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| These beta3-mutant mice lack the beta3 coding region of the Gabrb3 (gamma-aminobutyric acid (GABA-A) receptor, subunit beta 3) locus and may be useful in studying neurodevelopmental disorders such as cleft palate, seizures, epilepsy, and sensitivity to anesthetics and ethanol. In addition, the observed behavioral deficits (especially regarding social behaviors) indicate that mutant mice may be a useful model of autism spectrum disorders. Of note, several strains bearing gamma-aminobutyric acid (GABA-A) receptor mutations are available from this donating investigator (Dr. Gregg Homanics, University of Pittsburgh), including Gabra1 (Stock No. 004318), Gabra4 (Stock No. 006874), Gabra6 (Stock No. 002710), Gabrb3 (Stock No. 002711), Gabrd (Stock No. 003725), and Gabrg2 (Stock No. 003137). | |||||||||||||||
- 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 +N1
Generation DefinitionsDonating Investigator Dr. Gregg Homanics, University of Pittsburgh Description
The gamma-Aminobutyric acid type A receptors mediate the majority of rapid inhibitory synaptic transmission in the CNS. The beta3 subunit is an essential component of these receptors in many brain regions, especially during development, and is implicated in several pathophysiologic processes. The majority of mice homozygous for the Gabrb3tm1Geh mutation (or beta3-/-) die at birth with ~60% displaying cleft palate and the remaining ~35% die for unidentified reasons. Homozygous females that survive are fertile but do not care for their pups. Survivors have frequent myoclonus and occasional epileptic seizures, are hypersensitive to external stimuli and handling, have a lack of coordination and display altered responses to certain anesthesias. In addition, the observed behavioral deficits (especially regarding social behaviors) indicate that mutant mice may be a useful model of autism spectrum disorders.Of note, several strains bearing gamma-aminobutyric acid (GABA-A) receptor mutations are available from this donating investigator (Dr. Gregg Homanics, University of Pittsburgh), including Gabra1 (Stock No. 004318), Gabra4 (Stock No. 006874), Gabra6 (Stock No. 002710), Gabrb3 (Stock No. 002711), Gabrd (Stock No. 003725), and Gabrg2 (Stock No. 003137).
Development
This strain was developed in the laboratory of Dr. Gregg Homanics at the University of Pittsburgh. The vector containing Pgk-neo was inserted by homologous recombination and resulted in deletion of the promoter and exons 1 and 2 of the Gabrb3 gene. The 129X1/SvJ x 129S1/Sv-derived R1 ES cell line was used.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 101045 B6129SF2/J | (approximate) | |
| Considerations for Choosing Controls | ||
Related Strains
Facebase: models
View Facebase: models (58 strains)
008310 B6;129-Gabrb3tm2.1Geh/J
Additional Web Information
JAX® NOTES, Winter 2008; 512. JAX® Mice strain sheds new light on autism.
Phenotype
Phenotype Information
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Autism
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Epilepsy, Childhood Absence, Susceptibility to, 5; ECA5 (GABRB3)
Gamma-Aminobutyric Acid Receptor, Beta-3; GABRB3 (GABRB3)
assigned by genotype
Gabrb3tm1Geh/Gabrb3tm1Geh
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
- behavior/neurological phenotype
- abnormal behavior
- frequently seen sleeping away from nesting material (MGI Ref ID J:130259)
- abnormal response to novel object
- abnormal social/conspecific interaction
- fail to show a significant preference for spending time in the interaction chamber adjacent to the stimulus cage containing an unfamiliar mouse as opposed to spending time in the interaction chamber adjacent to an empty stimulus cage (MGI Ref ID J:130259)
- mice fail to exhibit a preference for interacting with a new mouse over a familiar mouse (MGI Ref ID J:130259)
- abnormal nest building behavior
- at 1, 24 and 48 hours after introduction of new nestlet material, mice utilize significantly less material than wild-type controls (MGI Ref ID J:130259)
- significant impairment in their ability to achieve the nest complexity exhibited by the controls (MGI Ref ID J:130259)
- location of nest construction is different (MGI Ref ID J:130259)
- circling (MGI Ref ID J:130259)
- decreased vertical activity
- hyperactivity
- nervous system phenotype
- abnormal cerebellum vermis lobule morphology (MGI Ref ID J:130259)
- abnormal cerebellum vermis lobule II morphology
- significant decrease in the surface area (MGI Ref ID J:130259)
- abnormal cerebellum vermis lobule III morphology
- significant decrease in the surface area (MGI Ref ID J:130259)
- abnormal cerebellum vermis lobule IV morphology
- significant decrease in the surface area (MGI Ref ID J:130259)
- abnormal cerebellum vermis lobule V morphology
- significant decrease in the surface area (MGI Ref ID J:130259)
- abnormal cerebellum vermis lobule VI morphology
- significant decrease in the surface area (MGI Ref ID J:130259)
- abnormal cerebellum vermis lobule VII morphology
- significant decrease in the surface area (MGI Ref ID J:130259)
Gabrb3tm1Geh/Gabrb3tm1Geh
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
- mortality/aging
- partial perinatal lethality
- premature death
- animals surviving to birth live an average of 18 weeks (MGI Ref ID J:39801)
- growth/size phenotype
- decreased body size
- 5-10% that survive to adulthood are runted until weaning but achieve normal body weight by adulthood (MGI Ref ID J:39801)
- behavior/neurological phenotype
- abnormal motor capabilities/coordination/movement (MGI Ref ID J:39801)
- circling (MGI Ref ID J:108890)
- many have been observed to run continuously in tight circles for extended periods of time (MGI Ref ID J:39801)
- hyperactivity (MGI Ref ID J:39801)
- impaired coordination
- have difficulty walking on grids and repeatedly fall off platforms and rotarods (MGI Ref ID J:39801)
- impaired swimming
- have difficulty swimming (MGI Ref ID J:39801)
- limb grasping (MGI Ref ID J:39801)
- abnormal parental behavior
- failure to nuture offspring (MGI Ref ID J:39801)
- hyperresponsive
- hyperresponsive to human contact and other sensory stimuli (MGI Ref ID J:39801)
- seizures
- variable severity of epileptic seizures in mice over 10 weeks of age (MGI Ref ID J:39801)
- hearing/vestibular/ear phenotype
- abnormal auditory brainstem response waveform shape
- at 6 weeks, suprathreshold ABR amplitudes in homozygotes are significantly reduced in amplitude, by at least 50% at all test frequencies and sound levels (MGI Ref ID J:112951)
- abnormal cochlea morphology
- abnormal cochlear IHC afferent innervation pattern
- at >24 weeks, homozygotes display a significant reduction in the density of IHC afferent innervation relative to age-matched wild-type mice, indicating neuropathy (MGI Ref ID J:112951)
- abnormal cochlear OHC efferent innervation pattern
- at >24 weeks, homozygotes display a reduction in OHC efferent innervation, with fewer efferent axons crossing to OHCs at the level of the tunnel of Corti relative to age-matched wild-type mice (MGI Ref ID J:112951)
- cochlear inner hair cell degeneration
- at ~24 weeks, homozygotes display a nearly complete loss of IHCs throughout the basal 15% of the cochlear spiral, i.e., from 40 to 90 kHz according to the mouse cochlear frequency map (MGI Ref ID J:112951)
- cochlear outer hair cell degeneration
- at ~24 weeks, homozygotes display a nearly complete loss of OHCs throughout the basal 15% of the cochlear spiral, i.e., from 40 to 90 kHz according to the mouse cochlear frequency map (MGI Ref ID J:112951)
- type IV spiral ligament fibrocyte degeneration
- at >24 weeks, homozygotes display widespread loss of type IV fibrocytes, spreading farther apically (MGI Ref ID J:112951)
- abnormal distortion product otoacoustic emission
- at 6 weeks, homozygotes display significantly elevated DPOAE thresholds across all test frequencies relative to wild-type mice, with DPOAE thresholds of >60 dB at high frequencies (MGI Ref ID J:112951)
- at 16 kHz (middle cochlear region), ABR shifts are similar in magnitude to the observed DPOAE shifts, suggesting that the threshold shift arises at, or before, the stage of OHC transduction and amplification (MGI Ref ID J:112951)
- increased or absent threshold for auditory brainstem response
- at 6 weeks, homozygotes display severe cochlear dysfunction, as shown by highly significant ABR threshold elevations of 20-45 dB across a range of test frequencies, with peak loss occurring at 22.6 kHz (MGI Ref ID J:112951)
- ABR threshold elevation corresponds to >2 orders of magnitude of stimulus amplitude (MGI Ref ID J:112951)
- sensorineural hearing loss (MGI Ref ID J:112951)
- nervous system phenotype
- abnormal CNS synaptic transmission
- 80% decrease in the maximal amplitude of GABA-activated chloride currents in dorsal root ganglion (MGI Ref ID J:39801)
- abnormal cochlear IHC afferent innervation pattern
- at >24 weeks, homozygotes display a significant reduction in the density of IHC afferent innervation relative to age-matched wild-type mice, indicating neuropathy (MGI Ref ID J:112951)
- abnormal cochlear OHC efferent innervation pattern
- at >24 weeks, homozygotes display a reduction in OHC efferent innervation, with fewer efferent axons crossing to OHCs at the level of the tunnel of Corti relative to age-matched wild-type mice (MGI Ref ID J:112951)
- abnormal cochlear nerve morphology
- at >24 weeks, homozygotes display clear signs of cochlear nerve abnormalities (progressive loss of afferent terminals) (MGI Ref ID J:112951)
- cochlear ganglion degeneration
- at >24 weeks, homozygotes show partial loss of spiral ganglion cells but only in cochlear regions in which IHCs are degenerated (MGI Ref ID J:112951)
- cochlear inner hair cell degeneration
- at ~24 weeks, homozygotes display a nearly complete loss of IHCs throughout the basal 15% of the cochlear spiral, i.e., from 40 to 90 kHz according to the mouse cochlear frequency map (MGI Ref ID J:112951)
- cochlear outer hair cell degeneration
- at ~24 weeks, homozygotes display a nearly complete loss of OHCs throughout the basal 15% of the cochlear spiral, i.e., from 40 to 90 kHz according to the mouse cochlear frequency map (MGI Ref ID J:112951)
- seizures
- variable severity of epileptic seizures in mice over 10 weeks of age (MGI Ref ID J:39801)
- small cochlear ganglion
- mutant calretinin-negative cells are smaller at each sampled location in the spiral ganglion relative to wild-type cells (MGI Ref ID J:108890)
- the reduction in mean somatic area of mutant calretinin-negative cells is 5.2% in the basal turn, 8.7% in the middle turn, and 12.2% in the apical turn of the spiral ganglion relative to wild-type cells (MGI Ref ID J:108890)
- adult homozygotes display significantly smaller cochlear ganglion cell areas at every sampled region in the spiral ganglion, except the apical cochlear turn (MGI Ref ID J:108890)
- in contrast, mutant calretinin-positive ganglion cells are of normal size and proportion relative to wild-type cells (MGI Ref ID J:108890)
- cochlear ganglion hypoplasia
- small vestibular ganglion
- adult homozygotes display significantly smaller ganglion cell areas in both divisions of Scarpa's ganglion (superior and inferior) relative to wild-type mice (MGI Ref ID J:108890)
- mutant calretinin-negative cells are smaller in both divisions of Scarpa's ganglion relative to wild-type cells (MGI Ref ID J:108890)
- the reduction in mean somatic area of mutant calretinin-negative cells is 9.5% in the inferior division and 21.5% in the superior division of Scarpa's ganglion (MGI Ref ID J:108890)
- in contrast, mutant calretinin-positive ganglion cells are of normal size and proportion relative to wild-type cells (MGI Ref ID J:108890)
- craniofacial phenotype
- cleft palate
- about 57% exhibit cleft palate (MGI Ref ID J:39801)
- digestive/alimentary phenotype
- cleft palate
- about 57% exhibit cleft palate (MGI Ref ID J:39801)
- skeleton phenotype
- type IV spiral ligament fibrocyte degeneration
- at >24 weeks, homozygotes display widespread loss of type IV fibrocytes, spreading farther apically (MGI Ref ID J:112951)
This mouse can be used to support research in many areas including:
Gabrb3tm1Geh relatedNeurobiology Research
Epilepsy
Neurodevelopmental Defects
Autism
Receptor Defects
GABA receptor
Cell Biology Research
Channel and Transporter Defects
chloride
chloride: GABAA receptor
Developmental Biology Research
Neurodevelopmental Defects
Neurobiology Research
Behavioral and Learning Defects
Channel and Transporter Defects
chloride
chloride: GABAA receptor
Epilepsy
Neurodevelopmental Defects
Neurotransmitter Receptor and Synaptic Vesicle Defects
Receptor Defects
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Gabrb3tm1Geh | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Gregg E Homanics | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | beta3-; | ||
| Mutation Made By | Dr. Gregg Homanics, University of Pittsburgh | ||
| Strain of Origin | (129X1/SvJ x 129S1/Sv)F1-Kitl<+> | ||
| ES Cell Line Name | R1 | ||
| ES Cell Line Strain | (129X1/SvJ x 129S1/Sv)F1-Kitl<+> | ||
| Gene Symbol and Name | Gabrb3, gamma-aminobutyric acid (GABA) A receptor, subunit beta 3 | ||
| Chromosome | 7 | ||
| Gene Common Name(s) | A230092K12Rik; AW049585; Cp1; ECA5; Gabrb-3; RIKEN cDNA A230092K12 gene; beta3; cleft palate 1; expressed sequence AW049585; | ||
| Molecular Note | A neomycin resistance cassette replaced 2.8 kb of sequence, including exons 1-3. [MGI Ref ID J:39801] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Gabrb3tm1Geh, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Delorey TM; Sahbaie P; Hashemi E; Homanics GE; Clark JD. 2008. Gabrb3 gene deficient mice exhibit impaired social and exploratory behaviors, deficits in non-selective attention and hypoplasia of cerebellar vermal lobules: A potential model of autism spectrum disorder. Behav Brain Res 187(2):207-20. [PubMed: 17983671] [MGI Ref ID J:130259]
Homanics GE; DeLorey TM; Firestone LL; Quinlan JJ; Handforth A ; Harrison NL ; Krasowski MD ; Rick CE ; Korpi ER ; Makela R ; Brilliant MH ; Hagiwara N ; Ferguson C ; Snyder K ; Olsen RW. 1997. Mice devoid of gamma-aminobutyrate type A receptor beta3 subunit have epilepsy, cleft palate, and hypersensitive behavior. Proc Natl Acad Sci U S A 94(8):4143-8. [PubMed: 9108119] [MGI Ref ID J:39801]
Additional References
Dellovade TL; Davis AM; Ferguson C; Sieghart W; Homanics GE; Tobet SA. 2001. GABA influences the development of the ventromedial nucleus of the hypothalamus. J Neurobiol 49(4):264-76. [PubMed: 11745664] [MGI Ref ID J:79217]
Gabrb3tm1Geh relatedDeLorey TM; Handforth A; Anagnostaras SG; Homanics GE; Minassian BA ; Asatourian A ; Fanselow MS ; Delgado-Escueta A ; Ellison GD ; Olsen RW. 1998. Mice lacking the beta3 subunit of the GABAA receptor have the epilepsy phenotype and many of the behavioral characteristics of Angelman syndrome. J Neurosci 18(20):8505-14. [PubMed: 9763493] [MGI Ref ID J:50564]
DeLorey TM; Sahbaie P; Hashemi E; Li WW; Salehi A; Clark DJ. 2011. Somatosensory and sensorimotor consequences associated with the heterozygous disruption of the autism candidate gene, Gabrb3. Behav Brain Res 216(1):36-45. [PubMed: 20699105] [MGI Ref ID J:174161]
Hagiwara N; Katarova Z; Siracusa LD; Brilliant MH. 2003. Nonneuronal expression of the GABA(A) beta3 subunit gene is required for normal palate development in mice. Dev Biol 254(1):93-101. [PubMed: 12606284] [MGI Ref ID J:83131]
Hashemi E; Sahbaie P; Davies MF; Clark JD; DeLorey TM. 2007. Gabrb3 gene deficient mice exhibit increased risk assessment behavior, hypotonia and expansion of the plexus of locus coeruleus dendrites. Brain Res 1129(1):191-9. [PubMed: 17156762] [MGI Ref ID J:117697]
Huntsman MM; Porcello DM; Homanics GE; DeLorey TM; Huguenard JR. 1999. Reciprocal inhibitory connections and network synchrony in the mammalian thalamus. Science 283(5401):541-3. [PubMed: 9915702] [MGI Ref ID J:124675]
Koo JW; Homanics GE; Balaban CD. 2002. Hypoplasia of spiral and Scarpa's ganglion cells in GABA(A) receptor beta(3) subunit knockout mice. Hear Res 167(1-2):71-80. [PubMed: 12117532] [MGI Ref ID J:108890]
Krasowski MD; Rick CE; Harrison NL; Firestone LL; Homanics GE. 1998. A deficit of functional GABA(A) receptors in neurons of beta 3 subunit knockout mice. Neurosci Lett 240(2):81-4. [PubMed: 9486477] [MGI Ref ID J:107951]
Liljelund P; Handforth A; Homanics GE; Olsen RW. 2005. GABA(A) receptor beta3 subunit gene-deficient heterozygous mice show parent-of-origin and gender-related differences in beta3 subunit levels, EEG, and behavior. Brain Res Dev Brain Res 157(2):150-61. [PubMed: 15878204] [MGI Ref ID J:99362]
Maison SF; Rosahl TW; Homanics GE; Liberman MC. 2006. Functional role of GABAergic innervation of the cochlea: phenotypic analysis of mice lacking GABA(A) receptor subunits alpha1, alpha2, alpha5, alpha6, beta2, beta3, or delta. J Neurosci 26(40):10315-26. [PubMed: 17021187] [MGI Ref ID J:112951]
Nusser Z; Kay LM; Laurent G; Homanics GE; Mody I. 2001. Disruption of GABA(A) receptors on GABAergic interneurons leads to increased oscillatory power in the olfactory bulb network. J Neurophysiol 86(6):2823-33. [PubMed: 11731539] [MGI Ref ID J:104000]
Olexova L; Talarovicova A; Lewis-Evans B; Borbelyova V; Krskova L. 2012. Animal models of autism with a particular focus on the neural basis of changes in social behaviour: an update article. Neurosci Res 74(3-4):184-94. [PubMed: 23142422] [MGI Ref ID J:192363]
Quinlan JJ; Homanics GE; Firestone LL. 1998. Anesthesia sensitivity in mice that lack the beta3 subunit of the gamma-aminobutyric acid type A receptor. Anesthesiology 88(3):775-80. [PubMed: 9523823] [MGI Ref ID J:46728]
Ramadan E; Fu Z; Losi G; Homanics GE; Neale JH; Vicini S. 2003. GABA(A) receptor beta3 subunit deletion decreases alpha2/3 subunits and IPSC duration. J Neurophysiol 89(1):128-34. [PubMed: 12522165] [MGI Ref ID J:102972]
Resnick A; Homanics GE; Jung BJ; Peris J. 1999. Increased acute cocaine sensitivity and decreased cocaine sensitization in GABA(A) receptor beta3 subunit knockout mice. J Neurochem 73(4):1539-48. [PubMed: 10501199] [MGI Ref ID J:57686]
Sinkkonen ST; Homanics GE; Korpi ER. 2003. Mouse models of Angelman syndrome, a neurodevelopmental disorder, display different brain regional GABA(A) receptor alterations. Neurosci Lett 340(3):205-8. [PubMed: 12672542] [MGI Ref ID J:108025]
Ugarte SD; Homanics GE; Firestone LL; Hammond DL. 2000. Sensory thresholds and the antinociceptive effects of GABA receptor agonists in mice lacking the beta3 subunit of the GABA(A) receptor Neuroscience 95(3):795-806. [PubMed: 10670447] [MGI Ref ID J:60491]
Ugarte SD; Homanics GE; Hammond DL. 2001. Effect of embryonic knock-down of GABA(A) receptors on the levels of monoamines and their metabolites in the CNS of the mouse. Brain Res 904(2):290-7. [PubMed: 11406127] [MGI Ref ID J:70367]
Wisor JP; DeLorey TM; Homanics GE; Edgar DM. 2002. Sleep states and sleep electroencephalographic spectral power in mice lacking the beta(3) subunit of the GABA(A) receptor. Brain Res 955(1-2):221-8. [PubMed: 12419540] [MGI Ref ID J:80484]
Wong SM; Cheng G; Homanics GE; Kendig JJ. 2001. Enflurane actions on spinal cords from mice that lack the beta3 subunit of the GABA(A) receptor. Anesthesiology 95(1):154-64. [PubMed: 11465553] [MGI Ref ID J:106235]
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 This strain is currently maintained on a mixed C57BL/6J x 129 genetic background. It is maintained by mating heterozygous mice to normal wildtype siblings. Diet Information LabDiet® 5K52/5K67
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* $3175.00 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* $4127.50 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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|
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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.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 101045 B6129SF2/J | (approximate) | |
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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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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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.