes BA; Hollon NG; Van Bockstaele EJ; Chavkin C; Phillips PE. 2012. Severe stress switches CRF action in the nucleus accumbens from appetitive to aversive. Nature 490(7420):402-6. [PubMed: 22992525] [MGI Ref ID J:189229]
Paladini CA; Robinson S; Morikawa H; Williams JT; Palmiter RD. 2003. Dopamine controls the firing pattern of dopamine neurons via a network feedback mechanism. Proc Natl Acad Sci U S A 100(5):2866-71. [PubMed: 12604788] [MGI Ref ID J:82388]
Robinson S; Smith DM; Mizumori SJ; Palmiter RD. 2004. Firing properties of dopamine neurons in freely moving dopamine-deficient mice: effects of dopamine receptor activation and anesthesia. Proc Natl Acad Sci U S A 101(36):13329-34. [PubMed: 15317940] [MGI Ref ID J:92402]
Seeman P; Weinshenker D; Quirion R; Srivastava LK; Bhardwaj SK; Grandy DK; Premont RT; Sotnikova TD; Boksa P; El-Ghundi M; O'dowd BF; George SR; Perreault ML; Mannisto PT; Robinson S; Palmiter RD; Tallerico T. 2005. Dopamine supersensitivity correlates with D2High states, implying many paths to psychosis. Proc Natl Acad Sci U S A 102(9):3513-8. [PubMed: 15716360] [MGI Ref ID J:96985]
Sotak BN; Hnasko TS; Robinson S; Kremer EJ; Palmiter RD. 2005. Dysregulation of dopamine signaling in the dorsal striatum inhibits feeding. Brain Res 1061(2):88-96. [PubMed: 16226228] [MGI Ref ID J:124410]
Szczypka MS; Kwok K; Brot MD; Marck BT; Matsumoto AM; Donahue BA; Palmiter RD. 2001. Dopamine production in the caudate putamen restores feeding in dopamine-deficient mice. Neuron 30(3):819-28. [PubMed: 11430814] [MGI Ref ID J:70162]
Szczypka MS; Rainey MA; Palmiter RD. 2000. Dopamine is required for hyperphagia in Lep(ob/ob) mice. Nat Genet 25(1):102-4. [PubMed: 10802666] [MGI Ref ID J:61883]
Chartoff EH; Marck BT; Matsumoto AM; Dorsa DM; Palmiter RD. 2001. Induction of stereotypy in dopamine-deficient mice requires striatal D1 receptor activation. Proc Natl Acad Sci U S A 98(18):10451-6. [PubMed: 11517332] [MGI Ref ID J:126668]
Denenberg VH; Kim DS; Palmiter RD. 2004. The role of dopamine in learning, memory, and performance of a water escape task. Behav Brain Res 148(1-2):73-8. [PubMed: 14684249] [MGI Ref ID J:87763]
Hasbani DM; Perez FA; Palmiter RD; O'Malley KL. 2005. Dopamine depletion does not protect against acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxicity in vivo. J Neurosci 25(41):9428-33. [PubMed: 16221852] [MGI Ref ID J:123449]
Kim DS; Szczypka MS; Palmiter RD. 2000. Dopamine-deficient mice are hypersensitive to dopamine receptor agonists. J Neurosci 20(12):4405-13. [PubMed: 10844009] [MGI Ref ID J:120532]
Sotak BN; Hnasko TS; Robinson S; Kremer EJ; Palmiter RD. 2005. Dysregulation of dopamine signaling in the dorsal striatum inhibits feeding. Brain Res 1061(2):88-96. [PubMed: 16226228] [MGI Ref ID J:124410]
Szczypka MS; Rainey MA; Palmiter RD. 2000. Dopamine is required for hyperphagia in Lep(ob/ob) mice. Nat Genet 25(1):102-4. [PubMed: 10802666] [MGI Ref ID J:61883]
Tsahai Tafari A; Thomas SA; Palmiter RD. 1997. Norepinephrine facilitates the development of the murine sweat response but is not essential. J Neurosci 17(11):4275-81. [PubMed: 9151744] [MGI Ref ID J:40429]
Zhou QY; Quaife CJ; Palmiter RD. 1995. Targeted disruption of the tyrosine hydroxylase gene reveals that catecholamines are required for mouse fetal development. Nature 374(6523):640-3. [PubMed: 7715703] [MGI Ref ID J:24347]
Health & husbandry
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Health & Colony Maintenance Information
Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.Colony Maintenance
Breeding & Husbandry When maintaining a live colony, mice heterozygous for both targeted alleles may be bred together. DD mice (homozygous for the TH mutant allele and heterozygous for the DBH-TH mutant allele; Th-/-;DbhTh/+) become hypoactive and hypophagic around two weeks of age and usually die before 4 weeks of age. Further backcrossing to the C57BL/6 genetic background may result in declining birth rates and increased mortality of DD mice.
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
|
Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2085.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
| Pricing for International shipping destinations |
|
Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2710.50 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
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|
|
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Control Information
| Control | ||
|---|---|---|
| 101043 B6129SF1/J | (approximate) | |
| 101045 B6129SF2/J | (approximate) | |
| 000664 C57BL/6J | (approximate) | |
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Important Note
Dopamine-deficient (DA-deficient, DA-/-, or DD) mice are homozygous for the TH mutant allele and heterozygous for the DBH-TH mutant allele (Th-/-; DbhTh/+). When maintained as congenic on a C57BL/6 genetic background, Th-/-; DbhTh/+ mice may exhibit declining birth rates and increased mortality (Hnasko et al 2007 J Neurosci 27:12484-8). Therefore, the colony at The Jackson Laboratory is maintained as heterozygous for both mutant alleles.
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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 Information
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For Licensing and Use Restrictions view the link(s) below:
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JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (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. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
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MICE and PRODUCTS 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 JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON 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 JACKSON, 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 JACKSON, 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 or services by JACKSON.