Overview

Also Known As:Mecp2^-

This Mecp2 knockout strain is a mouse model of human Rett Syndrome. Mecp2-deficient males (Mecp2^-/Y) exhibit mobility problems and a range of Rett Syndrome-like characteristics at 3-8 weeks of age. Heterozygous females exhibit a much later onset (~6 months of age).

Our preclinical efficacy testing services offer scientific expertise and an array of target-based and phenotype-based outcome measures, both in vivo and at endpoint, for flexible study designs and assay development in mouse models of Rett Syndrome. See our full service platform.

Donating Investigator

Adrian Bird, University of Edinburgh

Genetic overview

Genetic Background	Generation
	N4+N36pN1 (2021-07-16 00:00:00)

Mecp2^tm1.1Bird

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Mecp2	methyl CpG binding protein 2

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Research Applications

Neurobiology Research
Mouse/Human Gene Homologs

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Base Price

Starting at:

$205.90 Domestic price for female 4-week

232.12 Domestic price for breeder pair

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Details

Detailed Description

The Mecp2 knockout mutation is X-linked; therefore the Mecp2-deficient mice are Mecp2^-/- (homozygous) females and Mecp2^-/Y (hemizygous) males.
Mecp2 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 approximately 50-60 days.
Heterozygous female mice display mobility problems and hindlimb clasping starting at about 6 months, but the symptoms are reported not to be progressive.
This Mecp2 knockout strain is useful for studying Rett Syndrome.

The Jackson Laboratory maintains this strain by breeding females heterozygous for the X-linked Mecp2 knockout mutation with C57BL/6J males. It has been our experience that less than 1% of all offspring genotype as "homozygous" females (120 of 36,437 females; July 2020). A cohort of "homozygous" females examined for karyotype were found to be XO. In general, the "homozygous" females present much the same as hemizygous males, with obesity, hind limb clasping, gradual decline in hind limb mobility and death between 50-100 days of age. In addition, rare instances of obese heterozygous females have also been noted in the colony, which could possibly represent the same phenomenon. When identified in our colony, "homozygous" females are removed and the breeding unit that produced it is discontinued. Furthermore, heterozygous females commonly exhibit seizures which are sometimes fatal.

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

Development

A targeting vector was designed to insert loxP sites around exons 3 and 4 of the methyl CpG binding protein 2 gene (Mecp2) on the X chromosome. The construct 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 CMV-Cre 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 germline recombined null 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 Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

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):322-6PubMed: 11242117 MGI: 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):96-109PubMed: 23026749 MGI: J:189576

View All References

Genetics

Mecp2^tm1.1Bird

Allele Symbol: Mecp2^tm1.1Bird

Allele Name	targeted mutation 1.1, Adrian Bird
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Mecp2^-; MeCP2^Bird; Mecp2^tm1+1Bird; Mecp2^tm1-1Bird
Gene Symbol and Name	Mecp2, methyl CpG binding protein 2
Gene Synonym(s)
Strain of Origin	129P2/OlaHsd
Chromosome	X
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.
Mutations Made By	Adrian Bird, University of Edinburgh

Disease/Phenotype

Disease Terms

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

Research Areas By Phenotype

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

Genotype: Mecp2^tm1.1Bird related

Neurobiology Research
- Neurodevelopmental Defects
  - Rett's syndrome
- Ataxia (Movement) Defects
Mouse/Human Gene Homologs
- Rett syndrome

Mammalian Phenotype Terms by Genotype

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

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * 129S6/SvEvTac

behavior/neurological phenotype

decreased startle reflex
- even in mice treated with fluvastatin

lethargy

impaired coordination
- Normal - however, treatment with fluvastatin or lovastatin improves coordination

limb grasping

tremors

hypoactivity
- Normal - however, treatment with fluvastatin or lovastatin improves open-field activity

homeostasis/metabolism phenotype

increased circulating LDL cholesterol level
- at P56

increased brain cholesterol level
- at P56, but not P70

increased liver triglyceride level
- Normal - however, treatment with fluvastatin or lovastatin improves liver lipid levels
- at P56

increased circulating triglyceride level
- at P56

increased circulating cholesterol level
- at P56
- Normal - however, statin treatment decreases serum cholesterol concentrations

liver/biliary system phenotype

increased liver triglyceride level
- Normal - however, treatment with fluvastatin or lovastatin improves liver lipid levels
- at P56

mortality/aging

premature death
- Normal - however, treatment with fluvastatin improves lifespan

nervous system phenotype

increased brain cholesterol level
- at P56, but not P70

respiratory system phenotype

increased pulmonary respiratory rate
- even in mice treated with fluvastatin

skeleton phenotype

malocclusion

craniofacial phenotype

malocclusion

growth/size/body region phenotype

malocclusion

decreased body weight

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd

mammalian phenotype

nervous system phenotype
- Normal - no alteration in synaptic release probability is detected in neurons

nervous system phenotype

abnormal hippocampus physiology
- at P40, hippocampal NOVA1 (neuro-oncological ventral antigen 1) mRNA and protein levels are significantly upregulated relative to those in wild-type controls

abnormal miniature excitatory postsynaptic currents
- mEPSCs show a significant decrease in frequency compared to wild-type

abnormal excitatory postsynaptic currents
- evoked EPSC amplitudes show a 46% reduction compared to wild-type

decreased CNS synapse formation
- 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

abnormal synaptic vesicle number
- neurons exhibit a 41% reduction in RRP charge relative to wild-type

abnormal nervous system physiology
- neurospecific isoforms of lysine (K)-specific demethylase 1A (KDM1A, also known as LSD1) are significantly upregulated in the hippocampus, cerebellum and cortex, along with a corresponding decrease in the ubiquitous KDM1A isoforms, suggesting that NOVA1-mediated upregulation of neurospecific KDM1A isoforms could be causally linked to hyperexcitability

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * C57BL/6 * CBA

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

behavior/neurological phenotype

abnormal motor coordination/balance

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

limb grasping
- subtle clasping is observed starting at 6 weeks of age

growth/size/body region phenotype

increased body weight
- 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
- male mice become obese with increased weight of fat pads by 14-17 weeks

mammalian phenotype

behavior/neurological phenotype
- Normal - anxiety-related behaviors are similar to wild-type mice
- Normal - visual placing reflex and response to a soft touch to the side of the face are normal relative to wild-type
- Normal - ability to grip a wire and remain suspended for 1 minute is normal in mutants
- Normal - olfaction and motivation to eat were normal in mutants

Genotype: Mecp2^tm1.1Bird/Mecp2^tm1.1Bird
involves: 129P2/OlaHsd * C57BL/6

respiratory system phenotype

abnormal breathing pattern
- most mutants exhibit irregular breathing after 3-8 weeks of age

skeleton phenotype

abnormal jaw morphology
- frequently exhibit misalignment of the jaws

abnormal tooth morphology
- frequently exhibit uneven wearing of the teeth

behavior/neurological phenotype

hypoactivity
- exhibit reduced spontaneous movement between 3 and 8 weeks of age

limb grasping
- most mutants develop hindlimb clasping after 7 weeks of age

abnormal gait
- develop a stiff, uncoordinated gait between 3 and 8 weeks of age

craniofacial phenotype

abnormal tooth morphology
- frequently exhibit uneven wearing of the teeth

abnormal jaw morphology
- frequently exhibit misalignment of the jaws

growth/size/body region phenotype

weight loss
- variable progression of symptoms leads to rapid weight loss and death at about 54 days of age

abnormal tooth morphology
- frequently exhibit uneven wearing of the teeth

hearing/vestibular/ear phenotype

abnormal hearing physiology
- some mutants fail to respond to sound, although neither motor defects nor sensory defects are detected

mortality/aging

premature death
- variable progression of symptoms leads to rapid weight loss and death at about 54 days of age

Genotype: Mecp2^tm1.1Bird/Mecp2⁺
involves: 129P2/OlaHsd * C57BL/6

behavior/neurological phenotype

limb grasping
- acquire hindlimb clasping at ages greater than 3 months

hypoactivity
- ols
- 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
- although heterozygous females initially show no symptoms and raise normal litters, they acquire inertia at ages greater than 3 months

respiratory system phenotype

abnormal breathing pattern
- often exhibit breathing irregularities by 9 months of age

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * C57BL/6

craniofacial phenotype

abnormal tooth morphology
- frequently exhibit uneven wearing of the teeth

abnormal jaw morphology
- frequently exhibit misalignment of the jaws

endocrine/exocrine gland phenotype

cryptorchism
- testes of mutant males are always internal

growth/size/body region phenotype

increased body weight
- Background Sensitivity - 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

decreased body weight
- Background Sensitivity - mutants mated to C57BL/6 (mixed 129P2/OlaHsd and C57BL/6 background) mice are substantially underweight from 4 weeks with full penatrance

abnormal tooth morphology
- frequently exhibit uneven wearing of the teeth

weight loss
- variable progression of symptoms leads to rapid weight loss and death at about 54 days of age

hearing/vestibular/ear phenotype

abnormal hearing physiology
- some mutants fail to respond to sound, although neither motor defects nor sensory defects are detected

homeostasis/metabolism phenotype

decreased noradrenaline level
- 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
- mutants do not exhibit an increase in norepinephrine in the hippocampus from 3 to 8 weeks of age as seen in wild-type mice
- 36% reduction in levels of norepinephrine within the vestibular nuclei

decreased serotonin level
- 5-HT turnover is increased in the prefrontal cortex and motor cortex
- 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
- 5-HT levels are decreased in the hippocampus at 8 weeks of age but not at 3 weeks
- 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

mortality/aging

premature death
- variable progression of symptoms leads to rapid weight loss and death at about 54 days of age

nervous system phenotype

abnormal neurotransmitter level
- during progression of disease, noradrenergic and serotonergic transmission is also altered in the hippocampus and cerebellum
- at 3 weeks of age, noradrenergic and serotonergic transmission is altered in the prefrontal and motor cortices

decreased noradrenaline level
- 36% reduction in levels of norepinephrine within the vestibular nuclei
- 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
- mutants do not exhibit an increase in norepinephrine in the hippocampus from 3 to 8 weeks of age as seen in wild-type mice

decreased serotonin level
- 5-HT levels are decreased in the hippocampus at 8 weeks of age but not at 3 weeks
- 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
- 5-HT turnover is increased in the prefrontal cortex and motor cortex
- 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

reproductive system phenotype

cryptorchism
- testes of mutant males are always internal

respiratory system phenotype

abnormal breathing pattern
- most mutants exhibit irregular breathing after 3-8 weeks of age

skeleton phenotype

abnormal jaw morphology
- frequently exhibit misalignment of the jaws

abnormal tooth morphology
- frequently exhibit uneven wearing of the teeth

behavior/neurological phenotype

abnormal locomotor coordination
- in the gait onset test, males take longer to exit a circle at 3 and 8 weeks of age

limb grasping
- most mutants develop hindlimb clasping after 7 weeks of age

short stride length
- stride length is shorter than in wild-type mice at 8 weeks of age but not at 3 weeks of age

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

abnormal gait
- develop a stiff, uncoordinated gait between 3 and 8 weeks of age
- males exhibit a greater front-base width overall and a larger hind-base width than wild-type mice by 3 weeks of age

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

hypoactivity
- exhibit reduced spontaneous movement between 3 and 8 weeks of age

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * FVB

behavior/neurological phenotype

abnormal gait
- at all ages tested and severity increases with age

tremors
- at all ages tested and severity increases with age

growth/size/body region phenotype

increased body weight
- starting at 6 weeks of age and reaching a maximum weight by 8 weeks of age

integument phenotype

disheveled coat
- at 8 weeks of age

mortality/aging

premature death
- median lifespan of 76 days

nervous system phenotype

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

abnormal brain development
- brain weight peaks at 7 weeks (1 week earlier than in controls) then declines

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

decreased brain weight
- brain weight peaks at 7 weeks (1 week earlier than in controls) then declines

Genotype: Mecp2^tm1.1Bird/Mecp2⁺
involves: 129P2/OlaHsd

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%)

nervous system phenotype

abnormal hippocampus morphology
- decrease in the number of ATRX containing foci in null cells only

decreased neuron number
- 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
- 7-9 week old adults have 33% the number of Mecp2-expressing neurons compared to young adult wild-type

abnormal cerebral cortex morphology
- decrease in the number of ATRX containing foci in null cells only

Genotype: Mecp2^tm1.1Bird/Y Tg(MECP2)1Hzo/0
involves: 129P2/OlaHsd * FVB

mammalian phenotype

mortality/aging
- Normal - premature death in male Mecp2-null mice at 10-11 weeks is rescued

behavior/neurological phenotype
- Normal - neurological abnormalities seen in single transgenic mutant are rescued by loss of Mecp2

nervous system phenotype
- Normal - glutamatergic synaptic density is normalized in double mutant brains compared to either single mutant brain
- Normal - amplitudes of EPSCs, RRP size, and mEPSC frequency, amplitude, and decay kinetics are normalized in double mutant brains compared to either single mutant brain

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * C57BL/6J * FVB/N

behavior/neurological phenotype

seizures
- electrographic seizures are measured in cultured neurons from constitutive null mice

nervous system phenotype

seizures
- electrographic seizures are measured in cultured neurons from constitutive null mice

abnormal miniature inhibitory postsynaptic currents
- electrographic seizures are measured in cultured neurons from constitutive null mice

abnormal nervous system electrophysiology
- non-seizure hyperexcitability discharges are observed in recordings from in cultured neurons from constitutive null mice

The following phenotype relates to a compound genotype created using this strain

Genotype: Mecp2^tm1.1Bird/Y
B6.129P2(C)-Mecp2/J

behavior/neurological phenotype

hypoactivity
- mice exhibit decreased activity levels during the light cycle but not the dark cycle

homeostasis/metabolism phenotype

decreased body temperature
- mice exhibit decreased temperature during both light and dark cycles

nervous system phenotype

abnormal sympathetic nervous system physiology
- mice have a blunted response to either sympathetic blockade with propranolol or activation with isoproterenol

abnormal parasympathetic nervous system physiology
- mice are sensitive to parasympathetic blockade with atropine but have a blunted response to parasympathetic activation with carbachol, indicating excessive parasympathetic tone

cardiovascular system phenotype

irregular heartbeat
- 2 month old males present with a variety of spontaneous cardiac arrhythmias ranging from sinus pauses and atrioventricular block to aberrant ventricular contractions
- treatment with atropine results in a drop in the frequency of arrhythmias
- treatment with propranolol does not decrease heart rate but increases sinus pauses
- treatment with both atropine and propranolol decreases the rate of sinus pauses but has little effect on the overall heart rate
- treatment with isoproterenol decreases the rate of sinus pauses
- treatment with propranolol or carbachol does not reduce the rate of sinus pauses
- 2-3 month old males exhibit erratic heart rate patterns, with sudden pauses in the regular rhythm of the heart rate and bradycardic events

ventricular premature beat
- 2 month old males are susceptible to premature ventricular contractions

atrioventricular block
- atrioventricular block is seen at a higher rate in 2 month old males

decreased heart rate
- males show decreased heart rate during both the light and dark periods and have a higher incidence of sudden bradycardic events
- the initial heart rate increase seen in wild-type mice after saline injection is blunted in mutants

increased heart rate variability

References

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):322-6PubMed: 11242117 MGI: 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):96-109PubMed: 23026749 MGI: 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):1275-86PubMed: 15115765 MGI: J:91193

Additional - Mecp2^tm1.1Bird related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Mecp2
- Standard PCR:Mecp2
- Separated PCR:Mecp2
- Standard PCR:Mecp2
- Standard PCR:Mecp2
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

The Mecp2 knockout mutation is X-linked; therefore the Mecp2-deficient mice are Mecp2^-/- (homozygous) females and Mecp2^-/Y (hemizygous) males.
When maintaining a live colony at The Jackson Laboratory, heterozygous females are bred to C57BL/6J inbred males (Stock No. 000664). Heterozygous females breed best when under 6 months of age, and are prone to seizures which may be progressive with age. Coat color expected from breeding is black.
- Additional Breeding and Husbandry Support
Mating System
- Heterozygote x C57BL/6J (000664)
Citation
When using the Mecp2^- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003890 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX11 (Maximum)

Pricing & Availability

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Age

Genotype

Price

weeks

Breeder Pair

Sex

Genotype

Price

Female
Male

Cryorecovery - Pricing

Service/Product	Description	Price
> >	X linked - Heterozygous Females and Wild-type Males for Mecp2<tm1.1Bird> 2 pair minimum

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:Mecp2-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Mecp2tm1.1Bird

Allele Symbol: Mecp2tm1.1Bird

Disease Terms

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).

Research Areas By Phenotype

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

Genotype: Mecp2tm1.1Bird related

Mammalian Phenotype Terms by Genotype

Genotype: Mecp2tm1.1Bird/Yinvolves: 129P2/OlaHsd * 129S6/SvEvTac

behavior/neurological phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

mortality/aging

nervous system phenotype

respiratory system phenotype

skeleton phenotype

craniofacial phenotype

growth/size/body region phenotype

Genotype: Mecp2tm1.1Bird/Yinvolves: 129P2/OlaHsd

mammalian phenotype

nervous system phenotype

Genotype: Mecp2tm1.1Bird/Yinvolves: 129P2/OlaHsd * C57BL/6 * CBA

adipose tissue phenotype

behavior/neurological phenotype

growth/size/body region phenotype

mammalian phenotype

Genotype: Mecp2tm1.1Bird/Mecp2tm1.1Birdinvolves: 129P2/OlaHsd * C57BL/6

respiratory system phenotype

skeleton phenotype

behavior/neurological phenotype

craniofacial phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

mortality/aging

Genotype: Mecp2tm1.1Bird/Mecp2+involves: 129P2/OlaHsd * C57BL/6

behavior/neurological phenotype

respiratory system phenotype

Genotype: Mecp2tm1.1Bird/Yinvolves: 129P2/OlaHsd * C57BL/6

craniofacial phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

homeostasis/metabolism phenotype

mortality/aging

nervous system phenotype

reproductive system phenotype

respiratory system phenotype

skeleton phenotype

behavior/neurological phenotype

Genotype: Mecp2tm1.1Bird/Yinvolves: 129P2/OlaHsd * FVB

behavior/neurological phenotype

growth/size/body region phenotype

integument phenotype

mortality/aging

nervous system phenotype

Genotype: Mecp2tm1.1Bird/Mecp2+involves: 129P2/OlaHsd

cellular phenotype

nervous system phenotype

Genotype: Mecp2tm1.1Bird/Y Tg(MECP2)1Hzo/0involves: 129P2/OlaHsd * FVB

mammalian phenotype

Genotype: Mecp2tm1.1Bird/Yinvolves: 129P2/OlaHsd * C57BL/6J * FVB/N

behavior/neurological phenotype

nervous system phenotype

Genotype: Mecp2tm1.1Bird/YB6.129P2(C)-Mecp2/J

behavior/neurological phenotype

homeostasis/metabolism phenotype

nervous system phenotype

cardiovascular system phenotype

References

Additional References

Also Known As:Mecp2^-

Mecp2^tm1.1Bird

Allele Symbol: Mecp2^tm1.1Bird

Genotype: Mecp2^tm1.1Bird related

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * 129S6/SvEvTac

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * C57BL/6 * CBA

Genotype: Mecp2^tm1.1Bird/Mecp2^tm1.1Bird
involves: 129P2/OlaHsd * C57BL/6

Genotype: Mecp2^tm1.1Bird/Mecp2⁺
involves: 129P2/OlaHsd * C57BL/6

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * C57BL/6

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * FVB

Genotype: Mecp2^tm1.1Bird/Mecp2⁺
involves: 129P2/OlaHsd

Genotype: Mecp2^tm1.1Bird/Y Tg(MECP2)1Hzo/0
involves: 129P2/OlaHsd * FVB

Genotype: Mecp2^tm1.1Bird/Y
involves: 129P2/OlaHsd * C57BL/6J * FVB/N

Genotype: Mecp2^tm1.1Bird/Y
B6.129P2(C)-Mecp2/J

Additional - Mecp2^tm1.1Bird related