Strain Name:

B6CBACa Aw-J/A-EdaTa/J-XO

Stock Number:

000314

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Availability:

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Common Names: 39,X;     XO (Turner syndrome model);    
Females of this strain have only one X chromosome, and may be useful in studies of Turner Syndrome in humans.

Description

Strain Information

Former Names B6CBACa-Aw-J/A-EdaTa/O    (Changed: 26-JUL-10 )
B6CBACa Aw-J/A-EdaTa/O/J    (Changed: 15-MAY-07 )
B6CBACa-Aw-J/A-EdaTa/O    (Changed: 15-DEC-04 )
Type Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemOutcross-Intercross         (Female x Male)   01-MAR-06
TJL Breeding Scheme: hemizygote x F1 then (X/O) wild type sibling x hemizygote
TJL Breeding Summary: genotypes of breeders are EdaTa/O x B6CBCaF1Aw-J/A in the first generation then +/O x EdaTa/Y in the second generation. Viable offspring produced from the first generation breeder pair are EdaTa/+ females, +/O females, and EdaTa/Y males.
Viable offspring produced from the second generation breeder pair are EdaTa/+ females, normal +/Y males, and EdaTa/O females.
Specieslaboratory mouse
GenerationN74F2 (28-OCT-13)
Generation Definitions

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 EdaTa/O females or Aw-J/A? EdaTa/O females or A/A EdaTa/Y males or Aw-J/A? EdaTa/Y males

agouti with mosaic striped coat
Related Genotype: A/A EdaTa/+ females

white-bellied agouti with mosaic striped coat
Related Genotype: Aw-J/A? EdaTa/+ 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: Aw-J/A? +/+ or Aw-J/A? +/O females or Aw-J/A? +/Y

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 Information

  Control
   +/+, EdaTa/+ or +/Y from the colony
   001201 B6CBACaF1/J-Aw-J/A (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   EdaTa allele
000287   B6CBACa Aw-J/A-Plp1jp EdaTa/J
000569   C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J
000583   STOCK T(X;16)16H +/+ EdaTa
View Strains carrying   EdaTa     (3 strains)

View Strains carrying other alleles of Eda     (8 strains)

Additional Web Information

JAX® NOTES, January 1990, 440. Tabby Stocks Available from The Jackson Laboratory.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Ectodermal Dysplasia 1, Hypohidrotic, X-Linked; XHED   (EDA)
Tooth Agenesis, Selective, X-Linked, 1; STHAGX1   (EDA)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

EdaTa/Eda+

        B6CBACa Aw-J/A-EdaTa/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   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga V abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • ruga V is more often absent compared to in homozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped less often than in homozygotes   (MGI Ref ID J:147677)
  • 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   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga V abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • ruga V is more often absent compared to in homozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped less often than in homozygotes   (MGI Ref ID J:147677)
  • growth/size/body 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   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga V abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • ruga V is more often absent compared to in homozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped less often than in homozygotes   (MGI Ref ID J:147677)

EdaTa/EdaTa

        B6CBACa Aw-J/A-EdaTa/J-XO
  • craniofacial phenotype
  • abnormal palatal rugae morphology
    • only 13% of mice exhibit a normal palatal rugae pattern   (MGI Ref ID J:147677)
    • 32% of mice exhibit different number of rugae on the left and right side compared to 25% of wild-type mice   (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga VI and VII abnormalities than in heterozygotes   (MGI Ref ID J:147677)
    • mice exhibit more ruga V abnormalities than in heterozygotes   (MGI Ref ID J:147677)
    • ruga V is less often absent compared to in heterozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped more often than in heterozygotes and wild-type mice   (MGI Ref ID J:147677)
  • digestive/alimentary phenotype
  • abnormal palatal rugae morphology
    • only 13% of mice exhibit a normal palatal rugae pattern   (MGI Ref ID J:147677)
    • 32% of mice exhibit different number of rugae on the left and right side compared to 25% of wild-type mice   (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga VI and VII abnormalities than in heterozygotes   (MGI Ref ID J:147677)
    • mice exhibit more ruga V abnormalities than in heterozygotes   (MGI Ref ID J:147677)
    • ruga V is less often absent compared to in heterozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped more often than in heterozygotes and wild-type mice   (MGI Ref ID J:147677)
  • growth/size/body phenotype
  • abnormal palatal rugae morphology
    • only 13% of mice exhibit a normal palatal rugae pattern   (MGI Ref ID J:147677)
    • 32% of mice exhibit different number of rugae on the left and right side compared to 25% of wild-type mice   (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga VI and VII abnormalities than in heterozygotes   (MGI Ref ID J:147677)
    • mice exhibit more ruga V abnormalities than in heterozygotes   (MGI Ref ID J:147677)
    • ruga V is less often absent compared to in heterozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped more often than in heterozygotes and wild-type mice   (MGI Ref ID J:147677)

EdaTa/Y

        B6CBACa Aw-J/A-EdaTa/J-XO
  • craniofacial phenotype
  • abnormal palatal rugae morphology
    • only 13% of mice exhibit a normal palatal rugae pattern   (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
  • digestive/alimentary phenotype
  • abnormal palatal rugae morphology
    • only 13% of mice exhibit a normal palatal rugae pattern   (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
  • growth/size/body phenotype
  • abnormal palatal rugae morphology
    • only 13% of mice exhibit a normal palatal rugae pattern   (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, absence of rugae, S-shaped rugae, and rugae discordance   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)

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

EdaTa/Eda+

        C57BL/6J-Aw-J-EdaTa +/+ ArTfm/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   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga V abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • ruga V is more often absent compared to in homozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped less often than in homozygotes   (MGI Ref ID J:147677)
  • 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   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga V abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • ruga V is more often absent compared to in homozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped less often than in homozygotes   (MGI Ref ID J:147677)
  • growth/size/body 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   (MGI Ref ID J:147677)
    • rugae V and VI are most often affected   (MGI Ref ID J:147677)
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • mice exhibit fewer ruga V abnormalities than in homozygotes   (MGI Ref ID J:147677)
    • ruga V is more often absent compared to in homozygotes   (MGI Ref ID J:147677)
    • ruga IV is S-shaped less often than in homozygotes   (MGI Ref ID J:147677)

EdaTa/Eda+

        Background Not Specified
  • pigmentation phenotype
  • abnormal coat/hair pigmentation   (MGI Ref ID J:249)
    • absent hair follicle pheomelanosome pheomelanin
      • restricted loss of agouti hair color contributes to the appearance of transverse markings on an agouti background   (MGI Ref ID J:249)
    • irregular coat pigmentation
      • transverse markings are the result of regional loss of phaeomelanin from agouti hairs and absence or significant loss of of zigzag hairs   (MGI Ref ID J:249)
      • transverse fur striping
        • this appearance is the result of regional loss of phaeomelanin from agouti hairs and absence of zigzag hairs   (MGI Ref ID J:249)
  • integument phenotype
  • abnormal coat/hair pigmentation   (MGI Ref ID J:249)
    • absent hair follicle pheomelanosome pheomelanin
      • restricted loss of agouti hair color contributes to the appearance of transverse markings on an agouti background   (MGI Ref ID J:249)
    • irregular coat pigmentation
      • transverse markings are the result of regional loss of phaeomelanin from agouti hairs and absence or significant loss of of zigzag hairs   (MGI Ref ID J:249)
      • transverse fur striping
        • this appearance is the result of regional loss of phaeomelanin from agouti hairs and absence of zigzag hairs   (MGI Ref ID J:249)
  • abnormal hair texture
    • a result of loss of zigzag type hairs   (MGI Ref ID J:249)
  • absent zigzag hairs
    • transverse markings are most distinct where this hair type is absent   (MGI Ref ID J:249)
  • decreased zigzag hair amount
    • scarce or absent   (MGI Ref ID J:249)
  • striated fur
    • transverse black banding characterizes the appearance of this mouse on an agouti background   (MGI Ref ID J:249)
    • on non-agouti or albino background significant regional loss or absence of zigzag hairs alone results in transverse markings   (MGI Ref ID J:249)

EdaTa/Y

        Background Not Specified
  • craniofacial phenotype
  • abnormal nose morphology   (MGI Ref ID J:249)
    • abnormal nasal cavity morphology
      • accumulation of hair in nasal cavities results in "snuffling"   (MGI Ref ID J:249)
  • limbs/digits/tail phenotype
  • abnormal tail morphology
    • devoid or nearly devoid of hair and tail rings   (MGI Ref ID J:249)
    • usually a few sharp kinks are seen at the tip   (MGI Ref ID J:249)
    • hairless tail   (MGI Ref ID J:249)
    • kinked tail   (MGI Ref ID J:249)
  • pigmentation phenotype
  • abnormal coat/hair pigmentation   (MGI Ref ID J:249)
    • absent hair follicle pheomelanosome pheomelanin
      • absence of agouti-banding on dorsal hair results in a dark stripe in that region   (MGI Ref ID J:249)
  • abnormal skin pigmentation
    • noteably delayed   (MGI Ref ID J:249)
  • respiratory system phenotype
  • abnormal nose morphology   (MGI Ref ID J:249)
    • abnormal nasal cavity morphology
      • accumulation of hair in nasal cavities results in "snuffling"   (MGI Ref ID J:249)
  • vision/eye phenotype
  • narrow eye opening   (MGI Ref ID J:249)
  • integument phenotype
  • abnormal coat/ hair morphology   (MGI Ref ID J:249)
    • abnormal coat/hair pigmentation   (MGI Ref ID J:249)
      • absent hair follicle pheomelanosome pheomelanin
        • absence of agouti-banding on dorsal hair results in a dark stripe in that region   (MGI Ref ID J:249)
    • abnormal hair growth
      • hair does not develop behind the ears and on the tail   (MGI Ref ID J:249)
    • abnormal hair texture
      • due to the absence of guard-hairs and zig-zag hairs   (MGI Ref ID J:249)
    • absent guard hair   (MGI Ref ID J:249)
    • absent zigzag hairs   (MGI Ref ID J:249)
  • abnormal hair follicle development
    • E14-17 embryos lack the complement of prominent hair follicles for this age   (MGI Ref ID J:249)
  • abnormal skin pigmentation
    • noteably delayed   (MGI Ref ID J:249)
  • abnormal vibrissa number
    • the post-orbital vibrissa is absent   (MGI Ref ID J:249)
    • usually there is one rather than two supra-orbital vibrissae   (MGI Ref ID J:249)
  • thin skin
    • noted a few days after birth   (MGI Ref ID J:249)
  • growth/size/body phenotype
  • abnormal nose morphology   (MGI Ref ID J:249)
    • abnormal nasal cavity morphology
      • accumulation of hair in nasal cavities results in "snuffling"   (MGI Ref ID J:249)
View Research Applications

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

Reproductive Biology Research
Fertility Defects
      Turner's syndrome

EdaTa related

Dermatology Research
Color and White Spotting Defects
Skin and Hair Texture Defects

Developmental Biology Research
Eye Defects

Sensorineural Research
Eye Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol EdaTa
Allele Name tabby
Allele Type Spontaneous
Common Name(s) Ta; Ta3; TaFa; Taf;
Strain of Originstock including A, C57BL, CBA, and RIII
Gene Symbol and Name Eda, ectodysplasin-A
Chromosome X
Gene Common Name(s) EDA1; Ed1; Eda-A1; Eda-A2; RGD1563178; Ta; tabby;
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 (Edaraddcr) and downless (Edardl) mice and with homozygous or heterozygous sleek (Dlslk) 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 EdaTa 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 EdaTa/+ females has been extensively studied because of its relevance to the X-inactivation theory of dosage compensation (J:5018, J:5238).EdaTa and the related mutations Edaraddcr and Edardl 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 EdaTa 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 EdaTa 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. [MGI Ref ID J:42614] [MGI Ref ID J:44605]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Deckers JF; Van der Kroon PH. 1981. Some characteristics of the XO mouse (Mus musculus L.) I. Vitality: Growth adn metabolism Genetica 55:179-185.  [MGI Ref ID J:139220]

Green MC. 1967. XO mosaic origin Mouse News Lett 37:33.  [MGI Ref ID 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):173-82. [PubMed: 17367875]  [MGI Ref ID 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):512-7. [PubMed: 18499648]  [MGI Ref ID 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):76-93. [PubMed: 15136142]  [MGI Ref ID J:92174]

Agulnik AI; Harrison WR; Bishop CE. 2001. Smcy transgene does not rescue spermatogenesis in sex-reversed mice. Mamm Genome 12(2):112-6. [PubMed: 11210179]  [MGI Ref ID J:69107]

Cattanach BM. 1962. Flecked Mouse News Lett 27:31.  [MGI Ref ID 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):182-8. [PubMed: 10771195]  [MGI Ref ID 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):322-31. [PubMed: 12629675]  [MGI Ref ID 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):180-92. [PubMed: 11570810]  [MGI Ref ID J:71957]

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):554-560. [PubMed: 16590412]  [MGI Ref ID J:13126]

EdaTa related

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):76-93. [PubMed: 15136142]  [MGI Ref ID J:92174]

Blecher SR; Kapalanga J; Lalonde D. 1990. Induction of sweat glands by epidermal growth factor in murine X-linked anhidrotic ectodermal dysplasia. Nature 345(6275):542-4. [PubMed: 2348861]  [MGI Ref ID J:42660]

Boran T; Lesot H; Peterka M; Peterkova R. 2005. Increased apoptosis during morphogenesis of the lower cheek teeth in tabby/EDA mice. J Dent Res 84(3):228-33. [PubMed: 15723861]  [MGI Ref ID J:112546]

Cerghet M; Bessert DA; Nave KA; Skoff RP. 2001. Differential expression of apoptotic markers in jimpy and in Plp overexpressors: evidence for different apoptotic pathways. J Neurocytol 30(9-10):841-55. [PubMed: 12165674]  [MGI Ref ID J:121313]

Charles C; Pantalacci S; Peterkova R; Peterka M; Laudet V; Viriot L. 2007. Disruption of the palatal rugae pattern in Tabby (eda) mutant mice. Eur J Oral Sci 115(6):441-8. [PubMed: 18028050]  [MGI Ref ID J:147677]

Charles C; Pantalacci S; Tafforeau P; Headon D; Laudet V; Viriot L. 2009. Distinct impacts of Eda and Edar loss of function on the mouse dentition. PLoS ONE 4(4):e4985. [PubMed: 19340299]  [MGI Ref ID J:148176]

Claxton JH. 1967. The initiation and development of the hair follicle population in tabby mice. Genet Res 10:161-171.  [MGI Ref ID J:12100]

Dulos GJ; Bagchus WM. 2001. Androgens indirectly accelerate thymocyte apoptosis. Int Immunopharmacol 1(2):321-8. [PubMed: 11360932]  [MGI Ref ID J:109877]

FALCONER DS. 1953. [Total sex-linkage in the house mouse.] Z Indukt Abstamm Vererbungsl 85(2):210-9. [PubMed: 13103353]  [MGI Ref ID J:249]

Falconer DS; Latyszewski M. 1952. The environment in relation to selection for size in mice J Genet 51:67-80.  [MGI Ref ID J:78116]

Ferguson BM; Brockdorff N; Formstone E; Ngyuen T; Kronmiller JE; Zonana J. 1997. Cloning of Tabby, the murine homolog of the human EDA gene: evidence for a membrane-associated protein with a short collagenous domain. Hum Mol Genet 6(9):1589-94. [PubMed: 9285798]  [MGI Ref ID J:42614]

Fliniaux I; Mikkola ML; Lefebvre S; Thesleff I. 2008. Identification of dkk4 as a target of Eda-A1/Edar pathway reveals an unexpected role of ectodysplasin as inhibitor of Wnt signalling in ectodermal placodes. Dev Biol 320(1):60-71. [PubMed: 18508042]  [MGI Ref ID J:138365]

Fraser AS; Kindred BM. 1960. Selection for an invariant character, vibrissa number, in the house mouse. II. Limits to variability Aust J Biol Sci 13:48-58.  [MGI Ref ID J:14912]

Gruneberg H. 1965. Genes and genotypes affecting the teeth of the mouse. J Embryol Exp Morphol 14(2):137-59. [PubMed: 5893447]  [MGI Ref ID J:12999]

Gruneberg H. 1971. The glandular aspects of the tabby syndrome in the mouse. J Embryol Exp Morphol 25(1):1-19. [PubMed: 5548211]  [MGI Ref ID J:5193]

Gruneberg H. 1966. The molars of the tabby mouse, and a test of the 'single-active X-chromosome' hypothesis. J Embryol Exp Morphol 15(2):223-44. [PubMed: 5959976]  [MGI Ref ID J:5018]

Gruneberg H. 1971. The tabby syndrome in the mouse. Proc R Soc Lond B Biol Sci 179(55):139-56. [PubMed: 4399988]  [MGI Ref ID J:5246]

Gruneberg H. 1969. Threshold phenomena versus cell heredity in the manifestation of sex-linked genes in mammals. J Embryol Exp Morphol 22(2):145-79. [PubMed: 5361553]  [MGI Ref ID J:5137]

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Huh SH; Narhi K; Lindfors PH; Haara O; Yang L; Ornitz DM; Mikkola ML. 2013. Fgf20 governs formation of primary and secondary dermal condensations in developing hair follicles. Genes Dev 27(4):450-8. [PubMed: 23431057]  [MGI Ref ID J:193958]

Isaacs K; Brown G; Moore GP. 1998. Interactions between epidermal growth factor and the Tabby mutation in skin. Exp Dermatol 7(5):273-80. [PubMed: 9832315]  [MGI Ref ID J:53635]

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Kowalczyk-Quintas C; Schuepbach-Mallepell S; Willen L; Smith TK; Huttner K; Kirby N; Headon DJ; Schneider P. 2015. Pharmacological stimulation of edar signaling in the adult enhances sebaceous gland size and function. J Invest Dermatol 135(2):359-68. [PubMed: 25207818]  [MGI Ref ID J:218060]

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Laurikkala J; Mikkola M; Mustonen T; Aberg T; Koppinen P; Pispa J; Nieminen P; Galceran J; Grosschedl R; Thesleff I. 2001. TNF signaling via the ligand-receptor pair ectodysplasin and edar controls the function of epithelial signaling centers and is regulated by Wnt and activin during tooth organogenesis. Dev Biol 229(2):443-55. [PubMed: 11203701]  [MGI Ref ID J:67054]

Laurikkala J; Pispa J; Jung HS; Nieminen P; Mikkola M; Wang X; Saarialho-Kere U; Galceran J; Grosschedl R; Thesleff I. 2002. Regulation of hair follicle development by the TNF signal ectodysplasin and its receptor Edar. Development 129(10):2541-53. [PubMed: 11973284]  [MGI Ref ID J:75943]

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Miard S; Peterkova R; Vonesch JL; Peterka M; Ruch JV; Lesot H. 1999. Alterations in the incisor development in the Tabby mouse. Int J Dev Biol 43(6):517-29. [PubMed: 10610025]  [MGI Ref ID J:104871]

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Mustonen T; Ilmonen M; Pummila M; Kangas AT; Laurikkala J; Jaatinen R; Pispa J; Gaide O; Schneider P; Thesleff I; Mikkola ML. 2004. Ectodysplasin A1 promotes placodal cell fate during early morphogenesis of ectodermal appendages. Development 131(20):4907-19. [PubMed: 15371307]  [MGI Ref ID J:128256]

Narhi K; Jarvinen E; Birchmeier W; Taketo MM; Mikkola ML; Thesleff I. 2008. Sustained epithelial {beta}-catenin activity induces precocious hair development but disrupts hair follicle down-growth and hair shaft formation. Development 135(6):1019-28. [PubMed: 18256193]  [MGI Ref ID J:131961]

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Peterkova R; Lesot H; Viriot L; Peterka M. 2005. The supernumerary cheek tooth in tabby/EDA mice-a reminiscence of the premolar in mouse ancestors. Arch Oral Biol 50(2):219-25. [PubMed: 15721153]  [MGI Ref ID J:98533]

Pispa J; Jung HS; Jernvall J; Kettunen P; Mustonen T; Tabata MJ; Kere J; Thesleff I. 1999. Cusp patterning defect in Tabby mouse teeth and its partial rescue by FGF. Dev Biol 216(2):521-34. [PubMed: 10642790]  [MGI Ref ID J:59068]

Pispa J; Pummila M; Barker PA; Thesleff I; Mikkola ML. 2008. Edar and Troy signalling pathways act redundantly to regulate initiation of hair follicle development. Hum Mol Genet 17(21):3380-91. [PubMed: 18689798]  [MGI Ref ID J:140329]

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Schmidt-Ullrich R; Tobin DJ; Lenhard D; Schneider P; Paus R; Scheidereit C. 2006. NF-{kappa}B transmits Eda A1/EdaR signalling to activate Shh and cyclin D1 expression, and controls post-initiation hair placode down growth. Development 133(6):1045-57. [PubMed: 16481354]  [MGI Ref ID J:106549]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           FGB27

Colony Maintenance

Mating SystemOutcross-Intercross         (Female x Male)   01-MAR-06
TJL Breeding Scheme: hemizygote x F1 then (X/O) wild type sibling x hemizygote
TJL Breeding Summary: genotypes of breeders are EdaTa/O x B6CBCaF1Aw-J/A in the first generation then +/O x EdaTa/Y in the second generation. Viable offspring produced from the first generation breeder pair are EdaTa/+ females, +/O females, and EdaTa/Y males.
Viable offspring produced from the second generation breeder pair are EdaTa/+ females, normal +/Y males, and EdaTa/O females.
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $246.90Female or MaleHemizygous for EdaTa  
$246.90FemaleHemizygous for X  
Individual Mouse $246.90FemaleHeterozygous for EdaTa  
Price per Pair (US dollars $)Pair Genotype
$386.80Hemizygous for EdaTa x B6CBACaF1/J-Aw-J/A (001201)  
$493.80Hemizygous for X x Hemizygous for EdaTa  

Standard Supply

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

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $321.00Female or MaleHemizygous for EdaTa  
$321.00FemaleHemizygous for X  
Individual Mouse $321.00FemaleHeterozygous for EdaTa  
Price per Pair (US dollars $)Pair Genotype
$502.90Hemizygous for EdaTa x B6CBACaF1/J-Aw-J/A (001201)  
$642.00Hemizygous for X x Hemizygous for EdaTa  

Standard Supply

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

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

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

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

Control Information

  Control
   +/+, EdaTa/+ or +/Y from the colony
   001201 B6CBACaF1/J-Aw-J/A (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

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The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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