Overview

Also Known As:XO (Turner syndrome model), 39,X

Females of this strain have only one X chromosome, and may be useful in studies of Turner Syndrome in humans.

Genetic overview

Genetic Background	Generation

Eda^Ta

Allele Type	Gene Symbol	Gene Name
Spontaneous	Eda	ectodysplasin-A

View Genetics

Research Applications

Reproductive Biology Research
Dermatology Research
Developmental Biology Research
Sensorineural Research
Mouse/Human Gene Homologs

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

XO or monsomy X mice lack a second sex chromosome. The condition is inherited as an X-linked dominant trait with male lethality. XO mice exhibit some degree of growth retardation, high frequency hearing loss, reduced thyroid activity, reduced body temperature and some behavioral abnormalities. Unlike Turner Syndrome in humans, XO females are fertile. The two-step mating system for this strain (described under Mating System) incorporates the X-linked coat color marker tabby so that mice can be identified by a combination of coat color and sex. This strain may be useful for studies of Turner Syndrome or X-linked recessive alleles.

Development

The female progenitor of the X/O line now maintained at the Jackson Laboratory was a Ta+/+Bn, Ta+/O mosaic. She was the offspring of a Mo+/+Ta x Bn/Y cross and looked like a Ta/O non-Bn female except for faint transverse striping across the rump. Seven of her apparently wild type daughters after mating her to a wild type male were mated with Ta/Y males. One produced Ta/O daughters and was apparently +/O. (from M.C. Green, Mouse News Letter 1967 33:37)

Control Suggestions

+/+, Eda^Ta/+ or +/Y from the colony

Approximate Controls

001201 B6CBACaF1/J-A^w-J/A

Additional Information

Considerations for Choosing Controls

Selected References

Deckers JF; Van der Kroon PH. 1981. Some characteristics of the XO mouse (Mus musculus L.) I. Vitality: Growth and metabolism Genetica 55:179-185MGI: J:139220
Green MC. 1967. XO mosaic origin Mouse News Lett 37:33MGI: J:166122
Lynn PM; Davies W. 2007. The 39,XO mouse as a model for the neurobiology of Turner syndrome and sex-biased neuropsychiatric disorders. Behav Brain Res 179(2):173-82PubMed: 17367875 MGI: J:120158
Probst FJ; Cooper ML; Cheung SW; Justice MJ. 2008. Genotype, phenotype, and karyotype correlation in the XO mouse model of Turner Syndrome. J Hered 99(5):512-7PubMed: 18499648 MGI: J:138994

View All References

Genetics

Eda^Ta

Allele Symbol: Eda^Ta

Allele Name	tabby
Allele Type	Spontaneous
Allele Synonym(s)	Ta; Ta^f; Ta^Fa; Ta3
Gene Symbol and Name	Eda, ectodysplasin-A
Gene Synonym(s)
Strain of Origin	stock including A, C57BL, CBA, and RIII
Chromosome	X
General Note	This mutation arose in a strain selected for large size. Hemizygous mutant males breed satisfactorily, but homozygous mutant females are often sterile. Hemizygous mutant females are fully fertile (J:249).Hemizygous males and homozygous females are identical in phenotype with homozygous crinkled (Edaradd^cr) and downless (Edar^dl) mice and with homozygous or heterozygous sleek (Dl^slk) mice. They are characterized by absence of guard hairs and zigzags in the coat, a bald patch behind the ear, bald tail with a few kinks near the tip, reduced aperture of the eyelids, a respiratory disorder, and a modified agouti pattern (J:249). The number of vibrissae is reduced (J:14912). The incisors may be reduced or absent, and the molars are usually smaller than normal with the third molar often absent (J:5018, J:5138). There are defects of many endocrine glands. The structures affected by the mutation all arise embryologically as downgrowths of solid epithelial cords, not by invagination with a lumen or by outgrowths from deep grooves (J:5246).Hemizygous mutant females are most easily recognized if they are agouti, in which case they show transverse stripes of light-colored normal and dark tabby hair. They have normal incisors but may have mutant or intermediate-type molars (J:5138). A small proportion of heterozygous females may show some slight defects of some of the exocrine glands (J:5193).In the development of the coat of homozygous and hemizygous mutant mice, hair follicle initiation begins at 17 days of gestation, 3 days later than normal, and ends 1 or 2 days after birth, several days earlier than normal. The hairs are of only one type and resemble abnormal awls (J:12100, J:5137). By use of dermal--epidermal recombination grafts of embryonic flank skin, it was shown that Eda^Ta acts in the epidermis in its effects on structure of the hairs (J:6041). The effect of the mutation in preventing growth of hair on the tail may be either dermal or epidermal. The mutation may act directly on hair cells or via a diffusible product (J:7450). The phenotype of Eda^Ta/+ females has been extensively studied because of its relevance to the X-inactivation theory of dosage compensation (J:5018, J:5238).Eda^Ta and the related mutations Edaradd^cr and Edar^dl disrupt normal development of certain epidermal derivatives, including sweat glands. Although the sensory innervation of footpad skin and the sympathetic innervation of blood vessels in the foot pad is normal in these mutants, the sympathetic fibers that normally innervate the sweat glands fail to develop (J:19910).A candidate gene for the human familial X-linked disorder hypohidrotic ectodermal dysplasia (EDA)(OMIM 305100) has been partially cloned. Eda, a candidate for which has also been cloned, is the homologous gene in the mouse, on the basis of phenotype - hypoplasia of sweat glands, teeth, and hair - and of homologous mapping. There is high sequence identity between the cloned portions of the two genes. Known Eda mutations have been identified in the candidate mouse gene. An extracellular collagenous domain of the mouse gene, not yet identified in the EDA gene, may represent the location of mutations in 85-90% of human families (J:42614). A mouse gene Eda (ectodysplasin-A) has been proposed as the site of the tabby mutations (J:44605).Exogenous epidermal growth factor can reverse phenotypic features of Eda^Ta mice, advancing the delayed opening of eyelids and eruption of incisors (J:42661) and inducing development of dermal ridges and functional sweat glands (J:42660). Expression of epidermal growth factor receptor is reduced in EDA and in Eda^Ta mice (J:33361).
Molecular Note	This allele is characterized by an ~ 2 kb deletion: Genomic DNA was hybridized with an exon 1 probe showing a deletion including the coding region and primers for DNA flanking exon 1 failed to amplify in a PCR assay.

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).

hypohidrotic ectodermal dysplasia

Research Areas By Phenotype

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

Reproductive Biology Research
- Fertility Defects
  - Turner's syndrome

Genotype: Eda^Ta related

Dermatology Research
- Color and White Spotting Defects
- Skin and Hair Texture Defects
Developmental Biology Research
- Eye Defects
Sensorineural Research
- Eye Defects
Mouse/Human Gene Homologs
- hypohidrotic ectodermal dysplasia

Mammalian Phenotype Terms by Genotype

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

Genotype: Eda^Ta/Eda⁺
C57BL/6J-A-Eda +/+ Ar/J

craniofacial phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
- mice exhibit fewer ruga V abnormalities than in homozygotes
- mice exhibit more ruga VI and VII abnormalities than in homozygotes
- ruga IV is S-shaped less often than in homozygotes
- ruga V is more often absent compared to in homozygotes
- rugae V and VI are most often affected

growth/size/body region phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
- mice exhibit fewer ruga V abnormalities than in homozygotes
- mice exhibit more ruga VI and VII abnormalities than in homozygotes
- ruga IV is S-shaped less often than in homozygotes
- ruga V is more often absent compared to in homozygotes
- rugae V and VI are most often affected

digestive/alimentary phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
- mice exhibit fewer ruga V abnormalities than in homozygotes
- mice exhibit more ruga VI and VII abnormalities than in homozygotes
- ruga IV is S-shaped less often than in homozygotes
- ruga V is more often absent compared to in homozygotes
- rugae V and VI are most often affected

Genotype: Eda^Ta/Y
Not Specified

craniofacial phenotype

abnormal lateral nasal gland morphology
- branching of lateral nasal gland 3 is defective at a more rostral location
- only lateral nasal gland 3 and 8 develop in mutants, while no other ducts of the other lateral nasal glands are found either in the lateral nasal wall or middle conchal lip

abnormal nasal cavity morphology
- accumulation of hair in nasal cavities results in "snuffling"

abnormal nasal gland morphology
- Normal - however, the Steno's gland (lateral nasal gland 1) and maxillary sinus gland develop normally
- medial nasal glands are completely absent

abnormal nose morphology

growth/size/body region phenotype

abnormal lateral nasal gland morphology
- branching of lateral nasal gland 3 is defective at a more rostral location
- only lateral nasal gland 3 and 8 develop in mutants, while no other ducts of the other lateral nasal glands are found either in the lateral nasal wall or middle conchal lip

abnormal nasal cavity morphology
- accumulation of hair in nasal cavities results in "snuffling"

abnormal nasal gland morphology
- Normal - however, the Steno's gland (lateral nasal gland 1) and maxillary sinus gland develop normally
- medial nasal glands are completely absent

abnormal nose morphology

integument phenotype

abnormal coat/ hair morphology

abnormal coat/hair pigmentation

abnormal hair follicle development
- E14-17 embryos lack the complement of prominent hair follicles for this age

abnormal hair growth
- hair does not develop behind the ears and on the tail

abnormal hair texture
- due to the absence of guard-hairs and zig-zag hairs

abnormal skin pigmentation
- noteably delayed

abnormal tail ring morphology
- devoid or nearly devoid of tail rings

abnormal vibrissa number
- the post-orbital vibrissa is absent
- usually there is one rather than two supra-orbital vibrissae

absent guard hair

absent hair follicle pheomelanosome pheomelanin
- absence of agouti-banding on dorsal hair results in a dark stripe in that region

absent zigzag hairs

thin skin
- noted a few days after birth

limbs/digits/tail phenotype

hairless tail
- devoid or nearly devoid of hair

kinked tail
- usually a few sharp kinks are seen at the tip

pigmentation phenotype

abnormal coat/hair pigmentation

abnormal skin pigmentation
- noteably delayed

absent hair follicle pheomelanosome pheomelanin
- absence of agouti-banding on dorsal hair results in a dark stripe in that region

respiratory system phenotype

abnormal lateral nasal gland morphology
- branching of lateral nasal gland 3 is defective at a more rostral location
- only lateral nasal gland 3 and 8 develop in mutants, while no other ducts of the other lateral nasal glands are found either in the lateral nasal wall or middle conchal lip

abnormal nasal cavity morphology
- accumulation of hair in nasal cavities results in "snuffling"

abnormal nasal gland morphology
- Normal - however, the Steno's gland (lateral nasal gland 1) and maxillary sinus gland develop normally
- medial nasal glands are completely absent

abnormal nose morphology

vision/eye phenotype

narrow eye opening

endocrine/exocrine gland phenotype

abnormal lateral nasal gland morphology
- branching of lateral nasal gland 3 is defective at a more rostral location
- only lateral nasal gland 3 and 8 develop in mutants, while no other ducts of the other lateral nasal glands are found either in the lateral nasal wall or middle conchal lip

abnormal nasal gland morphology
- Normal - however, the Steno's gland (lateral nasal gland 1) and maxillary sinus gland develop normally
- medial nasal glands are completely absent

Genotype: Eda^Ta/Eda⁺
Not Specified

integument phenotype

abnormal coat/hair pigmentation

abnormal hair texture
- Background Sensitivity - a result of loss of zigzag type hairs

absent hair follicle pheomelanosome pheomelanin
- Background Sensitivity - restricted loss of agouti hair color contributes to the appearance of transverse markings on an agouti background

absent zigzag hairs
- transverse markings are most distinct where this hair type is absent

decreased zigzag hair amount
- scarce or absent

irregular coat pigmentation
- Background Sensitivity - transverse markings are the result of regional loss of phaeomelanin from agouti hairs and absence or significant loss of of zigzag hairs

striated fur
- Background Sensitivity - on non-agouti or albino background significant regional loss or absence of zigzag hairs alone results in transverse markings
- Background Sensitivity - transverse black banding characterizes the appearance of this mouse on an agouti background

transverse fur striping
- Background Sensitivity - this appearance is the result of regional loss of phaeomelanin from agouti hairs and absence of zigzag hairs

pigmentation phenotype

abnormal coat/hair pigmentation

absent hair follicle pheomelanosome pheomelanin
- Background Sensitivity - restricted loss of agouti hair color contributes to the appearance of transverse markings on an agouti background

irregular coat pigmentation
- Background Sensitivity - transverse markings are the result of regional loss of phaeomelanin from agouti hairs and absence or significant loss of of zigzag hairs

transverse fur striping
- Background Sensitivity - this appearance is the result of regional loss of phaeomelanin from agouti hairs and absence of zigzag hairs

Genotype: Eda^Ta/Y
B6.Cg-A Eda/JGbms

integument phenotype

abnormal hair follicle development
- lack of tylotrich follicles at E14.5, E16 and E17

thin epidermis
- at E17

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

Genotype: Eda^Ta/Eda^Ta
B6CBACa A/A-Eda/J-XO

craniofacial phenotype

abnormal palatal rugae morphology
- 32% of mice exhibit different number of rugae on the left and right side compared to 25% of wild-type mice
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance
- mice exhibit fewer ruga VI and VII abnormalities than in heterozygotes
- mice exhibit more ruga V abnormalities than in heterozygotes
- only 13% of mice exhibit a normal palatal rugae pattern
- ruga IV is S-shaped more often than in heterozygotes and wild-type mice
- ruga V is less often absent compared to in heterozygotes
- rugae V and VI are most often affected

growth/size/body region phenotype

abnormal palatal rugae morphology
- 32% of mice exhibit different number of rugae on the left and right side compared to 25% of wild-type mice
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance
- mice exhibit fewer ruga VI and VII abnormalities than in heterozygotes
- mice exhibit more ruga V abnormalities than in heterozygotes
- only 13% of mice exhibit a normal palatal rugae pattern
- ruga IV is S-shaped more often than in heterozygotes and wild-type mice
- ruga V is less often absent compared to in heterozygotes
- rugae V and VI are most often affected

digestive/alimentary phenotype

abnormal palatal rugae morphology
- 32% of mice exhibit different number of rugae on the left and right side compared to 25% of wild-type mice
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance
- mice exhibit fewer ruga VI and VII abnormalities than in heterozygotes
- mice exhibit more ruga V abnormalities than in heterozygotes
- only 13% of mice exhibit a normal palatal rugae pattern
- ruga IV is S-shaped more often than in heterozygotes and wild-type mice
- ruga V is less often absent compared to in heterozygotes
- rugae V and VI are most often affected

Genotype: Eda^Ta/Eda⁺
B6CBACa A/A-Eda/J-XO

craniofacial phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
- mice exhibit fewer ruga V abnormalities than in homozygotes
- mice exhibit more ruga VI and VII abnormalities than in homozygotes
- ruga IV is S-shaped less often than in homozygotes
- ruga V is more often absent compared to in homozygotes
- rugae V and VI are most often affected

growth/size/body region phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
- mice exhibit fewer ruga V abnormalities than in homozygotes
- mice exhibit more ruga VI and VII abnormalities than in homozygotes
- ruga IV is S-shaped less often than in homozygotes
- ruga V is more often absent compared to in homozygotes
- rugae V and VI are most often affected

digestive/alimentary phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
- mice exhibit fewer ruga V abnormalities than in homozygotes
- mice exhibit more ruga VI and VII abnormalities than in homozygotes
- ruga IV is S-shaped less often than in homozygotes
- ruga V is more often absent compared to in homozygotes
- rugae V and VI are most often affected

Genotype: Eda^Ta/Y
B6CBACa A/A-Eda/J-XO

craniofacial phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance
- only 13% of mice exhibit a normal palatal rugae pattern
- rugae V and VI are most often affected

digestive/alimentary phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance
- only 13% of mice exhibit a normal palatal rugae pattern
- rugae V and VI are most often affected

growth/size/body region phenotype

abnormal palatal rugae morphology
- mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance
- only 13% of mice exhibit a normal palatal rugae pattern
- rugae V and VI are most often affected

References

Deckers JF; Van der Kroon PH. 1981. Some characteristics of the XO mouse (Mus musculus L.) I. Vitality: Growth and metabolism Genetica 55:179-185MGI: J:139220
Green MC. 1967. XO mosaic origin Mouse News Lett 37:33MGI: J:166122
Lynn PM; Davies W. 2007. The 39,XO mouse as a model for the neurobiology of Turner syndrome and sex-biased neuropsychiatric disorders. Behav Brain Res 179(2):173-82PubMed: 17367875 MGI: J:120158
Probst FJ; Cooper ML; Cheung SW; Justice MJ. 2008. Genotype, phenotype, and karyotype correlation in the XO mouse model of Turner Syndrome. J Hered 99(5):512-7PubMed: 18499648 MGI: J:138994

Additional References

Aberg T; Wang XP; Kim JH; Yamashiro T; Bei M; Rice R; Ryoo HM; Thesleff I. 2004. Runx2 mediates FGF signaling from epithelium to mesenchyme during tooth morphogenesis. Dev Biol 270(1):76-93PubMed: 15136142 MGI: J:92174
Agulnik AI; Harrison WR; Bishop CE. 2001. Smcy transgene does not rescue spermatogenesis in sex-reversed mice. Mamm Genome 12(2):112-6PubMed: 11210179 MGI: J:69107
Cattanach BM. 1962. Flecked Mouse News Lett 27:31MGI: J:31415
Hultcrantz M; Stenberg AE; Fransson A; Canlon B. 2000. Characterization of hearing in an X,0 'Turner mouse'. Hear Res 143(1-2):182-8PubMed: 10771195 MGI: J:108844
Jaskoll T; Zhou YM; Trump G; Melnick M. 2003. Ectodysplasin receptor-mediated signaling is essential for embryonic submandibular salivary gland development. Anat Rec A Discov Mol Cell Evol Biol 271(2):322-31PubMed: 12629675 MGI: J:105968
Koppinen P; Pispa J; Laurikkala J; Thesleff I; Mikkola ML. 2001. Signaling and subcellular localization of the TNF receptor Edar. Exp Cell Res 269(2):180-92PubMed: 11570810 MGI: J:71957
Miura K; Murata C; Harikae K; Suzuki H; Kanai-Azuma M; Kurohmaru M; Tsunekawa N; Kanai Y. 2017. Defects in the first wave of folliculogenesis in mouse XO ovaries. J Reprod Dev 63(3):333-338PubMed: 28392504 MGI: J:261218
Raznahan A; Probst F; Palmert MR; Giedd JN; Lerch JP. 2013. High resolution whole brain imaging of anatomical variation in XO, XX, and XY mice. Neuroimage 83:962-8PubMed: 23891883 MGI: J:275053
Russell WL; Russell LB; Gower JS. 1959. Exceptional inheritance of a sex-linked gene in the mouse explained on the basis that the X/O sex-chromosome constitution is female. Proc Natl Acad Sci U S A 45(4):554-560PubMed: 16590412 MGI: J:13126

Additional - Eda^Ta related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Separated PCR:A A A
- Separated PCR:A A A Alternate2
- Genotyping resources and troubleshooting
Mating System
- Outcross-Intercross
- TJL Breeding Scheme: hemizygote x F1 then (X/O) wild type sibling x hemizygote
  TJL Breeding Summary: genotypes of breeders are Eda^Ta/O x B6CBCaF1A^w-J/A in the first generation then +/O x Eda^Ta/Y in the second generation. Viable offspring produced from the first generation breeder pair are Eda^Ta/+ females, +/O females, and Eda^Ta/Y males.
  Viable offspring produced from the second generation breeder pair are Eda^Ta/+ females, normal +/Y males, and Eda^Ta/O females
Appearance
- tabby (yellow coat, no hair on ears and tail, bald patch behind ears, no guard hairs; tails may show epidermal ulcers)
  Related Genotype: A/A Eda^Ta/O females or A^w-J/A^? Eda^Ta/O females or A/A Eda^Ta/Y males or A^w-J/A^? Eda^Ta/Y males
  
  agouti with mosaic striped coat
  Related Genotype: A/A Eda^Ta/+ females
  
  white-bellied agouti with mosaic striped coat
  Related Genotype: A^w-J/A^? Eda^Ta/+ females
  
  agouti, no striping in coat
  Related Genotype: A/A +/+ or A/A +/O females or A/A +/Y
  
  white-bellied agouti, no striping in coat
  Related Genotype: A^w-J/A^? +/+ or A^w-J/A^? +/O females or A^w-J/A^? +/Y
Citation
When using the B6CBACa A^w-J/A-Eda^Ta/J-XO mouse strain in a publication, please cite the originating article(s) and include JAX stock #000314 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
	Minimum of two pair provided, Ta/0 x XY

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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:XO (Turner syndrome model), 39,X

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

EdaTa

Allele Symbol: EdaTa

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: EdaTa related

Mammalian Phenotype Terms by Genotype

Genotype: EdaTa/Eda+C57BL/6J-A-Eda +/+ Ar/J

craniofacial phenotype

growth/size/body region phenotype

digestive/alimentary phenotype

Genotype: EdaTa/YNot Specified

craniofacial phenotype

growth/size/body region phenotype

integument phenotype

limbs/digits/tail phenotype

pigmentation phenotype

respiratory system phenotype

vision/eye phenotype

endocrine/exocrine gland phenotype

Genotype: EdaTa/Eda+Not Specified

integument phenotype

pigmentation phenotype

Genotype: EdaTa/YB6.Cg-A Eda/JGbms

integument phenotype

Genotype: EdaTa/EdaTaB6CBACa A/A-Eda/J-XO

craniofacial phenotype

growth/size/body region phenotype

digestive/alimentary phenotype

Genotype: EdaTa/Eda+B6CBACa A/A-Eda/J-XO

craniofacial phenotype

growth/size/body region phenotype

digestive/alimentary phenotype

Genotype: EdaTa/YB6CBACa A/A-Eda/J-XO

craniofacial phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

References

Additional References

Additional - EdaTa related

Genotyping Protocols

Mating System

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

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JAX® Mice, Products & Services Conditions of Use

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Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

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Eda^Ta

Allele Symbol: Eda^Ta

Genotype: Eda^Ta related

Genotype: Eda^Ta/Eda⁺
C57BL/6J-A-Eda +/+ Ar/J

Genotype: Eda^Ta/Y
Not Specified

Genotype: Eda^Ta/Eda⁺
Not Specified

Genotype: Eda^Ta/Y
B6.Cg-A Eda/JGbms

Genotype: Eda^Ta/Eda^Ta
B6CBACa A/A-Eda/J-XO

Genotype: Eda^Ta/Eda⁺
B6CBACa A/A-Eda/J-XO

Genotype: Eda^Ta/Y
B6CBACa A/A-Eda/J-XO

Additional - Eda^Ta related