Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Mating System Heterozygote x Inbred         (Female x Male)   01-MAR-06 Species laboratory mouse Generation N4+18 (01-JAN-09)   Donating Investigator Adrian Bird,   University of Edinburgh

Description
Homozygous null mice are viable and appear normal at birth. No Mecp2 gene product (mRNA or protein) is detected in tissues. Mobility problems are apparent at 3-8 weeks of age. Mice exhibit hindlimb clasping and uneven breathing. An uneven wearing of teeth associated with misalignment of the jaws is observed in 50% of the animals. Adult males do not mate and their testes remain internal although sperm are present in the cauda epididymis. Symptom progression is variable, but mice can be expected to undergo weight loss, shivering, continued mobility problems before succumbing. Expected lifespan is about 50-60 days. Heterozygous female mice display mobility problems and hindlimb clasping starting at about 6 months, but the symptoms appear not to be progressive. This mutant mouse strain represents a model that may be useful in studies related to Rett Syndrome.

Importation of this model was supported in part by the Rett Syndrome Research Foundation.

Development
A targeting vector designed to insert loxP sites around exons 3 and 4 was transfected into 129P2/OlaHsd-derived E14TG2a embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Chimeric offspring were bred to C57BL/6 mice to produce heterozygous floxed females. The floxed line was bred to homozygosity and maintained in this form. Homozygous floxed female mice were crossed with male CMVCre mice (BALB/c background) in which the Cre gene is located on the X chromosome and is ubiquitously expressed. The resulting female mice, heterozygous for the recombined allele, were mated with wild type C57BL/6 animals. Each subsequent generation of heterozygous females have been mated to inbred C57BL/6 males to maintain the line.

Control Information

	Control
	Wild-type from the colony
	000664 C57BL/6J
Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Mecp2

007177	B6.129P2-Mecp2tm1Bird/J
006849	B6.129P2-Mecp2tm2Bird/J
005439	B6.129S-Mecp2tm1Hzo/J
006847	B6;129P2-Mecp2tm1Bird/J

View Strains carrying other alleles of Mecp2     (4 strains)

Additional Web Information

JAX^® NOTES, Summer 2002; 486. New Mouse Model for Rett Syndrome.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms

Rett Syndrome; RTT - Models with phenotypic similarity to human disease where etiologies involve orthologs.1

1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

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.

Mecp2^tm1.1Bird/Mecp2⁺

        involves: 129P2/OlaHsd * C57BL/6

• behavior/neurological phenotype
• hypoactivity (MGI Ref ID J:67910)
  • although heterozygous females initially show no symptoms and raise normal litters, they acquire inertia at ages greater than 3 months
  • in an open field test, visit fewer squares, spend more time being immotile and rear less than controls, however this is not due to increased anxiety, as fecal bolus counts, grooming times and time spent in different zones of the field are similar to controls
• limb grasping (MGI Ref ID J:67910)
  • acquire hindlimb clasping at ages greater than 3 months
• respiratory system phenotype
• abnormal breathing (MGI Ref ID J:67910)
  • often exhibit breathing irregularities by 9 months of age

Mecp2^tm1.1Bird/Mecp2⁺

        involves: 129P2/OlaHsd

• nervous system phenotype
• decreased neuron number (MGI Ref ID J:108953)
  • 7-9 week old adults have 33% the number of Mecp2-expressing neurons compared to young adult wild-type
  • compared to age-matched wild-type adults, 24-95 week old heterozygotes have 68% the number of Mecp2-expressing cortical neurons; number of Mecp2-expressing neurons is significantly higher in younger mutants than in older mutants
• other phenotype
• other aberrant phenotype (MGI Ref ID J:108953)
  • X-chromosome inactivation becomes unbalance in older mutants, with a larger percentage expressing Mecp2 compared to younger mutants (>50%)

Mecp2^tm1.1Bird/Mecp2^tm1.1Bird

        involves: 129P2/OlaHsd * C57BL/6

• life span-post-weaning/aging
• premature death (MGI Ref ID J:67910)
  • variable progression of symptoms leads to rapid weight loss and death at about 54 days of age
• behavior/neurological phenotype
• abnormal gait (MGI Ref ID J:67910)
  • develop a stiff, uncoordinated gait between 3 and 8 weeks of age
• hypoactivity (MGI Ref ID J:67910)
  • exhibit reduced spontaneous movement between 3 and 8 weeks of age
• limb grasping (MGI Ref ID J:67910)
  • most mutants develop hindlimb clasping after 7 weeks of age
• growth/size phenotype
• weight loss (MGI Ref ID J:67910)
  • variable progression of symptoms leads to rapid weight loss and death at about 54 days of age
• respiratory system phenotype
• abnormal breathing (MGI Ref ID J:67910)
  • most mutants exhibit irregular breathing after 3-8 weeks of age
• craniofacial phenotype
• abnormal jaw morphology (MGI Ref ID J:67910)
  • frequently exhibit misalignment of the jaws
• abnormal tooth morphology (MGI Ref ID J:67910)
  • frequently exhibit uneven wearing of the teeth
• skeleton phenotype
• abnormal jaw morphology (MGI Ref ID J:67910)
  • frequently exhibit misalignment of the jaws
• hearing/vestibular/ear phenotype
• abnormal hearing physiology (MGI Ref ID J:67910)
  • some mutants fail to respond to sound, although neither motor defects nor sensory defects are detected

Mecp2^tm1.1Bird/Y

        involves: 129P2/OlaHsd * C57BL/6

• life span-post-weaning/aging
• premature death (MGI Ref ID J:67910)
  • variable progression of symptoms leads to rapid weight loss and death at about 54 days of age
• behavior/neurological phenotype
• abnormal gait (MGI Ref ID J:67910)
  • develop a stiff, uncoordinated gait between 3 and 8 weeks of age
• hypoactivity (MGI Ref ID J:67910)
  • exhibit reduced spontaneous movement between 3 and 8 weeks of age
• limb grasping (MGI Ref ID J:67910)
  • most mutants develop hindlimb clasping after 7 weeks of age
• growth/size phenotype
• decreased body weight (MGI Ref ID J:67910)
  • mutants mated to C57BL/6 (mixed 129P2/OlaHsd and C57BL/6 background) mice are substantially underweight from 4 weeks with full penatrance
• weight loss (MGI Ref ID J:67910)
  • variable progression of symptoms leads to rapid weight loss and death at about 54 days of age
• weight gain (MGI Ref ID J:67910)
  • mutants on the mixed 129P2/OlaHsd and C57BL/6 background mated to 129 mice are the same weight as controls until 8 weeks of age, when they gain weight and become heavier than controls with an increase in deposited fat
• respiratory system phenotype
• abnormal breathing (MGI Ref ID J:67910)
  • most mutants exhibit irregular breathing after 3-8 weeks of age
• reproductive system phenotype
• cryptorchism (MGI Ref ID J:67910)
  • testes of mutant males are always internal
• craniofacial phenotype
• abnormal jaw morphology (MGI Ref ID J:67910)
  • frequently exhibit misalignment of the jaws
• abnormal tooth morphology (MGI Ref ID J:67910)
  • frequently exhibit uneven wearing of the teeth
• endocrine/exocrine gland phenotype
• cryptorchism (MGI Ref ID J:67910)
  • testes of mutant males are always internal
• skeleton phenotype
• abnormal jaw morphology (MGI Ref ID J:67910)
  • frequently exhibit misalignment of the jaws
• hearing/vestibular/ear phenotype
• abnormal hearing physiology (MGI Ref ID J:67910)
  • some mutants fail to respond to sound, although neither motor defects nor sensory defects are detected

Mecp2^tm1.1Bird/Y

        involves: 129P2/OlaHsd * FVB

• life span-post-weaning/aging
• *normal* life span-post-weaning/aging (MGI Ref ID J:94407)
  • premature death in male Mecp2-null mice at 10-11 weeks is rescued
• behavior/neurological phenotype
• *normal* behavior/neurological phenotype (MGI Ref ID J:94407)
  • neurological abnormalities seen in single transgenic mutant are rescued by loss of Mecp2
• nervous system phenotype
• *normal* nervous system phenotype (MGI Ref ID J:126964)
  • amplitudes of EPSCs, RRP size, and mEPSC frequency, amplitude, and decay kinetics are normalized in double mutant brains compared to either single mutant brain
  • glutamatergic synaptic density is normalized in double mutant brains compared to either single mutant brain

Mecp2^tm1.1Bird/Y

        involves: 129P2/OlaHsd

• nervous system phenotype
• *normal* nervous system phenotype (MGI Ref ID J:126964)
  • no alteration in synaptic release probability is detected in neurons
• abnormal excitatory postsynaptic currents (MGI Ref ID J:126964)
  • evoked EPSC amplitudes show a 46% reduction compared to wild-type
• abnormal miniature excitatory postsynaptic currents (MGI Ref ID J:126964)
  • mEPSCs show a significant decrease in frequency compared to wild-type
• abnormal synaptic vesicle number (MGI Ref ID J:126964)
  • neurons exhibit a 41% reduction in RRP charge relative to wild-type
• decreased CNS synapse formation (MGI Ref ID J:126964)
  • in vitro, density of synaptic markers is reduced by 39%
  • in vivo, at 2 weeks postnatal, number of glutamatergic synapses is reduced by 19%; by 5 weeks, difference is no longer significant

Mecp2^tm1.1Bird/Y

        involves: 129P2/OlaHsd * C57BL/6 * CBA

• growth/size phenotype
• increased body weight (MGI Ref ID J:135824)
  • male mutants become considerably heavier than littermates after 2 months, with noticeable weight differences at 9 weeks
  • at 17 weeks, males 39.7 g vs 32.1 g in wild-type
• obese (MGI Ref ID J:135824)
  • male mice become obese with increased weight of fat pads by 14-17 weeks
• behavior/neurological phenotype
• *normal* behavior/neurological phenotype (MGI Ref ID J:135824)
  • visual placing reflex and response to a soft touch to the side of the face are normal relative to wild-type
  • olfaction and motivation to eat were normal in mutants
  • anxiety-related behaviors are similar to wild-type mice
  • ability to grip a wire and remain suspended for 1 minute is normal in mutants
• abnormal motor coordination/ balance (MGI Ref ID J:135824)
• abnormal social investigation (MGI Ref ID J:135824)
  • mutants spend less time in chamber side containing familiar mouse than in side with a stranger relative to controls, although response to introduction of stranger is similar
• limb grasping (MGI Ref ID J:135824)
  • subtle clasping is observed starting at 6 weeks of age
• adipose tissue phenotype
• increased total fat pad weight (MGI Ref ID J:135824)
  • fat pads in 14-17 week old male mice weigh 2-3 times more than wild-type

View Research Applications

Research Applications

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

Mecp2^tm1.1Bird related

Mouse/Human Gene Homologs
Rett syndrome

Neurobiology Research
Ataxia (Movement) Defects
Neurodevelopmental Defects
      Rett's syndrome

Genes & Alleles

Gene & Allele Information

Allele Symbol		Mecp2tm1.1Bird
Allele Name		targeted mutation 1.1, Adrian Bird
Allele Type		Targeted (knock-out)
Common Name(s)		MeCP2Bird;
Mutation Made By		Adrian Bird,   University of Edinburgh
Strain of Origin		129P2/OlaHsd
ES Cell Line Name		E14TG2a
ES Cell Line Strain		129P2/OlaHsd
Gene Symbol and Name		Mecp2, methyl CpG binding protein 2
Chromosome		X
Gene Common Name(s)		1500041B07Rik; AUTSX3; BB130002; D630021H01Rik; DKFZp686A24160; MRX16; MRX79; MRXS13; MRXSL; Mbd5; PPMX; RIKEN cDNA 1500041B07 gene; RIKEN cDNA D630021H01 gene; RS; RTS; RTT; WBP10; expressed sequence BB130002;
Molecular Note		Insertion of a neomycin resistance cassette into the Mecp2 gene introduced loxP sites that flank exons 3 and 4, and added an intron and polyadenylation signal from the human beta globin gene. A CMV-Cre mediated recombination event in the germline then removed exons 3 and 4. Northern blot analysis did not detect Mecp2 mRNA in tissues of mutant male mice (-/y), nor did Western blot analysis detect protein in these tissues. [MGI Ref ID J:67910]

Genotyping

Genotyping Information

Genotyping Protocols

Mecp2^tm1.1Bird, Separated PCR

Helpful Links

Genotyping resources and troubleshooting

References

References

Selected Reference(s)

Guy J; Hendrich B; Holmes M; Martin JE; Bird A. 2001. A mouse Mecp2-null mutation causes neurological symptoms that mimic Rett syndrome. Nat Genet 27(3):322-6. [PubMed: 11242117]  [MGI Ref ID J:67910]

Additional References

Braunschweig D; Simcox T; Samaco RC; LaSalle JM. 2004. X-Chromosome inactivation ratios affect wild-type MeCP2 expression within mosaic Rett syndrome and Mecp2-/+ mouse brain. Hum Mol Genet 13(12):1275-86. [PubMed: 15115765]  [MGI Ref ID J:91193]

Mecp2^tm1.1Bird related

Alvarez-Saavedra M; Saez MA; Kang D; Zoghbi HY; Young JI. 2007. Cell-specific expression of wild-type MeCP2 in mouse models of Rett syndrome yields insight about pathogenesis. Hum Mol Genet 16(19):2315-25. [PubMed: 17635839]  [MGI Ref ID J:124365]

Asaka Y; Jugloff DG; Zhang L; Eubanks JH; Fitzsimonds RM. 2006. Hippocampal synaptic plasticity is impaired in the Mecp2-null mouse model of Rett syndrome. Neurobiol Dis 21(1):217-27. [PubMed: 16087343]  [MGI Ref ID J:104545]

Belichenko NP; Belichenko PV; Mobley WC. 2009. Evidence for both neuronal cell autonomous and nonautonomous effects of methyl-CpG-binding protein 2 in the cerebral cortex of female mice with Mecp2 mutation. Neurobiol Dis 34(1):71-7. [PubMed: 19167498]  [MGI Ref ID J:147302]

Bissonnette JM; Knopp SJ. 2008. Effect of inspired oxygen on periodic breathing in methy-CpG-binding protein 2 (Mecp2) deficient mice. J Appl Physiol 104(1):198-204. [PubMed: 18006868]  [MGI Ref ID J:149046]

Bissonnette JM; Knopp SJ; Maylie J; Thong T. 2007. Autonomic cardiovascular control in methyl-CpG-binding protein 2 (Mecp2) deficient mice. Auton Neurosci 136(1-2):82-9. [PubMed: 17544925]  [MGI Ref ID J:129856]

Braunschweig D; Simcox T; Samaco RC; LaSalle JM. 2004. X-Chromosome inactivation ratios affect wild-type MeCP2 expression within mosaic Rett syndrome and Mecp2-/+ mouse brain. Hum Mol Genet 13(12):1275-86. [PubMed: 15115765]  [MGI Ref ID J:91193]

Caballero IM; Hendrich B. 2005. MeCP2 in neurons: closing in on the causes of Rett syndrome. Hum Mol Genet 14 Spec No 1:R19-26. [PubMed: 15809268]  [MGI Ref ID J:97524]

Chao HT; Zoghbi HY; Rosenmund C. 2007. MeCP2 controls excitatory synaptic strength by regulating glutamatergic synapse number. Neuron 56(1):58-65. [PubMed: 17920015]  [MGI Ref ID J:126964]

Collins AL; Levenson JM; Vilaythong AP; Richman R; Armstrong DL; Noebels JL; David Sweatt J; Zoghbi HY. 2004. Mild overexpression of MeCP2 causes a progressive neurological disorder in mice. Hum Mol Genet 13(21):2679-89. [PubMed: 15351775]  [MGI Ref ID J:94407]

Deng V; Matagne V; Banine F; Frerking M; Ohliger P; Budden S; Pevsner J; Dissen GA; Sherman LS; Ojeda SR. 2007. FXYD1 is an MeCP2 target gene overexpressed in the brains of Rett syndrome patients and Mecp2-null mice. Hum Mol Genet 16(6):640-50. [PubMed: 17309881]  [MGI Ref ID J:121717]

Fukuda T; Itoh M; Ichikawa T; Washiyama K; Goto Y. 2005. Delayed maturation of neuronal architecture and synaptogenesis in cerebral cortex of Mecp2-deficient mice. J Neuropathol Exp Neurol 64(6):537-44. [PubMed: 15977646]  [MGI Ref ID J:104939]

Horike S; Cai S; Miyano M; Cheng JF; Kohwi-Shigematsu T. 2005. Loss of silent-chromatin looping and impaired imprinting of DLX5 in Rett syndrome. Nat Genet 37(1):31-40. [PubMed: 15608638]  [MGI Ref ID J:96437]

Ide S; Itoh M; Goto Y. 2005. Defect in normal developmental increase of the brain biogenic amine concentrations in the mecp2-null mouse. Neurosci Lett 386(1):14-7. [PubMed: 15975715]  [MGI Ref ID J:102566]

Jordan C; Francke U. 2006. Ube3a expression is not altered in Mecp2 mutant mice. Hum Mol Genet 15(14):2210-5. [PubMed: 16754645]  [MGI Ref ID J:112026]

Jugloff DG; Logan R; Eubanks JH. 2006. Breeding and maintenance of an Mecp2-deficient mouse model of Rett Syndrome J Neurosci Methods 154(1-2):89-95. [PubMed: 16439027]  [MGI Ref ID J:106418]

Jugloff DG; Vandamme K; Logan R; Visanji NP; Brotchie JM; Eubanks JH. 2008. Targeted delivery of an Mecp2 transgene to forebrain neurons improves the behavior of female Mecp2-deficient mice. Hum Mol Genet 17(10):1386-96. [PubMed: 18223199]  [MGI Ref ID J:135351]

Kerr B; Alvarez-Saavedra M; Saez MA; Saona A; Young JI. 2008. Defective body-weight regulation, motor control and abnormal social interactions in Mecp2 hypomorphic mice. Hum Mol Genet 17(12):1707-17. [PubMed: 18321865]  [MGI Ref ID J:135824]

Kriaucionis S; Paterson A; Curtis J; Guy J; Macleod N; Bird A. 2006. Gene expression analysis exposes mitochondrial abnormalities in a mouse model of Rett syndrome. Mol Cell Biol 26(13):5033-42. [PubMed: 16782889]  [MGI Ref ID J:110323]

Makedonski K; Abuhatzira L; Kaufman Y; Razin A; Shemer R. 2005. MeCP2 deficiency in Rett syndrome causes epigenetic aberrations at the PWS/AS imprinting center that affects UBE3A expression. Hum Mol Genet 14(8):1049-58. [PubMed: 15757975]  [MGI Ref ID J:98000]

Martin Caballero I; Hansen J; Leaford D; Pollard S; Hendrich BD. 2009. The methyl-CpG binding proteins Mecp2, Mbd2 and Kaiso are dispensable for mouse embryogenesis, but play a redundant function in neural differentiation. PLoS ONE 4(1):e4315. [PubMed: 19177165]  [MGI Ref ID J:144819]

Medrihan L; Tantalaki E; Aramuni G; Sargsyan V; Dudanova I; Missler M; Zhang W. 2008. Early defects of GABAergic synapses in the brain stem of a MeCP2 mouse model of Rett syndrome. J Neurophysiol 99(1):112-21. [PubMed: 18032561]  [MGI Ref ID J:147675]

Metcalf BM; Mullaney BC; Johnston MV; Blue ME. 2006. Temporal shift in methyl-CpG binding protein 2 expression in a mouse model of Rett syndrome. Neuroscience 139(4):1449-60. [PubMed: 16549272]  [MGI Ref ID J:108953]

Miralves J; Magdeleine E; Kaddoum L; Brun H; Peries S; Joly E. 2007. High Levels of MeCP2 Depress MHC Class I Expression in Neuronal Cells. PLoS ONE 2(12):e1354. [PubMed: 18159237]  [MGI Ref ID J:130960]

Nan X; Hou J; Maclean A; Nasir J; Lafuente MJ; Shu X; Kriaucionis S; Bird A. 2007. Interaction between chromatin proteins MECP2 and ATRX is disrupted by mutations that cause inherited mental retardation. Proc Natl Acad Sci U S A 104(8):2709-14. [PubMed: 17296936]  [MGI Ref ID J:125897]

Nelson ED; Kavalali ET; Monteggia LM. 2006. MeCP2-dependent transcriptional repression regulates excitatory neurotransmission. Curr Biol 16(7):710-6. [PubMed: 16581518]  [MGI Ref ID J:107739]

Peddada S; Yasui DH; LaSalle JM. 2006. Inhibitors of differentiation (ID1, ID2, ID3 and ID4) genes are neuronal targets of MeCP2 that are elevated in Rett syndrome. Hum Mol Genet 15(12):2003-14. [PubMed: 16682435]  [MGI Ref ID J:112064]

Rastegar M; Hotta A; Pasceri P; Makarem M; Cheung AY; Elliott S; Park KJ; Adachi M; Jones FS; Clarke ID; Dirks P; Ellis J. 2009. MECP2 isoform-specific vectors with regulated expression for Rett syndrome gene therapy. PLoS One 4(8):e6810. [PubMed: 19710912]  [MGI Ref ID J:152398]

Roux JC; Dura E; Villard L. 2008. Tyrosine hydroxylase deficit in the chemoafferent and the sympathoadrenergic pathways of the Mecp2 deficient mouse. Neurosci Lett 447(1):82-6. [PubMed: 18834926]  [MGI Ref ID J:143308]

Russell JC; Blue ME; Johnston MV; Naidu S; Hossain MA. 2007. Enhanced cell death in MeCP2 null cerebellar granule neurons exposed to excitotoxicity and hypoxia. Neuroscience 150(3):563-74. [PubMed: 17997046]  [MGI Ref ID J:130772]

Santos M; Silva-Fernandes A; Oliveira P; Sousa N; Maciel P. 2007. Evidence for abnormal early development in a mouse model of Rett syndrome. Genes Brain Behav 6(3):277-86. [PubMed: 16848781]  [MGI Ref ID J:135089]

Saywell V; Viola A; Confort-Gouny S; Le Fur Y; Villard L; Cozzone PJ. 2006. Brain magnetic resonance study of Mecp2 deletion effects on anatomy and metabolism. Biochem Biophys Res Commun 340(3):776-83. [PubMed: 16380085]  [MGI Ref ID J:104731]

Schule B; Li HH; Fisch-Kohl C; Purmann C; Francke U. 2007. DLX5 and DLX6 expression is biallelic and not modulated by MeCP2 deficiency. Am J Hum Genet 81(3):492-506. [PubMed: 17701895]  [MGI Ref ID J:134837]

Stettner GM; Huppke P; Brendel C; Richter DW; Gartner J; Dutschmann M. 2007. Breathing dysfunctions associated with impaired control of postinspiratory activity in Mecp2-/y knockout mice. J Physiol 579(Pt 3):863-76. [PubMed: 17204503]  [MGI Ref ID J:140841]

Viemari JC; Roux JC; Tryba AK; Saywell V; Burnet H; Pena F; Zanella S; Bevengut M; Barthelemy-Requin M; Herzing LB; Moncla A; Mancini J; Ramirez JM; Villard L; Hilaire G. 2005. Mecp2 deficiency disrupts norepinephrine and respiratory systems in mice. J Neurosci 25(50):11521-30. [PubMed: 16354910]  [MGI Ref ID J:104053]

Viola A; Saywell V; Villard L; Cozzone PJ; Lutz NW. 2007. Metabolic fingerprints of altered brain growth, osmoregulation and neurotransmission in a Rett syndrome model. PLoS ONE 2(1):e157. [PubMed: 17237885]  [MGI Ref ID J:129328]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX12

Colony Maintenance

Breeding & Husbandry	Heterozygous females breed best when under 6 months of age. Coat color expected from breeding:Black
Mating System	Heterozygote x Inbred         (Female x Male)   01-MAR-06
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 approximately 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 two business days following order placement.

Supply Notes

Hemizygotes are not available as a pair, only males are available. Usually shipped between four and eight weeks of age. This strain is included in the Induced Mutant Resource Colony collection. Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	Wild-type from the colony
	000664 C57BL/6J
Considerations for Choosing Controls
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX^® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX^® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX^® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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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.