Overview

Mice homozygous for the mocha spontaneous mutation (Ap3d1^mh) have increased perinatal mortality. They are recognizable at birth by the absence of visible pigment in the eyes, which darken to deep red in adults. The hairs have considerably smaller and fewer melanin granules than normal. Behavior is abnormal, characterized by hyperactivity, tilted heads, and in some the inability to swim. All homozygotes show degenerative changes in the organ of Corti, stria vascularis, and spiral ganglion, and most show abnormalities of the otoliths in the saccule and utricle. This degeneration can be lessened by the administration of supplemental manganese or, to a lesser degree, zinc to the dam during pregnancy. Evoked auditory brainstem responses appear normal in young homozygotes, but decrease with age coincident with the cochlear degeneration with no response detected after six months of age. At three months of age, mice homozygous for the Ap3d1^mh allele have si...

Genetic overview

Genetic Background	Generation

Mfsd12^gr

Allele Type	Gene Symbol	Gene Name
Spontaneous	Mfsd12	major facilitator superfamily domain containing 12

Ap3d1^mh

Allele Type	Gene Symbol	Gene Name
Spontaneous	Ap3d1	adaptor-related protein complex 3, delta 1 subunit

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Research Applications

Dermatology Research
Neurobiology Research
Sensorineural Research
Hematological Research
Developmental Biology Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Important Note

This strain is homozygous for the retinal degeneration allele Pde6b^rd1.

Detailed Description

Mice homozygous for the mocha spontaneous mutation (Ap3d1^mh) have increased perinatal mortality. They are recognizable at birth by the absence of visible pigment in the eyes, which darken to deep red in adults. The hairs have considerably smaller and fewer melanin granules than normal. Behavior is abnormal, characterized by hyperactivity, tilted heads, and in some the inability to swim. All homozygotes show degenerative changes in the organ of Corti, stria vascularis, and spiral ganglion, and most show abnormalities of the otoliths in the saccule and utricle. This degeneration can be lessened by the administration of supplemental manganese or, to a lesser degree, zinc to the dam during pregnancy. Evoked auditory brainstem responses appear normal in young homozygotes, but decrease with age coincident with the cochlear degeneration with no response detected after six months of age. At three months of age, mice homozygous for the Ap3d1^mh allele have significantly increased auditory evoked potentials after the first of two paired tones. Ap3d1^mh-2J homozygotes also show an increased response to thefirst tone but this has not been proven with statistical significance. Homozygotes also show prolonged bleeding times due to a platelet storage pool deficiency (SPD) associated with reduced granulation of the platelets. Consistent with this defective vesicle transport, homozygotes also have decreased levels of renal lysosomal enzymes in the urine. Mocha is thus a mouse mutation that, like pa (pallid) and mu (muted), offers a model for human Hermansky-Pudlak syndrome, combining pigment and otolith abnormalities with platelet SPD. Electrocorticograms from awake Ap3d1^mh homozygotes show a constant, high voltage, bilaterally synchronous theta wave pattern that is diminished by chloral-hydrate anesthetization. Heterozygotes also have occasional brief bursts of lower voltage theta waves. Ap3d1^mh-2J homozygotes do not display hypersynchronized electrocorticograms but have spike-wave and tonic clonic seizures. Ap3d1^mh homozygotes may be fertile but are poor breeders. (Lane and Deol, 1974; Rolfson and Erway, 1984; Noebels and Sidman, 1989; Miller et al., 1999; Peden et al., 2002; Kantheti et al., 1998 and 2003.)

This strain is also segregating for the grizzled (gr) spontaneous mutation. gr is a recessive mutation that occasionally causes tail kinks and consistently causes dilution of the yellow pigment but not the black pigment of the hair. The coat color has been described as similar to chinchilla (Tyr^c-ch/Tyr^c-ch) but with the black pigment remaining undiluted. On the agouti JIGR/Dn background the gr/gr coat color is grayish agouti. On a non-agouti background the hair in the ears and around the genitalia is white. The gr mutation causes 40-50% mortality prior to phenotypic classification and this affects males more than females. This mortality is both postnatal and prenatal from approximately 10 days onward. Pregnant dams expected to carry some homozygotes have been found to carry some dead embryos some of which had craneofacial abnormalities including shortened snout and swollen optic and occipital regions. At birth homozygotes weigh an average of one quarter less than their wildtype siblings. Although they increase in weight as suckling pups, as adults they still weigh 5-25% less than their wildtype siblings. (Falconer, 1950; Bloom and Falconer, 1966.)

This strain is homozygous for the rd1 allele of Pde6b resulting in early onset retinal degeneration in all pups. (Lane and Deol, 1974; Qiao et al., 2003.)

Development

The Ap3d1^mh mutation arose spontaneously on the B6.C3-pi/+ background (then at N8) at The Jackson Laboratory in 1963 and was subsequently crossed to a variety of linkage testing stocks (including one carrying Ra, Os, and Pt, one carrying Kcnj6^wv, one carrying Re, Mcoln^Va, and Sd, and one carrying Gli3^Xt-J, Lyst^bg-J, and Edaradd^cr) before then being crossed to JIGR/Dn (then at F13) which carries Atcay^ji and gr maintained in repulsion. Atcay^ji was bred out and the resulting balanced stock with Ap3d1^mh in repulsion with Mfsd12^gr was then inbred via sibling mating. It reached F5 in 1972, F14 in 1975, F26 in 1978, F35 in 1980, F41 in 1982, F49 in 1984, and in 1989 doubly heterozygous (Mfsd12^gr +/+ Ap3d1^mh) females and males at F69 or F70 were sibling mated to generate embryos for freezing.

Control Suggestions

? +/+ ? untested from colony

Additional Information

Considerations for Choosing Controls

Selected References

Crawford NG; Kelly DE; Hansen MEB; Beltrame MH; Fan S; Bowman SL; Jewett E; Ranciaro A; Thompson S; Lo Y; Pfeifer SP; Jensen JD; Campbell MC; Beggs W; Hormozdiari F; Mpoloka SW; Mokone GG; Nyambo T; Meskel DW; Belay G; Haut J; Rothschild H; Zon L; Zhou Y; Kovacs MA; Xu M; Zhang T; Bishop K; Sinclair J; Rivas C; Elliot E; Choi J; Li SA; Hicks B; Burgess S; Abnet C; Watkins-Chow DE; Oceana E; Song YS; Eskin E; Brown KM; Marks MS; Loftus SK; Pavan WJ; Yeager M; Chanock S; Tishkoff SA. 2017. Loci associated with skin pigmentation identified in African populations. Science 358(6365)PubMed: 29025994 MGI: J:243759

View All References

Genetics

Mfsd12^gr

Allele Symbol: Mfsd12^gr

Allele Name	grizzled
Allele Type	Spontaneous
Allele Synonym(s)	grizzled; Mfsd12^gr
Gene Symbol and Name	Mfsd12, major facilitator superfamily domain containing 12
Gene Synonym(s)	C19orf28; F630110N24Rik; PP3501; RGD1307722; F630110N24Rik; Wdt1; RIKEN cDNA F630110N24 gene; grizzled; gr; gr
Strain of Origin	A x STOCK-Sgk3^fz
Chromosome	10
Molecular Note	A spontaneous mutation deletes 9 base pairs in-frame within exon 2.

Ap3d1^mh

Allele Symbol: Ap3d1^mh

Allele Name	mocha
Allele Type	Spontaneous
Allele Synonym(s)	Ap3d1^mh; mocha
Gene Symbol and Name	Ap3d1, adaptor-related protein complex 3, delta 1 subunit
Gene Synonym(s)	hBLVR; ADTD; Bolvr; bovine leukemia virus receptor; mh; expressed sequence AA407035; mBLVR1; mocha; Ap3d; AA407035; Bolvr; HPS10
Strain of Origin	B6.C3-Grxcr1^pi
Chromosome	10
Molecular Note	The mutation is a 12 kb deletion that removes at least two exons, resulting in a 496 bp deletion of coding material shortly after the initiating ATG codon and causing an out of frame translation followed by a premature termination site.

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).

Hermansky-Pudlak syndrome 2

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

platelet storage pool deficiency

Research Areas By Genotype

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

Genotype: Ap3d1^mh related

Dermatology Research
- Color and White Spotting Defects
Neurobiology Research
- Epilepsy
- Hearing Defects
Sensorineural Research
- Hearing Defects
Hematological Research
- Platelet Defects
  - platelet storage pool deficiency

Genotype: Mfsd12^gr related

Dermatology Research
- Color and White Spotting Defects
Developmental Biology Research
- Craniofacial and Palate Defects
- Growth Defects
- Postnatal Lethality
- Perinatal Lethality
  - Homozygous

Mammalian Phenotype Terms by Genotype

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

Genotype: Mfsd12^gr/Mfsd12^gr
involves: A * STOCK fz

craniofacial phenotype

abnormal craniofacial bone morphology
- commom among E16-18 fetuses; not seen among pups after birth

abnormal cranium morphology

abnormal jaw morphology
- most frequent abnormaity among E16-18 fetuses; not seen among pups after birth

integument phenotype

absent coat pigmentation
- on a non-agouti background hairs on the ears and genitalia normally yellow are white

diluted coat color
- agouti mice look like chinchilla (A/A;c^ch/c^ch)
- dilutes yellow pigment (phaeomelanin)

limbs/digits/tail phenotype

abnormal tail morphology

kinked tail
- occasionally seen

mortality/aging

postnatal lethality, incomplete penetrance
- more females than males survive
- some mutants survive to maturity

premature death
- mortality occurs at all stages with loss of 50-60% of mutants

prenatal lethality, incomplete penetrance
- cranial-facial defects commonly seen may contribute to mortality
- some survive to birth

pigmentation phenotype

absent coat pigmentation
- on a non-agouti background hairs on the ears and genitalia normally yellow are white

diluted coat color
- agouti mice look like chinchilla (A/A;c^ch/c^ch)
- dilutes yellow pigment (phaeomelanin)

reproductive system phenotype

abnormal ovulation

decreased ovulation rate
- although low compared to normal, ovulation rate is consistent with smaller size of mutant mice

skeleton phenotype

abnormal craniofacial bone morphology
- commom among E16-18 fetuses; not seen among pups after birth

abnormal cranium morphology

abnormal jaw morphology
- most frequent abnormaity among E16-18 fetuses; not seen among pups after birth

abnormal skeleton morphology

growth/size/body region phenotype

abnormal body weight
- weight is 25% less than normal at birth and remains 10-20% below weight of normal littermates

abnormal postnatal growth/weight/body size

decreased body size
- 10% smaller than normal littermates as adults
- 20-30% smaller than normal littermates at birth
- reduced body size

decreased body weight
- weight data between 2 and 6 weeks of age show females are 75-80% of normal weight; males are 90-95% of normal weight

Genotype: Ap3d1^mh/Ap3d1^mh
B6.C3-Grxcr1

behavior/neurological phenotype

abnormal motor capabilities/coordination/movement

head tilt
- all do not overtly display this but all show imbalance when handled

hyperactivity
- contributes to poor breeding and offspring neglect

homeostasis/metabolism phenotype

abnormal mineral level
- loss of vesicular zinc

increased bleeding time
- greater than 15 minutes compared to normal 2 minute bleeding time

integument phenotype

diluted coat color
- both yellow (phaeomelanin) and black (eumelanin) hairs are diluted
- hairs in ear and around genitalia are white

mortality/aging

postnatal lethality, incomplete penetrance
- 50-70% die between birth and 4 weeks of age depending on genetic background

nervous system phenotype

cochlear ganglion degeneration
- severe loss of cells in the spiral ganglion in animals over 100-days-old

pigmentation phenotype

decreased eye pigmentation
- absence of visible eye pigment at birth
- eyes of adult mice appear deep red

diluted coat color
- both yellow (phaeomelanin) and black (eumelanin) hairs are diluted
- hairs in ear and around genitalia are white

reproductive system phenotype

abnormal fertility/fecundity
- hyperactivity contributes to poor breeding performance and offspring neglect

vision/eye phenotype

decreased eye pigmentation
- absence of visible eye pigment at birth
- eyes of adult mice appear deep red

growth/size/body region phenotype

postnatal growth retardation
- at all ages mice are smaller than normal littermates

hearing/vestibular/ear phenotype

abnormal hearing physiology
- hearing loss progresses to complete deafness between 3-6 months of age
- mice are initially hypersensitive to sound

abnormal inner ear morphology
- in surviving homozygous ranging 27 days or more

abnormal inner ear vestibule morphology

abnormal otolith morphology
- inconsistent occurrence of variable amounts and distribution of crystals in some mutants

abnormal stria vascularis morphology
- almost always reduced

absent linear vestibular evoked potential

organ of Corti degeneration
- >by 100 days of age there is extensive loss of hair cells and distortion of supporting cells

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

Genotype: Ap3d1^mh/Ap3d1^mh
STOCK Mfsd12 +/+ Ap3d1/J

behavior/neurological phenotype

abnormal spike wave discharge
- spike discharge episodes of .25-1 mV amplitude and approximately 0.5-2 seconds duration observed for 4 of 5 mocha homozygotes, more frequent than in mocha 2 Jackson homozygotes

homeostasis/metabolism phenotype

decreased platelet aggregation
- decreased aggregation both in the presence of high or low concentrations of collagen

decreased platelet serotonin level
- platelet serotonin levels are less than 6% those of normal

increased bleeding time
- bleed time is greater than 15 minutes

mammalian phenotype

hematopoietic system phenotype
- Normal - MHC class II transport, peptide binding, and surface expression are normal
- Normal - the invariant chain appears to mature and be degraded with normal kinetics, and to have a normal half-life in LPS stimulated antigen presenting cells,

mortality/aging

postnatal lethality
- the percent homozygotes surviving to weaning is between 16% and 23% of Mendelian prediction, with some variation over time
- the percent of newborn homozygotes is between 47% and 97% of Mendelian prediction, with many dying within the first two or three days after birth

nervous system phenotype

abnormal brain wave pattern
- electrocorticograms from most awake homozygotes show a constant, high voltage (300-600 microvolts), bilaterally synchronous theta wave pattern that is diminished by chloral-hydrate anesthetization
- in some homozygotes there is unilateral hemispheric predominance of the altered theta frequency
- sleep onset causes generalized slowing of cortical activity with sharp waves similar to normal controls

abnormal nervous system physiology
- synaptic zinc levels are reduced throughout the brain

abnormal spike wave discharge
- spike discharge episodes of .25-1 mV amplitude and approximately 0.5-2 seconds duration observed for 4 of 5 mocha homozygotes, more frequent than in mocha 2 Jackson homozygotes

abnormal synaptic dopamine release
- a significant decrease in evoked dopamine release in dorsolateral striatum of

decreased platelet serotonin level
- platelet serotonin levels are less than 6% those of normal

enhanced sensorimotor gating

cellular phenotype

decreased lysosomal enzyme secretion
- lysosomal enzyme levels are increased in kidneys and there is an associated decrease in secretion into the urine
- thrombin-induced secretion of platelet lysosomal enzymes glucuronidase and galactosidase is only 30% to 45% of normal values and is not corrected by the addition of adenosine diphosphate

pigmentation phenotype

abnormal retinal pigment epithelium morphology
- although homozygotes do not have the giant granules that are found in the retinal pigment epithelial cells of beige mice, they do have enlarged retinal pigment granules

renal/urinary system phenotype

abnormal proximal convoluted tubule morphology
- higher than normal autofluorescence, typical of ceroid-like pigment, is found in proximal tubules

vision/eye phenotype

abnormal retinal pigment epithelium morphology
- although homozygotes do not have the giant granules that are found in the retinal pigment epithelial cells of beige mice, they do have enlarged retinal pigment granules

hearing/vestibular/ear phenotype

abnormal auditory brainstem response
- the S1 response, but not the S2 response, is markedly greater than in controls and the auditory gating is significantly enhanced as a result

abnormal inner ear vestibule morphology
- greatly reduced pigmentation within the vestibular portions of the inner ear, and this is not corrected by supplementing the mother's diet with manganese-zinc

absent linear vestibular evoked potential
- VESPs are absent at the maximum stimulus intensity used

absent otoliths
- on a normal diet most mocha homozygotes lack otoconia in both the utricle and saccule of one or both ears, but this developmental defect can be greatly prevented in pups by supplementing the mother's diet with manganese-zinc

hematopoietic system phenotype

abnormal platelet dense granule morphology
- although a normal number of dense granules stain with mepacrine, UV flashing is reduced by more than fivefold indicating an abnormal intragranular environment

decreased platelet aggregation
- decreased aggregation both in the presence of high or low concentrations of collagen

decreased platelet dense granule number
- platelets nearly devoid of dense granules

decreased platelet serotonin level
- platelet serotonin levels are less than 6% those of normal

Genotype: Ap3d1^mh Mfsd12⁺/Ap3d1⁺ Mfsd12^gr
STOCK Mfsd12 +/+ Ap3d1/J

nervous system phenotype

abnormal brain wave pattern
- electrocorticograms of mocha heterozygotes show occasional brief bursts of lower voltage theta waves, which are a less pronounced abnormality than in homozygotes

References

Crawford NG; Kelly DE; Hansen MEB; Beltrame MH; Fan S; Bowman SL; Jewett E; Ranciaro A; Thompson S; Lo Y; Pfeifer SP; Jensen JD; Campbell MC; Beggs W; Hormozdiari F; Mpoloka SW; Mokone GG; Nyambo T; Meskel DW; Belay G; Haut J; Rothschild H; Zon L; Zhou Y; Kovacs MA; Xu M; Zhang T; Bishop K; Sinclair J; Rivas C; Elliot E; Choi J; Li SA; Hicks B; Burgess S; Abnet C; Watkins-Chow DE; Oceana E; Song YS; Eskin E; Brown KM; Marks MS; Loftus SK; Pavan WJ; Yeager M; Chanock S; Tishkoff SA. 2017. Loci associated with skin pigmentation identified in African populations. Science 358(6365)PubMed: 29025994 MGI: J:243759

Additional References

Simpson F; Peden AA; Christopoulou L; Robinson MS. 1997. Characterization of the adaptor-related protein complex, AP-3. J Cell Biol 137(4):835-45PubMed: 9151686 MGI: J:20036
Swank RT; Reddington M; Howlett O; Novak EK. 1991. Platelet storage pool deficiency associated with inherited abnormalities of the inner ear in the mouse pigment mutants muted and mocha. Blood 78(8):2036-44PubMed: 1912584 MGI: J:29151
Lane PW; Deol MS. 1974. Mocha, a new coat color and behavior mutation on chromosome 10 of the mouse. J Hered 65(6):362-4PubMed: 4448900 MGI: J:5511
Rolfsen RM; Erway LC. 1984. Trace metals and otolith defects in mocha mice. J Hered 75(3):159-62PubMed: 6736600 MGI: J:7485
Elewaut D; Lawton AP; Nagarajan NA; Maverakis E; Khurana A; Honing S; Benedict CA; Sercarz E; Bakke O; Kronenberg M; Prigozy TI. 2003. The adaptor protein AP-3 is required for CD1d-mediated antigen presentation of glycosphingolipids and development of Valpha14i NKT cells. J Exp Med 198(8):1133-46PubMed: 14557411 MGI: J:86243
Qiao X; Pennesi M; Seong E; Gao H; Burmeister M; Wu SM. 2003. Photoreceptor degeneration and rd1 mutation in the grizzled/mocha mouse strain. Vision Res 43(8):859-65PubMed: 12668055 MGI: J:88031
Jones SM; Erway LC; Johnson KR; Yu H; Jones TA. 2004. Gravity receptor function in mice with graded otoconial deficiencies. Hear Res 191(1-2):34-40PubMed: 15109702 MGI: J:89392

Additional - Ap3d1^mh related

Additional - Mfsd12^gr related

Technical Support

Contact Technical Support

Genotyping Protocols
- Genotyping resources and troubleshooting
Appearance
- agouti grey
  Related Genotype: A/A Mfsd12^gr +/Mfsd12^gr ?
  
  mocha coat color
  Related Genotype: A/A Ap3d1^mh +/Ap3d1^mh ?
  
  agouti
  Related Genotype: A/A ? +/+ ? or A/A Mfsd12^gr +/+ Ap3d1^mh
Citation
When using the STOCK Mfsd12^gr +/+ Ap3d1^mh/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #000279 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

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Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Untyped repulsion heterozygotes or Ap3d1<mh> homozygotes or grizzled homozygotes

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

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Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Mfsd12gr

Allele Symbol: Mfsd12gr

Ap3d1mh

Allele Symbol: Ap3d1mh

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).

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Genotype

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

Genotype: Ap3d1mh related

Genotype: Mfsd12gr related

Mammalian Phenotype Terms by Genotype

Genotype: Mfsd12gr/Mfsd12grinvolves: A * STOCK fz

craniofacial phenotype

integument phenotype

limbs/digits/tail phenotype

mortality/aging

pigmentation phenotype

reproductive system phenotype

skeleton phenotype

growth/size/body region phenotype

Genotype: Ap3d1mh/Ap3d1mhB6.C3-Grxcr1

behavior/neurological phenotype

homeostasis/metabolism phenotype

integument phenotype

mortality/aging

nervous system phenotype

pigmentation phenotype

reproductive system phenotype

vision/eye phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

Genotype: Ap3d1mh/Ap3d1mhSTOCK Mfsd12 +/+ Ap3d1/J

behavior/neurological phenotype

homeostasis/metabolism phenotype

mammalian phenotype

mortality/aging

nervous system phenotype

cellular phenotype

pigmentation phenotype

renal/urinary system phenotype

vision/eye phenotype

hearing/vestibular/ear phenotype

hematopoietic system phenotype

Genotype: Ap3d1mh Mfsd12+/Ap3d1+ Mfsd12grSTOCK Mfsd12 +/+ Ap3d1/J

nervous system phenotype

References

Additional References

Additional - Ap3d1mh related

Additional - Mfsd12gr related

Genotyping Protocols

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

Mfsd12^gr

Allele Symbol: Mfsd12^gr

Ap3d1^mh

Allele Symbol: Ap3d1^mh

Genotype: Ap3d1^mh related

Genotype: Mfsd12^gr related

Genotype: Mfsd12^gr/Mfsd12^gr
involves: A * STOCK fz

Genotype: Ap3d1^mh/Ap3d1^mh
B6.C3-Grxcr1

Genotype: Ap3d1^mh/Ap3d1^mh
STOCK Mfsd12 +/+ Ap3d1/J

Genotype: Ap3d1^mh Mfsd12⁺/Ap3d1⁺ Mfsd12^gr
STOCK Mfsd12 +/+ Ap3d1/J

Additional - Ap3d1^mh related

Additional - Mfsd12^gr related