Overview

Also Known As:harlequin

Hemizygous male and homozygous female Harlequin mice are nearly bald with eventual, noticeable ataxia. These mice are characterized by delayed cerebellar cortical atrophy with an apoptotic loss of granule cells, a necrotic loss of Purkinje cells, and retinal degeneration. These mice may be useful in studies of neurodegenerative degeneration including Alzheimer's disease.

Genetic overview

Genetic Background	Generation

Aifm1^Hq

Allele Type	Gene Symbol	Gene Name
Spontaneous	Aifm1	apoptosis-inducing factor, mitochondrion-associated 1

A^w-J

Allele Type	Gene Symbol	Gene Name
Spontaneous	a	nonagouti

View Genetics

Research Applications

Cardiovascular Research
Apoptosis Research
Dermatology Research
Developmental Biology Research
Neurobiology Research
Sensorineural Research
Cell Biology Research

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11 months of age. Retinal degeneration is found beginning with ganglion and amacrine cell loss in the ganglion cell layer at 3 months of age, and progresses with cell loss in the inner and outer nuclear layers and reduction of rod and cone ERG responses at 4 months of age. By 10 months, the rod and cone ERG responses are gone, and at 11 months of age there isapparent cell loss in all layers of the retina. No cerebellar or retinal abnormalities were found in heterozygous females. Catalase activity and expression and total glutathione levels are increased in the cerebella of mutant mice, but not in other brain regions, and lipid hydroperoxidases are increased in brain and heart tissue. Primary granule cell cultures, but not cortical cultures, from harlequin mice show increased sensitivity to peroxide. Hemizygous males, homozygous females and hemizygous females are all viable and fertile. (Barber 1971; Falconer and Isaacson 1972; Bronson et al., 1990; Klein et al., 2002.)

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Klein JA; Longo-Guess CM; Rossmann MP; Seburn KL; Hurd RE; Frankel WN; Bronson RT; Ackerman SL. 2002. The harlequin mouse mutation downregulates apoptosis-inducing factor. Nature 419(6905):367-74PubMed: 12353028 MGI: J:78983

View All References

Genetics

Aifm1^Hq

Allele Symbol: Aifm1^Hq

Allele Name	harlequin
Allele Type	Spontaneous
Allele Synonym(s)	Hq; Pcdc8^hq
Gene Symbol and Name	Aifm1, apoptosis-inducing factor, mitochondrion-associated 1
Gene Synonym(s)
Strain of Origin	CF-1
Chromosome	X
General Note	Although initial reports indicated that ataxia was more severe in males than females, later unpublished reports indicate that there is no significant difference in severity of the ataxia phenotype between hemizygous males and homozygous females (S. Ackerman, personal communication)
Molecular Note	The harlequin mutation is an ecotropic proviral insertion at the Pdcd8 gene. This insertion leads to an 80% decrease in transcipt and protein levels, relative to wild-type controls.

A^w-J

Allele Symbol: A^w-J

Allele Name	white bellied agouti Jackson
Allele Type	Spontaneous
Allele Synonym(s)	A^WJ
Gene Symbol and Name	a, nonagouti
Gene Synonym(s)
Strain of Origin	C57BL/6J
Chromosome	2

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

mitochondrial complex I deficiency

Research Areas By Phenotype

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

Genotype: Aifm1^Hq related

Cardiovascular Research
Apoptosis Research
- Endogenous Regulators
Dermatology Research
- Skin and Hair Texture Defects
Developmental Biology Research
- Eye Defects
- Growth Defects
Neurobiology Research
- Neurodegeneration
- Tremor Defects
- Cerebellar Defects
  - Purkinje cell defect
Sensorineural Research
- Eye Defects
- Retinal Degeneration
Cell Biology Research
- Cell Cycle Regulation

Mammalian Phenotype Terms by Genotype

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

Genotype: Aifm1^Hq/Aifm1^Hq
involves: CF-1

growth/size/body region phenotype

decreased body weight
- adults are about 1/3 the weight of controls

integument phenotype

focal hair loss
- mice have bald patches of varying extent and distribution

Genotype: Aifm1^Hq/Y
involves: CF-1

growth/size/body region phenotype

decreased body weight
- adults are about 1/3 the weight of controls

integument phenotype

focal hair loss
- mice have bald patches of varying extent and distribution

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

Genotype: Aifm1^Hq/Aifm1^Hq
B6CBACa A/A-Aifm1/J

behavior/neurological phenotype

abnormal gait
- marked lateral swaying when moving and at rest by 9 months of age
- side by side unsteady gait at 5 months of age

abnormal motor capabilities/coordination/movement

abnormal seizure response to pharmacological agent
- mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed

ataxia
- age of onset is approximately 5 months of age
- ataxia is seen in most mice at 3 months of age and by 6 months of age, 90% of mice show severe ataxia while 8% have no signs of ataxia
- mild
- truncal ataxia by 9 months

impaired coordination
- mice show impaired coordination on the rotarod from 4 months of age

tremors
- a perceptible lateral tremor at rest by 9 months of age
- age of onset is approximately 5 months

cardiovascular system phenotype

abnormal cardiovascular system morphology

abnormal cardiovascular system physiology

abnormal myocardial fiber physiology
- cardiomyocytes more prone to die in response to exposure to hydrogen peroxide

altered response to myocardial infarction
- increased sensitivity to ischemia/reperfusion injury
- over 80% fail to survive 30minutes of left anterior descending artery occlusion followed by 2 to 24 hours of reperfusion

cardiac hypertrophy
- hypertrophy due to transverse aorting banding is twice as great as is seen in controls

decreased cardiac muscle contractility
- deterioration of cardiac contractility as a result of transverse aortic banding

dilated heart left ventricle
- increased left ventricular internal diameter relative to controls as a result of transverse aortic banding

increased cardiomyocyte apoptosis
- greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding

increased myocardial infarction size
- apoptosis in viable muscle cells is also increased
- experimental infarction size is increased by 50% over controls in 2 month old animals and by 78% in 6 month old animals

cellular phenotype

abnormal cell cycle
- cerebellar granule cells and retina cells re-enter the cell cycle with greater frequency than in controls
- number of cycling cells in the cerebellum and retina increase through 7 months and then declines

abnormal respiratory electron transport chain
- complex I deficiency is greatest by 1 month of age in the cerebellum and skeletal muscle, while it is modest or absent in the thalamus, cortex, and optic nerve at 1 month of age and reaches 50% by 6 months of age
- respiratory chain complex I activity is reduced by 20% in the spinal cord, by 10% in kidney, and by 30% in skeletal muscle and is normal in heart, liver, and testis
- respiratory chain complex I deficiency is detected at 1 month of age and is seen in the cerebellum, thalamus, cortical-enriched brain fractions, optic nerves, and retinas at 6 months of age, with activity about 50% of wild-type levels in the cerebellum

decreased susceptibility to neuronal excitotoxicity
- resistant to cell death induced by glutamate, NMDA, and kainic acid

increased cardiomyocyte apoptosis
- greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding

increased cellular sensitivity to hydrogen peroxide
- granule cells of the cerebellum in culture show increased sensitivity to hydrogen peroxide

oxidative stress
- increased sensitivity of the cerebellum to oxidative stress
- oxidative damage to mitochondria of the cerebellar granular layer and the ganglion layer of the retina
- slightly increased as a result of transverse aortic banding

growth/size/body region phenotype

cardiac hypertrophy
- hypertrophy due to transverse aorting banding is twice as great as is seen in controls

decreased birth weight

decreased body size

decreased body weight
- body weight varies widely

homeostasis/metabolism phenotype

altered response to myocardial infarction
- increased sensitivity to ischemia/reperfusion injury
- over 80% fail to survive 30minutes of left anterior descending artery occlusion followed by 2 to 24 hours of reperfusion

decreased susceptibility to neuronal excitotoxicity
- resistant to cell death induced by glutamate, NMDA, and kainic acid

increased catalase activity
- catalase activity increased in the cerebellum at 1 and 3 months of age
- mice exhibit moderately elevated catalase activities at 6 months of age in skeletal muscle

increased myocardial infarction size
- apoptosis in viable muscle cells is also increased
- experimental infarction size is increased by 50% over controls in 2 month old animals and by 78% in 6 month old animals

increased superoxide dismutase level
- mice exhibit moderately elevated superoxide dismutase activities at 6 months of age in skeletal muscle

integument phenotype

alopecia
- at 3 months of age, about 50% of mice are bald over more than 30% of their body and about 30% have near-normal fur, and 10% of mice have near-normal fur at 6 months of age
- complete baldness in most mice initially, followed by some hair growth resulting in a patchy or near-normal coat

sparse hair
- described as nearly bald

mortality/aging

increased sensitivity to induced morbidity/mortality
- significantly reduced survival at both 1 and 4 weeks after transverse aortic banding

premature death
- about 30% of mice die during the first 6 months, with most deaths occurring between 15 and 30 days of age

muscle phenotype

decreased cardiac muscle contractility
- deterioration of cardiac contractility as a result of transverse aortic banding

increased cardiomyocyte apoptosis
- greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding

nervous system phenotype

abnormal cerebellar cortex morphology

abnormal cerebellar granule cell morphology
- apoptotic granule cells seen at 4 months of age
- pyknotic granule cell nuclei at 4 months of age

abnormal cerebellar granule layer morphology
- losses are preferentially from the caudal vermis and hemispheres
- most caudal granule cells are lost by 12 months
- no reduction in the folia but extensive loss in the floccular lobes in mice 5-8 months of age

abnormal seizure response to pharmacological agent
- mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed

absent optic nerve
- ocular hypoplasia, with absence of the optic nerve in 40% of mice at 1 month of age

amacrine cell degeneration
- cell loss is seen in the ganglion layer after about 3 months of age

decreased susceptibility to neuronal excitotoxicity
- resistant to cell death induced by glutamate, NMDA, and kainic acid

Purkinje cell degeneration
- cell loss apparently due to necrosis
- described as mild and patchy in the folia, but extensive in the floccular lobes in mice 5-8 months of age
- many Purkinje cells are dead by 7 months of age
- Purkinje cell loss occurs later than granule cell loss

retinal ganglion cell degeneration
- ganglion cell loss is seen after about 3 months of age

small cerebellum
- Normal - cerebellum normal before 3 months
- much smaller at 7 months

vision/eye phenotype

abnormal eye electrophysiology
- both rod and cone ERG are diminished by 4 months of age
- ERG responses are completely abolished by 10 months of age

absent optic nerve
- ocular hypoplasia, with absence of the optic nerve in 40% of mice at 1 month of age

amacrine cell degeneration
- cell loss is seen in the ganglion layer after about 3 months of age

retinal degeneration
- cell loss is seen in all layers of the retina by 11 months
- onset of retinal degeneration is after 3 months of age

retinal ganglion cell degeneration
- ganglion cell loss is seen after about 3 months of age

thin retinal inner plexiform layer
- thinning by 11 months

thin retinal outer plexiform layer
- thinning by 11 months

Genotype: Aifm1^Hq/Y
B6CBACa A/A-Aifm1/J

behavior/neurological phenotype

abnormal gait
- marked lateral swaying when moving and at rest by 9 months of age
- side by side unsteady gait at 5 months of age

abnormal motor capabilities/coordination/movement

abnormal seizure response to pharmacological agent
- mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed

ataxia
- age of onset is approximately 5 months of age
- ataxia is seen in most mice at 3 months of age and by 6 months of age, 90% of mice show severe ataxia while 8% have no signs of ataxia
- mild
- truncal ataxia by 9 months

impaired coordination
- mice show impaired coordination on the rotarod from 4 months of age

tremors
- a perceptible lateral tremor at rest by 9 months of age
- age of onset is approximately 5 months

cardiovascular system phenotype

abnormal cardiovascular system morphology

abnormal cardiovascular system physiology

abnormal myocardial fiber physiology
- cardiomyocytes more prone to die in response to exposure to hydrogen peroxide

altered response to myocardial infarction
- increased sensitivity to ischemia/reperfusion injury
- over 80% fail to survive 30minutes of left anterior descending artery occlusion followed by 2 to 24 hours of reperfusion

cardiac hypertrophy
- hypertrophy due to transverse aorting banding is twice as great as is seen in controls

decreased cardiac muscle contractility
- deterioration of cardiac contractility as a result of transverse aortic banding

dilated heart left ventricle
- increased left ventricular internal diameter relative to controls as a result of transverse aortic banding

increased cardiomyocyte apoptosis
- greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding

increased myocardial infarction size
- apoptosis in viable muscle cells is also increased
- experimental infarction size is increased by 50% over controls in 2 month old animals and by 78% in 6 month old animals

cellular phenotype

abnormal cell cycle
- cerebellar granule cells and retina cells re-enter the cell cycle with greater frequency than in controls
- number of cycling cells in the cerebellum and retina increase through 7 months and then declines

abnormal respiratory electron transport chain
- complex I deficiency is greatest by 1 month of age in the cerebellum and skeletal muscle, while it is modest or absent in the thalamus, cortex, and optic nerve at 1 month of age and reaches 50% by 6 months of age
- respiratory chain complex I activity is reduced by 20% in the spinal cord, by 10% in kidney, and by 30% in skeletal muscle and is normal in heart, liver, and testis
- respiratory chain complex I deficiency is detected at 1 month of age and is seen in the cerebellum, thalamus, cortical-enriched brain fractions, optic nerves, and retinas at 6 months of age, with activity about 50% of wild-type levels in the cerebellum

decreased susceptibility to neuronal excitotoxicity
- resistant to cell death induced by glutamate, NMDA, and kainic acid

increased cardiomyocyte apoptosis
- greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding

increased cellular sensitivity to hydrogen peroxide
- granule cells of the cerebellum in culture show increased sensitivity to hydrogen peroxide

oxidative stress
- increased sensitivity of the cerebellum to oxidative stress
- oxidative damage to mitochondria of the cerebellar granular layer and the ganglion layer of the retina
- slightly increased as a result of transverse aortic banding

growth/size/body region phenotype

cardiac hypertrophy
- hypertrophy due to transverse aorting banding is twice as great as is seen in controls

decreased birth weight

decreased body size

decreased body weight
- body weight varies widely

postnatal growth retardation
- at 1 month of age, about half of the males show growth retardation with a greater than 30% decrease in body weight
- Normal - however, about 30% of males at 6 months of age do not show any growth retardation

homeostasis/metabolism phenotype

altered response to myocardial infarction
- increased sensitivity to ischemia/reperfusion injury
- over 80% fail to survive 30minutes of left anterior descending artery occlusion followed by 2 to 24 hours of reperfusion

decreased susceptibility to neuronal excitotoxicity
- resistant to cell death induced by glutamate, NMDA, and kainic acid

increased catalase activity
- catalase activity increased in the cerebellum at 1 and 3 months of age
- mice exhibit moderately elevated catalase activities at 6 months of age in skeletal muscle

increased myocardial infarction size
- apoptosis in viable muscle cells is also increased
- experimental infarction size is increased by 50% over controls in 2 month old animals and by 78% in 6 month old animals

increased superoxide dismutase level
- mice exhibit moderately elevated superoxide dismutase activities at 6 months of age in skeletal muscle

integument phenotype

alopecia
- at 3 months of age, about 50% of mice are bald over more than 30% of their body and about 30% have near-normal fur, and 10% of mice have near-normal fur at 6 months of age
- complete baldness in most mice initially, followed by some hair growth resulting in a patchy or near-normal coat

sparse hair
- described as nearly bald

mortality/aging

increased sensitivity to induced morbidity/mortality
- significantly reduced survival at both 1 and 4 weeks after transverse aortic banding

premature death
- about 30% of mice die during the first 6 months, with most deaths occurring between 15 and 30 days of age

muscle phenotype

decreased cardiac muscle contractility
- deterioration of cardiac contractility as a result of transverse aortic banding

increased cardiomyocyte apoptosis
- greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding

nervous system phenotype

abnormal cerebellar cortex morphology

abnormal cerebellar granule cell morphology
- apoptotic granule cells seen at 4 months of age
- pyknotic granule cell nuclei at 4 months of age

abnormal cerebellar granule layer morphology
- losses are preferentially from the caudal vermis and hemispheres
- most caudal granule cells are lost by 12 months
- no reduction in the folia but extensive loss in the floccular lobes in mice 5-8 months of age

abnormal seizure response to pharmacological agent
- mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed

absent optic nerve
- ocular hypoplasia, with absence of the optic nerve in 40% of mice at 1 month of age

amacrine cell degeneration
- cell loss is seen in the ganglion layer after 3 months of age

decreased susceptibility to neuronal excitotoxicity
- resistant to cell death induced by glutamate, NMDA, and kainic acid

Purkinje cell degeneration
- cell loss apparently due to necrosis
- described as mild and patchy in the folia, but extensive in the floccular lobes in mice 5-8 months of age
- many Purkinje cells are dead by 7 months of age
- Purkinje cell loss occurs later than granule cell loss

retinal ganglion cell degeneration
- ganglion cell loss is seen after about 3 months of age

small cerebellum
- Normal - cerebellum normal before 3 months
- much smaller at 7 months

vision/eye phenotype

abnormal eye electrophysiology
- both rod and cone ERG are diminished by 4 months of age
- ERG responses are completely abolished by 10 months of age

absent optic nerve
- ocular hypoplasia, with absence of the optic nerve in 40% of mice at 1 month of age

amacrine cell degeneration
- cell loss is seen in the ganglion layer after 3 months of age

retinal degeneration
- cell loss is seen in all layers of the retina by 11 months
- onset of retinal degeneration is after 3 months of age

retinal ganglion cell degeneration
- ganglion cell loss is seen after about 3 months of age

thin retinal inner plexiform layer
- thinning by 11 months

thin retinal outer plexiform layer
- thinning by 11 months

Genotype: Aifm1^Hq/Aifm1⁺
B6CBACa A/A-Aifm1/J

integument phenotype

sparse hair
- patchy irregular hair loss

mammalian phenotype

behavior/neurological phenotype
- Normal - heterozygotes are normal with respect to ataxia

nervous system phenotype
- Normal - no loss of granule cells seen to 26 months of age

References

Klein JA; Longo-Guess CM; Rossmann MP; Seburn KL; Hurd RE; Frankel WN; Bronson RT; Ackerman SL. 2002. The harlequin mouse mutation downregulates apoptosis-inducing factor. Nature 419(6905):367-74PubMed: 12353028 MGI: J:78983

Additional References

Cregan SP; Fortin A; MacLaurin JG; Callaghan SM; Cecconi F; Yu SW; Dawson TM; Dawson VL; Park DS; Kroemer G; Slack RS. 2002. Apoptosis-inducing factor is involved in the regulation of caspase-independent neuronal cell death. J Cell Biol 158(3):507-17PubMed: 12147675 MGI: J:78264
Daugas E; Nochy D; Ravagnan L; Loeffler M; Susin SA; Zamzami N; Kroemer G. 2000. Apoptosis-inducing factor (AIF): a ubiquitous mitochondrial oxidoreductase involved in apoptosis FEBS Lett 476(3):118-23PubMed: 10913597 MGI: J:63402
Joza N; Susin SA; Daugas E; Stanford WL; Cho SK; Li CY; Sasaki T; Elia AJ; Cheng HY; Ravagnan L; Ferri KF; Zamzami N; Wakeham A; Hakem R; Yoshida H; Kong YY; Mak TW; Zuniga-Pflucker JC; Kroemer G; Penninger JM. 2001. Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death. Nature 410(6828):549-54PubMed: 11279485 MGI: J:68434
Loeffler M; Daugas E; Susin SA; Zamzami N; Metivier D; Nieminen AL; Brothers G; Penninger JM; Kroemer G. 2001. Dominant cell death induction by extramitochondrially targeted apoptosis-inducing factor. FASEB J 15(3):758-67PubMed: 11259394 MGI: J:67944
Susin SA; Daugas E; Ravagnan L; Samejima K; Zamzami N; Loeffler M; Costantini P; Ferri KF; Irinopoulou T; Prevost MC; Brothers G; Mak TW; Penninger J; Earnshaw WC; Kroemer G. 2000. Two distinct pathways leading to nuclear apoptosis. J Exp Med 192(4):571-80PubMed: 10952727 MGI: J:64229

Additional - A^w-J related

Additional - Aifm1^Hq related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Separated PCR:Aifm1
- Separated PCR:A A A Alternate2
- Genotyping resources and troubleshooting
Breeding Considerations

Comments: Hq/Y males need to stay with their mothers an extra week or more because they are too small to wean at 3 weeks.
- Additional Breeding and Husbandry Support
Appearance
- balding, small, ataxic
  Related Genotype: Aifm1^Hq/Y male or Aifm1^Hq/Aifm1^Hq female
  
  possible patchy fur
  Related Genotype: Aifm1^Hq/+ female
Citation
When using the harlequin mouse strain in a publication, please cite the originating article(s) and include JAX stock #000501 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	X linked- Heterozygous females or Wild-type males for Hq, 1 pair minimum

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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

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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.

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Also Known As:harlequin

Genetic overview

Research Applications

Base Price

Detailed Description

Control Suggestions

Additional Information

Selected References

Aifm1Hq

Allele Symbol: Aifm1Hq

Aw-J

Allele Symbol: Aw-J

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Research Areas By Phenotype

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

Genotype: Aifm1Hq related

Mammalian Phenotype Terms by Genotype

Genotype: Aifm1Hq/Aifm1Hqinvolves: CF-1

growth/size/body region phenotype

integument phenotype

Genotype: Aifm1Hq/Yinvolves: CF-1

growth/size/body region phenotype

integument phenotype

Genotype: Aifm1Hq/Aifm1HqB6CBACa A/A-Aifm1/J

behavior/neurological phenotype

cardiovascular system phenotype

cellular phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

integument phenotype

mortality/aging

muscle phenotype

nervous system phenotype

vision/eye phenotype

Genotype: Aifm1Hq/YB6CBACa A/A-Aifm1/J

behavior/neurological phenotype

cardiovascular system phenotype

cellular phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

integument phenotype

mortality/aging

muscle phenotype

nervous system phenotype

vision/eye phenotype

Genotype: Aifm1Hq/Aifm1+B6CBACa A/A-Aifm1/J

integument phenotype

mammalian phenotype

References

Additional References

Additional - Aw-J related

Additional - Aifm1Hq related

Genotyping Protocols

Breeding Considerations

Appearance

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Aifm1^Hq

Allele Symbol: Aifm1^Hq

A^w-J

Allele Symbol: A^w-J

Genotype: Aifm1^Hq related

Genotype: Aifm1^Hq/Aifm1^Hq
involves: CF-1

Genotype: Aifm1^Hq/Y
involves: CF-1

Genotype: Aifm1^Hq/Aifm1^Hq
B6CBACa A/A-Aifm1/J

Genotype: Aifm1^Hq/Y
B6CBACa A/A-Aifm1/J

Genotype: Aifm1^Hq/Aifm1⁺
B6CBACa A/A-Aifm1/J

Additional - A^w-J related

Additional - Aifm1^Hq related