Strain Name:

B6.129P2(C)-Mecp2tm1.1Bird/J

Stock Number:

003890

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This Mecp2 KO mouse strain may have applications related to the study of Rett Syndrome. Mobility problems and a range of Rett Syndrome-like phenotypes are apparent at 3-8 weeks of age.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHeterozygote x Inbred         (Female x Male)   01-MAR-06
Specieslaboratory mouse
GenerationN4+29 (04-OCT-13)
Generation Definitions
 
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

View Strains carrying other alleles of Mecp2     (10 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 provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Rett Syndrome; RTT
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Angelman Syndrome; AS   (MECP2)
Autism, Susceptibility to, X-Linked 3; AUTSX3   (MECP2)
Encephalopathy, Neonatal Severe, Due to Mecp2 Mutations   (MECP2)
Lubs X-Linked Mental Retardation Syndrome; MRXSL   (MECP2)
Mental Retardation, X-Linked, Syndromic 13; MRXS13   (MECP2)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Mecp2tm1.1Bird/Mecp2+

        involves: 129P2/OlaHsd * C57BL/6
  • behavior/neurological phenotype
  • hypoactivity
    • although heterozygous females initially show no symptoms and raise normal litters, they acquire inertia at ages greater than 3 months   (MGI Ref ID J:67910)
    • 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   (MGI Ref ID J:67910)
  • limb grasping
    • acquire hindlimb clasping at ages greater than 3 months   (MGI Ref ID J:67910)
  • respiratory system phenotype
  • abnormal breathing pattern
    • often exhibit breathing irregularities by 9 months of age   (MGI Ref ID J:67910)

Mecp2tm1.1Bird/Mecp2+

        involves: 129P2/OlaHsd
  • nervous system phenotype
  • abnormal cerebral cortex morphology
    • decrease in the number of ATRX containing foci in null cells only   (MGI Ref ID J:194039)
  • abnormal hippocampus morphology
    • decrease in the number of ATRX containing foci in null cells only   (MGI Ref ID J:194039)
  • decreased neuron number
    • 7-9 week old adults have 33% the number of Mecp2-expressing neurons compared to young adult wild-type   (MGI Ref ID J:108953)
    • 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   (MGI Ref ID J:108953)
  • cellular phenotype
  • abnormal dosage compensation, by inactivation of X chromosome
    • X-chromosome inactivation becomes unbalance in older mutants, with a larger percentage expressing Mecp2 compared to younger mutants (>50%)   (MGI Ref ID J:108953)

Mecp2tm1.1Bird/Mecp2tm1.1Bird

        involves: 129P2/OlaHsd * C57BL/6
  • mortality/aging
  • premature death
    • variable progression of symptoms leads to rapid weight loss and death at about 54 days of age   (MGI Ref ID J:67910)
  • behavior/neurological phenotype
  • abnormal gait
    • develop a stiff, uncoordinated gait between 3 and 8 weeks of age   (MGI Ref ID J:67910)
  • hypoactivity
    • exhibit reduced spontaneous movement between 3 and 8 weeks of age   (MGI Ref ID J:67910)
  • limb grasping
    • most mutants develop hindlimb clasping after 7 weeks of age   (MGI Ref ID J:67910)
  • growth/size/body phenotype
  • abnormal tooth morphology
    • frequently exhibit uneven wearing of the teeth   (MGI Ref ID J:67910)
  • weight loss
    • variable progression of symptoms leads to rapid weight loss and death at about 54 days of age   (MGI Ref ID J:67910)
  • respiratory system phenotype
  • abnormal breathing pattern
    • most mutants exhibit irregular breathing after 3-8 weeks of age   (MGI Ref ID J:67910)
  • craniofacial phenotype
  • abnormal jaw morphology
    • frequently exhibit misalignment of the jaws   (MGI Ref ID J:67910)
  • abnormal tooth morphology
    • frequently exhibit uneven wearing of the teeth   (MGI Ref ID J:67910)
  • skeleton phenotype
  • abnormal jaw morphology
    • frequently exhibit misalignment of the jaws   (MGI Ref ID J:67910)
  • hearing/vestibular/ear phenotype
  • abnormal hearing physiology
    • some mutants fail to respond to sound, although neither motor defects nor sensory defects are detected   (MGI Ref ID J:67910)

Mecp2tm1.1Bird/Y

        involves: 129P2/OlaHsd * C57BL/6
  • mortality/aging
  • premature death
    • variable progression of symptoms leads to rapid weight loss and death at about 54 days of age   (MGI Ref ID J:67910)
  • behavior/neurological phenotype
  • abnormal locomotor activation
    • at 8 weeks of age, males show increased latency to start moving and to reach the wall of the open field apparatus   (MGI Ref ID J:165306)
    • hypoactivity
      • exhibit reduced spontaneous movement between 3 and 8 weeks of age   (MGI Ref ID J:67910)
  • abnormal locomotor coordination
    • in the gait onset test, males take longer to exit a circle at 3 and 8 weeks of age   (MGI Ref ID J:165306)
    • abnormal gait
      • develop a stiff, uncoordinated gait between 3 and 8 weeks of age   (MGI Ref ID J:67910)
      • males exhibit a greater front-base width overall and a larger hind-base width than wild-type mice by 3 weeks of age   (MGI Ref ID J:165306)
      • short stride length
        • stride length is shorter than in wild-type mice at 8 weeks of age but not at 3 weeks of age   (MGI Ref ID J:165306)
    • ataxia
      • males exhibit a greater front-base width overall and a larger hind-base width than wild-type mice by 3 weeks of age, a sign of ataxia   (MGI Ref ID J:165306)
  • limb grasping
    • most mutants develop hindlimb clasping after 7 weeks of age   (MGI Ref ID J:67910)
  • growth/size/body phenotype
  • abnormal tooth morphology
    • frequently exhibit uneven wearing of the teeth   (MGI Ref ID J:67910)
  • decreased body weight
    • mutants mated to C57BL/6 (mixed 129P2/OlaHsd and C57BL/6 background) mice are substantially underweight from 4 weeks with full penatrance   (MGI Ref ID J:67910)
    • weight loss
      • variable progression of symptoms leads to rapid weight loss and death at about 54 days of age   (MGI Ref ID J:67910)
  • increased body weight
    • 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   (MGI Ref ID J:67910)
  • respiratory system phenotype
  • abnormal breathing pattern
    • most mutants exhibit irregular breathing after 3-8 weeks of age   (MGI Ref ID J:67910)
  • reproductive system phenotype
  • cryptorchism
    • testes of mutant males are always internal   (MGI Ref ID J:67910)
  • craniofacial phenotype
  • abnormal jaw morphology
    • frequently exhibit misalignment of the jaws   (MGI Ref ID J:67910)
  • abnormal tooth morphology
    • frequently exhibit uneven wearing of the teeth   (MGI Ref ID J:67910)
  • endocrine/exocrine gland phenotype
  • cryptorchism
    • testes of mutant males are always internal   (MGI Ref ID J:67910)
  • skeleton phenotype
  • abnormal jaw morphology
    • frequently exhibit misalignment of the jaws   (MGI Ref ID J:67910)
  • hearing/vestibular/ear phenotype
  • abnormal hearing physiology
    • some mutants fail to respond to sound, although neither motor defects nor sensory defects are detected   (MGI Ref ID J:67910)
  • homeostasis/metabolism phenotype
  • abnormal noradrenaline level
    • 36% reduction in levels of norepinephrine within the vestibular nuclei   (MGI Ref ID J:165306)
    • males exhibit a 31%, 30%, and 61% decrease in norepinephrine in the prefrontal cortex at 3 weeks, the motor cortex at 3 weeks, and the cerebellum at 8 weeks of age   (MGI Ref ID J:165306)
    • mutants do not exhibit an increase in norepinephrine in the hippocampus from 3 to 8 weeks of age as seen in wild-type mice   (MGI Ref ID J:165306)
  • decreased serotonin level
    • males exhibit a 36%, 30%, and 55% decrease in 5-HT in the prefrontal cortex at 3 weeks, the motor cortex at 3 weeks, and the cerebellum at 8 weeks of age, respectively   (MGI Ref ID J:165306)
    • males exhibit a 34% and 55% decrease in the 5-HT precursor, 5-HIAA in the prefrontal cortex at 3 weeks and the cerebellum at 8 weeks of age, respectively   (MGI Ref ID J:165306)
    • 5-HT turnover is increased in the prefrontal cortex and motor cortex   (MGI Ref ID J:165306)
    • 5-HT levels are decreased in the hippocampus at 8 weeks of age but not at 3 weeks   (MGI Ref ID J:165306)
  • nervous system phenotype
  • abnormal neurotransmitter level
    • at 3 weeks of age, noradrenergic and serotonergic transmission is altered in the prefrontal and motor cortices   (MGI Ref ID J:165306)
    • during progression of disease, noradrenergic and serotonergic transmission is also altered in the hippocampus and cerebellum   (MGI Ref ID J:165306)

Mecp2tm1.1Bird/Y

        involves: 129P2/OlaHsd
  • nervous system phenotype
  • *normal* nervous system phenotype
    • no alteration in synaptic release probability is detected in neurons   (MGI Ref ID J:126964)
    • abnormal excitatory postsynaptic currents
      • evoked EPSC amplitudes show a 46% reduction compared to wild-type   (MGI Ref ID J:126964)
    • abnormal miniature excitatory postsynaptic currents
      • mEPSCs show a significant decrease in frequency compared to wild-type   (MGI Ref ID J:126964)
    • abnormal synaptic vesicle number
      • neurons exhibit a 41% reduction in RRP charge relative to wild-type   (MGI Ref ID J:126964)
    • decreased CNS synapse formation
      • in vitro, density of synaptic markers is reduced by 39%   (MGI Ref ID J:126964)
      • in vivo, at 2 weeks postnatal, number of glutamatergic synapses is reduced by 19%; by 5 weeks, difference is no longer significant   (MGI Ref ID J:126964)

Mecp2tm1.1Bird/Y

        involves: 129P2/OlaHsd * C57BL/6 * CBA
  • growth/size/body phenotype
  • increased body weight
    • male mutants become considerably heavier than littermates after 2 months, with noticeable weight differences at 9 weeks   (MGI Ref ID J:135824)
    • at 17 weeks, males 39.7 g vs 32.1 g in wild-type   (MGI Ref ID J:135824)
    • obese
      • male mice become obese with increased weight of fat pads by 14-17 weeks   (MGI Ref ID J:135824)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • visual placing reflex and response to a soft touch to the side of the face are normal relative to wild-type   (MGI Ref ID J:135824)
    • olfaction and motivation to eat were normal in mutants   (MGI Ref ID J:135824)
    • anxiety-related behaviors are similar to wild-type mice   (MGI Ref ID J:135824)
    • ability to grip a wire and remain suspended for 1 minute is normal in mutants   (MGI Ref ID J:135824)
    • abnormal motor coordination/ balance   (MGI Ref ID J:135824)
    • abnormal social investigation
      • 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   (MGI Ref ID J:135824)
    • limb grasping
      • subtle clasping is observed starting at 6 weeks of age   (MGI Ref ID J:135824)
  • adipose tissue phenotype
  • increased total fat pad weight
    • fat pads in 14-17 week old male mice weigh 2-3 times more than wild-type   (MGI Ref ID J:135824)

Mecp2tm1.1Bird/Y

        involves: 129P2/OlaHsd * C57BL/6J * FVB/N
  • behavior/neurological phenotype
  • seizures
    • electrographic seizures are measured in cultured neurons from constitutive null mice   (MGI Ref ID J:166851)
  • nervous system phenotype
  • abnormal miniature inhibitory postsynaptic currents
    • electrographic seizures are measured in cultured neurons from constitutive null mice   (MGI Ref ID J:166851)
  • abnormal nervous system electrophysiology
    • non-seizure hyperexcitability discharges are observed in recordings from in cultured neurons from constitutive null mice   (MGI Ref ID J:166851)
  • seizures
    • electrographic seizures are measured in cultured neurons from constitutive null mice   (MGI Ref ID J:166851)

Mecp2tm1.1Bird/Y

        involves: 129P2/OlaHsd * FVB
  • mortality/aging
  • premature death
    • median lifespan of 76 days   (MGI Ref ID J:194039)
  • growth/size/body phenotype
  • increased body weight
    • starting at 6 weeks of age and reaching a maximum weight by 8 weeks of age   (MGI Ref ID J:194039)
  • nervous system phenotype
  • abnormal brain development
    • brain weight peaks at 7 weeks (1 week earlier than in controls) then declines   (MGI Ref ID J:194039)
  • abnormal cerebral cortex morphology
    • decrease in the number of ATRX containing foci at 7 weeks of age and only a few foci are detected at 9 weeks of age   (MGI Ref ID J:194039)
  • abnormal hippocampus morphology
    • decrease in the number of ATRX containing foci at 7 weeks of age and only a few foci are detected at 9 weeks of age   (MGI Ref ID J:194039)
  • decreased brain weight
    • brain weight peaks at 7 weeks (1 week earlier than in controls) then declines   (MGI Ref ID J:194039)
  • behavior/neurological phenotype
  • abnormal gait
    • at all ages tested and severity increases with age   (MGI Ref ID J:194039)
  • tremors
    • at all ages tested and severity increases with age   (MGI Ref ID J:194039)
  • integument phenotype
  • disheveled coat
    • at 8 weeks of age   (MGI Ref ID J:194039)

Mecp2tm1.1Bird/Y

        involves: 129P2/OlaHsd * 129S6/SvEvTac
  • mortality/aging
  • premature death
    • however, treatment with fluvastatin improves lifespan   (MGI Ref ID J:198551)
  • behavior/neurological phenotype
  • decreased startle reflex
    • even in mice treated with fluvastatin   (MGI Ref ID J:198551)
  • hypoactivity
    • however, treatment with fluvastatin or lovastatin improves open-field activity   (MGI Ref ID J:198551)
  • impaired coordination
    • however, treatment with fluvastatin or lovastatin improves coordination   (MGI Ref ID J:198551)
  • lethargy   (MGI Ref ID J:198551)
  • limb grasping   (MGI Ref ID J:198551)
  • tremors   (MGI Ref ID J:198551)
  • homeostasis/metabolism phenotype
  • increased brain cholesterol level
    • at P56, but not P70   (MGI Ref ID J:198551)
  • increased circulating cholesterol level
    • at P56   (MGI Ref ID J:198551)
    • however, statin treatment decreases serum cholesterol concentrations   (MGI Ref ID J:198551)
    • increased circulating LDL cholesterol level
  • increased circulating triglyceride level
  • increased liver triglyceride level
    • at P56   (MGI Ref ID J:198551)
    • however, treatment with fluvastatin or lovastatin improves liver lipid levels   (MGI Ref ID J:198551)
  • craniofacial phenotype
  • malocclusion   (MGI Ref ID J:198551)
  • growth/size/body phenotype
  • decreased body weight   (MGI Ref ID J:198551)
  • liver/biliary system phenotype
  • increased liver triglyceride level
    • at P56   (MGI Ref ID J:198551)
    • however, treatment with fluvastatin or lovastatin improves liver lipid levels   (MGI Ref ID J:198551)
  • respiratory system phenotype
  • increased pulmonary respiratory rate
    • even in mice treated with fluvastatin   (MGI Ref ID J:198551)
  • skeleton phenotype
  • malocclusion   (MGI Ref ID J:198551)
  • nervous system phenotype
  • increased brain cholesterol level
    • at P56, but not P70   (MGI Ref ID J:198551)

The following phenotype relates to a compound genotype created using this strain.
Contact JAX® Services jaxservices@jax.org for customized breeding options.

Mecp2tm1.1Bird/Y Tg(MECP2)1Hzo/0

        involves: 129P2/OlaHsd * FVB
  • mortality/aging
  • *normal* mortality/aging
    • premature death in male Mecp2-null mice at 10-11 weeks is rescued   (MGI Ref ID J:94407)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • neurological abnormalities seen in single transgenic mutant are rescued by loss of Mecp2   (MGI Ref ID J:94407)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • amplitudes of EPSCs, RRP size, and mEPSC frequency, amplitude, and decay kinetics are normalized in double mutant brains compared to either single mutant brain   (MGI Ref ID J:126964)
    • glutamatergic synaptic density is normalized in double mutant brains compared to either single mutant brain   (MGI Ref ID J:126964)
View Research Applications

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

Mecp2tm1.1Bird related

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

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Mecp2tm1.1Bird
Allele Name targeted mutation 1.1, Adrian Bird
Allele Type Targeted (Null/Knockout)
Common Name(s) MeCP2Bird; Mecp2-; Mecp2tm1+1Bird; Mecp2tm1-1Bird;
Mutation Made By Adrian Bird,   University of Edinburgh
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14TG2a
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Mecp2, methyl CpG binding protein 2
Chromosome X
Gene Common Name(s) 1500041B07Rik; AUTSX3; BB130002; D630021H01Rik; 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

Mecp2tm1.1Bird-PROBE, QPCR
Mecp2tm1.1Bird, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

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]

Samaco RC; McGraw CM; Ward CS; Sun Y; Neul JL; Zoghbi HY. 2013. Female Mecp2+/- mice display robust behavioral deficits on two different genetic backgrounds providing a framework for pre-clinical studies. Hum Mol Genet 22(1):96-109. [PubMed: 23026749]  [MGI Ref ID J:189576]

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]

Mecp2tm1.1Bird related

Abdala AP; Dutschmann M; Bissonnette JM; Paton JF. 2010. Correction of respiratory disorders in a mouse model of Rett syndrome. Proc Natl Acad Sci U S A 107(42):18208-13. [PubMed: 20921395]  [MGI Ref ID J:165539]

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]

Baker SA; Chen L; Wilkins AD; Yu P; Lichtarge O; Zoghbi HY. 2013. An AT-Hook Domain in MeCP2 Determines the Clinical Course of Rett Syndrome and Related Disorders. Cell 152(5):984-96. [PubMed: 23452848]  [MGI Ref ID J:194039]

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]

Berghoff EG; Clark MF; Chen S; Cajigas I; Leib DE; Kohtz JD. 2013. Evf2 (Dlx6as) lncRNA regulates ultraconserved enhancer methylation and the differential transcriptional control of adjacent genes. Development 140(21):4407-16. [PubMed: 24089468]  [MGI Ref ID J:204597]

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]

Blue ME; Kaufmann WE; Bressler J; Eyring C; O'driscoll C; Naidu S; Johnston MV. 2011. Temporal and Regional Alterations in NMDA Receptor Expression in Mecp2-Null Mice. Anat Rec (Hoboken) 294(10):1624-34. [PubMed: 21901842]  [MGI Ref ID J:176669]

Braun S; Kottwitz D; Nuber UA. 2012. Pharmacological interference with the glucocorticoid system influences symptoms and lifespan in a mouse model of Rett syndrome. Hum Mol Genet 21(8):1673-80. [PubMed: 22186023]  [MGI Ref ID J:181897]

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]

Buchovecky CM; Turley SD; Brown HM; Kyle SM; McDonald JG; Liu B; Pieper AA; Huang W; Katz DM; Russell DW; Shendure J; Justice MJ. 2013. A suppressor screen in Mecp2 mutant mice implicates cholesterol metabolism in Rett Syndrome Nat Genet 45(9):1013-20. [PubMed: 23892605]  [MGI Ref ID J:198551]

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]

Castro J; Garcia RI; Kwok S; Banerjee A; Petravicz J; Woodson J; Mellios N; Tropea D; Sur M. 2014. Functional recovery with recombinant human IGF1 treatment in a mouse model of Rett Syndrome. Proc Natl Acad Sci U S A 111(27):9941-6. [PubMed: 24958891]  [MGI Ref ID J:212165]

Chahrour M; Jung SY; Shaw C; Zhou X; Wong ST; Qin J; Zoghbi HY. 2008. MeCP2, a key contributor to neurological disease, activates and represses transcription. Science 320(5880):1224-9. [PubMed: 18511691]  [MGI Ref ID J:136439]

Chao HT; Chen H; Samaco RC; Xue M; Chahrour M; Yoo J; Neul JL; Gong S; Lu HC; Heintz N; Ekker M; Rubenstein JL; Noebels JL; Rosenmund C; Zoghbi HY. 2010. Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes. Nature 468(7321):263-9. [PubMed: 21068835]  [MGI Ref ID J:166851]

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]

D'Cruz JA; Wu C; Zahid T; El-Hayek Y; Zhang L; Eubanks JH. 2010. Alterations of cortical and hippocampal EEG activity in MeCP2-deficient mice. Neurobiol Dis 38(1):8-16. [PubMed: 20045053]  [MGI Ref ID J:159940]

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]

Deogracias R; Yazdani M; Dekkers MP; Guy J; Ionescu MC; Vogt KE; Barde YA. 2012. Fingolimod, a sphingosine-1 phosphate receptor modulator, increases BDNF levels and improves symptoms of a mouse model of Rett syndrome. Proc Natl Acad Sci U S A 109(35):14230-5. [PubMed: 22891354]  [MGI Ref ID J:188569]

Derecki NC; Cronk JC; Lu Z; Xu E; Abbott SB; Guyenet PG; Kipnis J. 2012. Wild-type microglia arrest pathology in a mouse model of Rett syndrome. Nature 484(7392):105-9. [PubMed: 22425995]  [MGI Ref ID J:183878]

Durand S; Patrizi A; Quast KB; Hachigian L; Pavlyuk R; Saxena A; Carninci P; Hensch TK; Fagiolini M. 2012. NMDA receptor regulation prevents regression of visual cortical function in the absence of Mecp2. Neuron 76(6):1078-90. [PubMed: 23259945]  [MGI Ref ID J:197657]

Ebert DH; Gabel HW; Robinson ND; Kastan NR; Hu LS; Cohen S; Navarro AJ; Lyst MJ; Ekiert R; Bird AP; Greenberg ME. 2013. Activity-dependent phosphorylation of MeCP2 threonine 308 regulates interaction with NCoR. Nature 499(7458):341-5. [PubMed: 23770587]  [MGI Ref ID J:204723]

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]

Gantz SC; Ford CP; Neve KA; Williams JT. 2011. Loss of mecp2 in substantia nigra dopamine neurons compromises the nigrostriatal pathway. J Neurosci 31(35):12629-37. [PubMed: 21880923]  [MGI Ref ID J:176217]

Gonzales ML; Adams S; Dunaway KW; LaSalle JM. 2012. Phosphorylation of distinct sites in MeCP2 modifies cofactor associations and the dynamics of transcriptional regulation. Mol Cell Biol 32(14):2894-903. [PubMed: 22615490]  [MGI Ref ID J:186652]

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]

Isoda K; Morimoto M; Matsui F; Hasegawa T; Tozawa T; Morioka S; Chiyonobu T; Nishimura A; Yoshimoto K; Hosoi H. 2010. Postnatal changes in serotonergic innervation to the hippocampus of methyl-CpG-binding protein 2-null mice. Neuroscience 165(4):1254-60. [PubMed: 19932741]  [MGI Ref ID J:159547]

Itoh M; Tahimic CG; Ide S; Otsuki A; Sasaoka T; Noguchi S; Oshimura M; Goto Y; Kurimasa A. 2012. Methyl CpG-binding protein isoform MeCP2_e2 is dispensable for Rett syndrome phenotypes but essential for embryo viability and placenta development. J Biol Chem 287(17):13859-67. [PubMed: 22375006]  [MGI Ref ID J:184364]

Jin X; Cui N; Zhong W; Jin XT; Jiang C. 2013. GABAergic synaptic inputs of locus coeruleus neurons in wild-type and Mecp2-null mice. Am J Physiol Cell Physiol 304(9):C844-57. [PubMed: 23392116]  [MGI Ref ID J:198005]

Jin X; Zhong W; Jiang C. 2013. Time-dependent modulation of GABA(A)-ergic synaptic transmission by allopregnanolone in locus coeruleus neurons of Mecp2-null mice. Am J Physiol Cell Physiol 305(11):C1151-60. [PubMed: 24067915]  [MGI Ref ID J:210196]

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]

Kerr B; Silva PA; Walz K; Young JI. 2010. Unconventional transcriptional response to environmental enrichment in a mouse model of Rett syndrome. PLoS One 5(7):e11534. [PubMed: 20634955]  [MGI Ref ID J:163111]

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]

Kron M; Muller M. 2010. Impaired hippocampal Ca2+ homeostasis and concomitant K+ channel dysfunction in a mouse model of Rett syndrome during anoxia. Neuroscience 171(1):300-15. [PubMed: 20732392]  [MGI Ref ID J:169732]

Liao W; Gandal MJ; Ehrlichman RS; Siegel SJ; Carlson GC. 2012. MeCP2+/- mouse model of RTT reproduces auditory phenotypes associated with Rett syndrome and replicate select EEG endophenotypes of autism spectrum disorder. Neurobiol Dis 46(1):88-92. [PubMed: 22249109]  [MGI Ref ID J:182312]

Lioy DT; Garg SK; Monaghan CE; Raber J; Foust KD; Kaspar BK; Hirrlinger PG; Kirchhoff F; Bissonnette JM; Ballas N; Mandel G. 2011. A role for glia in the progression of Rett's syndrome. Nature 475(7357):497-500. [PubMed: 21716289]  [MGI Ref ID J:174777]

Macdonald JL; Verster A; Berndt A; Roskams AJ. 2010. MBD2 and MeCP2 regulate distinct transitions in the stage-specific differentiation of olfactory receptor neurons. Mol Cell Neurosci 44(1):55-67. [PubMed: 20188178]  [MGI Ref ID J:164144]

Maezawa I; Jin LW. 2010. Rett syndrome microglia damage dendrites and synapses by the elevated release of glutamate. J Neurosci 30(15):5346-56. [PubMed: 20392956]  [MGI Ref ID J:159848]

Maezawa I; Swanberg S; Harvey D; LaSalle JM; Jin LW. 2009. Rett syndrome astrocytes are abnormal and spread MeCP2 deficiency through gap junctions. J Neurosci 29(16):5051-61. [PubMed: 19386901]  [MGI Ref ID J:158156]

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]

McCauley MD; Wang T; Mike E; Herrera J; Beavers DL; Huang TW; Ward CS; Skinner S; Percy AK; Glaze DG; Wehrens XH; Neul JL. 2011. Pathogenesis of lethal cardiac arrhythmias in Mecp2 mutant mice: implication for therapy in Rett syndrome. Sci Transl Med 3(113):113ra125. [PubMed: 22174313]  [MGI Ref ID J:183640]

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]

Mellen M; Ayata P; Dewell S; Kriaucionis S; Heintz N. 2012. MeCP2 binds to 5hmC enriched within active genes and accessible chromatin in the nervous system. Cell 151(7):1417-30. [PubMed: 23260135]  [MGI Ref ID J:193327]

Mellios N; Woodson J; Garcia RI; Crawford B; Sharma J; Sheridan SD; Haggarty SJ; Sur M. 2014. beta2-Adrenergic receptor agonist ameliorates phenotypes and corrects microRNA-mediated IGF1 deficits in a mouse model of Rett syndrome. Proc Natl Acad Sci U S A 111(27):9947-52. [PubMed: 24958851]  [MGI Ref ID J:212180]

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]

Mironov SL; Skorova E; Hartelt N; Mironova LA; Hasan MT; Kugler S. 2009. Remodelling of the respiratory network in a mouse model of Rett syndrome depends on brain-derived neurotrophic factor regulated slow calcium buffering. J Physiol 587(Pt 11):2473-85. [PubMed: 19359374]  [MGI Ref ID J:176540]

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]

Noutel J; Hong YK; Leu B; Kang E; Chen C. 2011. Experience-dependent retinogeniculate synapse remodeling is abnormal in MeCP2-deficient mice. Neuron 70(1):35-42. [PubMed: 21482354]  [MGI Ref ID J:174711]

Panayotis N; Pratte M; Borges-Correia A; Ghata A; Villard L; Roux JC. 2011. Morphological and functional alterations in the substantia nigra pars compacta of the Mecp2-null mouse. Neurobiol Dis 41(2):385-97. [PubMed: 20951208]  [MGI Ref ID J:168648]

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]

Pitcher MR; Ward CS; Arvide EM; Chapleau CA; Pozzo-Miller L; Hoeflich A; Sivaramakrishnan M; Saenger S; Metzger F; Neul JL. 2013. Insulinotropic treatments exacerbate metabolic syndrome in mice lacking MeCP2 function. Hum Mol Genet 22(13):2626-33. [PubMed: 23462290]  [MGI Ref ID J:198235]

Pratte M; Panayotis N; Ghata A; Villard L; Roux JC. 2011. Progressive motor and respiratory metabolism deficits in post-weaning Mecp2-null male mice. Behav Brain Res 216(1):313-20. [PubMed: 20713094]  [MGI Ref ID J:165732]

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]

Roux JC; Zala D; Panayotis N; Borges-Correia A; Saudou F; Villard L. 2012. Modification of Mecp2 dosage alters axonal transport through the Huntingtin/Hap1 pathway. Neurobiol Dis 45(2):786-95. [PubMed: 22127389]  [MGI Ref ID J:182049]

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]

Samaco RC; Mandel-Brehm C; Chao HT; Ward CS; Fyffe-Maricich SL; Ren J; Hyland K; Thaller C; Maricich SM; Humphreys P; Greer JJ; Percy A; Glaze DG; Zoghbi HY; Neul JL. 2009. Loss of MeCP2 in aminergic neurons causes cell-autonomous defects in neurotransmitter synthesis and specific behavioral abnormalities. Proc Natl Acad Sci U S A :. [PubMed: 20007372]  [MGI Ref ID J:155808]

Samaco RC; Mandel-Brehm C; McGraw CM; Shaw CA; McGill BE; Zoghbi HY. 2012. Crh and Oprm1 mediate anxiety-related behavior and social approach in a mouse model of MECP2 duplication syndrome. Nat Genet 44(2):206-11. [PubMed: 22231481]  [MGI Ref ID J:181213]

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]

Santos M; Summavielle T; Teixeira-Castro A; Silva-Fernandes A; Duarte-Silva S; Marques F; Martins L; Dierssen M; Oliveira P; Sousa N; Maciel P. 2010. Monoamine deficits in the brain of methyl-CpG binding protein 2 null mice suggest the involvement of the cerebral cortex in early stages of Rett syndrome. Neuroscience 170(2):453-67. [PubMed: 20633611]  [MGI Ref ID J:165306]

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]

Singleton MK; Gonzales ML; Leung KN; Yasui DH; Schroeder DI; Dunaway K; LaSalle JM. 2011. MeCP2 is required for global heterochromatic and nucleolar changes during activity-dependent neuronal maturation. Neurobiol Dis 43(1):190-200. [PubMed: 21420494]  [MGI Ref ID J:174326]

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]

Szulwach KE; Li X; Li Y; Song CX; Wu H; Dai Q; Irier H; Upadhyay AK; Gearing M; Levey AI; Vasanthakumar A; Godley LA; Chang Q; Cheng X; He C; Jin P. 2011. 5-hmC-mediated epigenetic dynamics during postnatal neurodevelopment and aging. Nat Neurosci 14(12):1607-16. [PubMed: 22037496]  [MGI Ref ID J:180327]

Vermehren-Schmaedick A; Jenkins VK; Knopp SJ; Balkowiec A; Bissonnette JM. 2012. Acute intermittent hypoxia-induced expression of brain-derived neurotrophic factor is disrupted in the brainstem of methyl-CpG-binding protein 2 null mice. Neuroscience 206:1-6. [PubMed: 22297041]  [MGI Ref ID J:184632]

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]

Voituron N; Zanella S; Menuet C; Dutschmann M; Hilaire G. 2009. Early breathing defects after moderate hypoxia or hypercapnia in a mouse model of Rett syndrome. Respir Physiol Neurobiol 168(1-2):109-18. [PubMed: 19524074]  [MGI Ref ID J:155642]

Wang IT; Reyes AR; Zhou Z. 2013. Neuronal morphology in MeCP2 mouse models is intrinsically variable and depends on age, cell type, and Mecp2 mutation. Neurobiol Dis 58C:3-12. [PubMed: 23659895]  [MGI Ref ID J:197982]

Ward CS; Arvide EM; Huang TW; Yoo J; Noebels JL; Neul JL. 2011. MeCP2 Is Critical within HoxB1-Derived Tissues of Mice for Normal Lifespan. J Neurosci 31(28):10359-70. [PubMed: 21753013]  [MGI Ref ID J:174516]

Wither RG; Lang M; Zhang L; Eubanks JH. 2013. Regional MeCP2 expression levels in the female MeCP2-deficient mouse brain correlate with specific behavioral impairments. Exp Neurol 239:49-59. [PubMed: 23022455]  [MGI Ref ID J:196997]

Wood L; Shepherd GM. 2010. Synaptic circuit abnormalities of motor-frontal layer 2/3 pyramidal neurons in a mutant mouse model of Rett syndrome. Neurobiol Dis 38(2):281-7. [PubMed: 20138994]  [MGI Ref ID J:159917]

Yazdani M; Deogracias R; Guy J; Poot RA; Bird A; Barde YA. 2012. Disease modeling using embryonic stem cells: MeCP2 regulates nuclear size and RNA synthesis in neurons. Stem Cells 30(10):2128-39. [PubMed: 22865604]  [MGI Ref ID J:194651]

Zhang X; Cui N; Wu Z; Su J; Tadepalli JS; Sekizar S; Jiang C. 2010. Intrinsic membrane properties of locus coeruleus neurons in Mecp2-null mice. Am J Physiol Cell Physiol 298(3):C635-46. [PubMed: 20042730]  [MGI Ref ID J:157650]

Zhang X; Su J; Cui N; Gai H; Wu Z; Jiang C. 2011. The disruption of central CO2 chemosensitivity in a mouse model of Rett syndrome. Am J Physiol Cell Physiol 301(3):C729-38. [PubMed: 21307341]  [MGI Ref ID J:175673]

Zhang X; Su J; Rojas A; Jiang C. 2010. Pontine norepinephrine defects in Mecp2-null mice involve deficient expression of dopamine beta-hydroxylase but not a loss of catecholaminergic neurons. Biochem Biophys Res Commun 394(2):285-90. [PubMed: 20193660]  [MGI Ref ID J:158815]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryHeterozygous females breed best when under 6 months of age. Coat color expected from breeding:Black
Mating SystemHeterozygote x Inbred         (Female x Male)   01-MAR-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $199.90MaleHemizygous for Mecp2tm1.1Bird  
$199.90FemaleHeterozygous for Mecp2tm1.1Bird  
Price per Pair (US dollars $)Pair Genotype
$220.95Heterozygous for Mecp2tm1.1Bird x C57BL/6J (000664)  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Supply Notes

  • Hemizygous males are only available as individual mice and are not included as a component of a pair.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $259.90MaleHemizygous for Mecp2tm1.1Bird  
$259.90FemaleHeterozygous for Mecp2tm1.1Bird  
Price per Pair (US dollars $)Pair Genotype
$287.30Heterozygous for Mecp2tm1.1Bird x C57BL/6J (000664)  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Supply Notes

  • Hemizygous males are only available as individual mice and are not included as a component of a pair.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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" 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.

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