Strain Name:

STOCK T(X;16)16H +/+ EdaTa

Stock Number:

000583

Availability:

Cryopreserved - Ready for recovery

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names T16H    (Changed: 15-DEC-04 )
Type Chromosome Aberration; Translocation;
Additional information on Mice with Chromosomal Aberrations.
Type Mutant Stock;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse

Development
The T(X;16)16H translocation was identified in the 1960s and maintained on a non-inbred background by Anthony Searle, at MRC Harwell. The colony at The Jackson Laboratory is designated "STOCK" to indicate that its genetic background is a combination of C57BL/6J and CBA/J and the passenger genome from the stock of origin flanking the translocation breakpoints. Attempts to transfer this translocation onto an inbred strain background were not successful due to breeding difficulties encountered after a few generations of backcrossing, suggesting the need for some degree of hybrid vigor. For a time, hybrid vigor was occasionally refreshed by outcrossing to a (C57BL/6J-Aw-J x CBA/CaJ)F1. Many generations of colony breeding without refreshment proved this practice unnecessary, and so it was discontinued.

Related Strains

Reciprocal Translocations
000612   AEJ.Cg-T(10;14)8Rk/J
001138   AEJ.Cg-T(3;12)30Rk/J
001102   AEJ.Cg-T(5;8)3Rk/J
001538   B6 x B6C3Sn a/A-T(1;9)27H/J
000916   B6 x B6C3Sn a/A-T(5;12)31H/J
000602   B6 x B6C3Sn a/A-T(8;16)17H/J
000593   B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J
000599   B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J
002083   B6 x B6EiC3 a/A-T(7;16)235Dn/J
003759   B6 x B6EiC3Sn a/A-T(10;16)232Dn/J
002071   B6 x B6EiC3Sn a/A-T(11;17)202Dn/J
002113   B6 x B6EiC3Sn a/A-T(11A2;16B3)238Dn/J
002068   B6 x B6EiC3Sn a/A-T(11B1;16B5)233Dn/J
002069   B6 x B6EiC3Sn a/A-T(14E4or5;16B5)225Dn/J
001926   B6 x B6EiC3Sn a/A-T(15;16)198Dn/J
001832   B6 x B6EiC3Sn a/A-T(15E;16B1)60Dn/J
003758   B6 x B6EiC3Sn a/A-T(16C3-4;17A2)65Dn/J
001833   B6 x B6EiC3Sn a/A-T(1C2;16C3)45Dn/J
001903   B6 x B6EiC3Sn a/A-T(6F;18C)57Dn/J
001535   B6 x B6EiC3Sn a/A-T(8A4;12D1)69Dn/J
001831   B6 x B6EiC3Sn a/A-T(8C3;16B5)164Dn/J
000601   B6 x STOCK a/a T(7;18)50H/J
000951   B6 x STOCK T(10;18)18H/J
000597   B6 x STOCK T(2;16)28H/J
000961   B6 x STOCK T(2;3)24H/J
000592   B6 x STOCK T(2;4)13H a/J
000950   B6 x STOCK T(2;8)26H/J
000595   B6 x STOCK T(2;9)11H/J
001820   B6 x STOCK T(2D;11B5)4Dn/J
000600   B6-Gpi1b x B6CBCa Aw-J/A-T(7;15)9H Gpi1a/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
001752   B6CBCa Aw-J/A-T(7;15)9H/J
000584   C57BL/6J-+ T(1;2)5Ca/a +/J
000586   C57BL/6J-T(1;13)70H/J
001961   C57BL/6JEi x STOCK T T(16;17)43H/+ T(16;17)43H/Ei
000655   CBA/CaH-T(14;15)6Ca/J
001911   STOCK In(1)24Rk T(In1;13)2Rk/J
000596   STOCK T(2;11)30H/+ x AEJ-a Gdf5bp-H/J or A/J-a Gdf5bp-J/J
000970   STOCK T(2;16)28H A/T(2;16)28H a/J
000590   STOCK T(2;4)1Sn a/J
000594   STOCK T(2;8)26H a/T(2;8)26H a Tyrp1+/Tyrp1b/J
001101   STOCK T(3;4)5Rk Tyrp1b/J
001816   STOCK T(7;18)50H/J
001628   STOCK T(9;17)10Ad/J
000603   STOCK T(9;17)138Ca/J
000588   TF/GnLe-T(1;17)190Ca +/+ tf/J
View Reciprocal Translocations     (46 strains)

Strains carrying   EdaTa allele
000314   B6CBACa Aw-J/A-EdaTa/J-XO
000287   B6CBACa Aw-J/A-Plp1jp EdaTa/J
000569   C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J
View Strains carrying   EdaTa     (3 strains)

View Strains carrying other alleles of Eda     (8 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms
Ectodermal Dysplasia, Hypohidrotic, X-Linked; XHED - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

EdaTa/Eda+

        involves: A * C57BL * CBA * RIII
  • skin/coat/nails phenotype
  • abnormal coat/ hair morphology (MGI Ref ID J:249)
    • abnormal coat appearance (MGI Ref ID J:249)
      • mice are mosaic for transverse striping
      • on an agouti background, loss of yellow pigment in hair results in black hair in areas of skin containing the mutation
    • abnormal hair follicle melanocyte morphology (MGI Ref ID J:249)
    • tabby coat (MGI Ref ID J:249)
  • pigmentation phenotype
  • abnormal hair follicle melanocyte morphology (MGI Ref ID J:249)
  • tabby coat (MGI Ref ID J:249)

EdaTa/Eda+

        C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J
  • craniofacial phenotype
  • abnormal hard palate (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
    • rugae V and VI are most often affected
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes
    • mice exhibit fewer ruga V abnormalities than in homozygotes
    • ruga V is more often absent compared to in homozygotes
    • ruga IV is S-shaped less often than in homozygotes
  • digestive/alimentary phenotype
  • abnormal hard palate (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
    • rugae V and VI are most often affected
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes
    • mice exhibit fewer ruga V abnormalities than in homozygotes
    • ruga V is more often absent compared to in homozygotes
    • ruga IV is S-shaped less often than in homozygotes

EdaTa/Eda+

        B6CBACa Aw-J/A-EdaTa/J-XO
  • craniofacial phenotype
  • abnormal hard palate (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
    • rugae V and VI are most often affected
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes
    • mice exhibit fewer ruga V abnormalities than in homozygotes
    • ruga V is more often absent compared to in homozygotes
    • ruga IV is S-shaped less often than in homozygotes
  • digestive/alimentary phenotype
  • abnormal hard palate (MGI Ref ID J:147677)
    • mice exhibit abnormalities in the palatal rugae pattern including shortness of rugae, division of rugae, and S-shaped rugae and rugae discoradance
    • rugae V and VI are most often affected
    • mice exhibit more ruga VI and VII abnormalities than in homozygotes
    • mice exhibit fewer ruga V abnormalities than in homozygotes
    • ruga V is more often absent compared to in homozygotes
    • ruga IV is S-shaped less often than in homozygotes

EdaTa/EdaTa

        B6CBACa Aw-J/A-EdaTa/J-XO
  • craniofacial phenotype
  • abnormal hard palate (MGI Ref ID J:147677)
    • only 13% of mice exhibit a normal palatal rugae pattern
    • 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
    • rugae V and VI are most often affected
    • mice exhibit fewer ruga VI and VII abnormalities than in heterozygotes
    • mice exhibit more ruga V abnormalities than in heterozygotes
    • ruga V is less often absent compared to in heterozygotes
    • ruga IV is S-shaped more often than in heterozygotes and wild-type mice
  • digestive/alimentary phenotype
  • abnormal hard palate (MGI Ref ID J:147677)
    • only 13% of mice exhibit a normal palatal rugae pattern
    • 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
    • rugae V and VI are most often affected
    • mice exhibit fewer ruga VI and VII abnormalities than in heterozygotes
    • mice exhibit more ruga V abnormalities than in heterozygotes
    • ruga V is less often absent compared to in heterozygotes
    • ruga IV is S-shaped more often than in heterozygotes and wild-type mice

EdaTa/Y

        involves: A * C57BL * CBA * RIII
  • skin/coat/nails phenotype
  • abnormal coat/ hair morphology (MGI Ref ID J:249)
    • abnormal coat appearance (MGI Ref ID J:249)
    • abnormal guard hair (MGI Ref ID J:249)
      • absent guard hair (MGI Ref ID J:12999)
    • abnormal hair growth (MGI Ref ID J:249)
      • focal hair loss (MGI Ref ID J:12999)
        • hair does not develop behind the ears or on the tail
    • abnormal phaeomelanin content (MGI Ref ID J:249)
    • absent zigzag hairs (MGI Ref ID J:12999)
  • touch/vibrissae phenotype
  • abnormal vibrissa number (MGI Ref ID J:249)
    • usually one rather than two supra-orbital vibrissa
  • absent vibrissae (MGI Ref ID J:249)
    • post-orbital sinus follicle and vibrissa are absent
  • vision/eye phenotype
  • abnormal eye morphology (MGI Ref ID J:249)
    • abnormal eyelid morphology (MGI Ref ID J:249)
      • absent meibomian glands (MGI Ref ID J:249)
      • narrow eye opening (MGI Ref ID J:249)
  • endocrine/exocrine gland phenotype
  • absent meibomian glands (MGI Ref ID J:249)
  • absent palmar eccrine glands (MGI Ref ID J:42660)
    • lack palmar and volar sweat glands and exhibit anhidrosis
  • respiratory system phenotype
  • abnormal respiratory system morphology (MGI Ref ID J:249)
    • abnormal nose morphology (MGI Ref ID J:249)
      • unable to keep nasal cavities clear,impairing air flow causing "snuffling"
    • abnormal respiratory mucosa morphology (MGI Ref ID J:119848)
      • male mice lack submucosal glands
  • pigmentation phenotype
  • abnormal phaeomelanin content (MGI Ref ID J:249)
  • limbs/digits/tail phenotype
  • abnormal paw/hand/foot morphology (MGI Ref ID J:42660)
    • dermal ridges on the paws are absent in all adults; EGF injection postnatally can induce dermal ridge and sweat gland formation
    • absent palmar eccrine glands (MGI Ref ID J:42660)
      • lack palmar and volar sweat glands and exhibit anhidrosis
  • abnormal tail morphology (MGI Ref ID J:249)
    • kinked tail (MGI Ref ID J:12999)
      • usually there are multiple sharp kinks at the tail tip
  • skeleton phenotype
  • abnormal skeleton morphology (MGI Ref ID J:249)
  • craniofacial phenotype
  • abnormal enamel morphology (MGI Ref ID J:12999)
    • increase in enamel cover of the incisors
  • abnormal incisor morphology (MGI Ref ID J:12999)
    • absent incisors (MGI Ref ID J:5018)
      • often absent
    • short incisors (MGI Ref ID J:5018)
  • abnormal molar morphology (MGI Ref ID J:12999)
    • molars are abnormal; abnormalities of the upper molars are less variable than those of the lower ones
    • molars are variable in size, sometimes smaller or larger than in wild-type, depending on the size of the first molar; if the first molar is only slightly smaller, the rest of the molars are smaller, if it is much smaller, than the other molars tend to be larger
    • molars have 1-2 composite roots instead of the usual three roots
    • abnormal molar crown morphology (MGI Ref ID J:12999)
      • crown of molars shows a simplified cusp pattern
    • decreased molar number (MGI Ref ID J:12999)
      • third molar is often absent
    • small molars (MGI Ref ID J:5018)
      • molars are usually smaller than normal

EdaTa/Y

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

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

Research Tools
Genetics Research

EdaTa related

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

Developmental Biology Research
Eye Defects

Mouse/Human Gene Homologs
hypohidrotic ectodermal dysplasia

Sensorineural Research
Eye Defects

Genes & Alleles

Gene & Allele Information

 
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) ED1; ED1-A1; ED1-A2; EDA1; EDA2; Eda-A1; Eda-A2; HED; RGD1563178; Ta; XHED; XLHED; 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]
 
Allele Symbol T(X;16)16H
Allele Name reciprocal translocation, Chr X and 16, Harwell 16
Allele Type Not Applicable
Gene Symbol and Name T(X;16)16H, reciprocal translocation, Chr X and 16, Harwell 16
Chromosome 16
Gene Common Name(s) Searle's translocation; T16H;
 
Gene Symbol and Name T(X;16)16H, reciprocal translocation, Chr X and 16, Harwell 16
Chromosome X
Gene Common Name(s) Searle's translocation; T16H;

Genotyping

Genotyping Information

This strain will not have a genotyping protocol or one is not currently available.

Helpful Links

Genotyping resources and troubleshooting

References

References

Selected Reference(s)

LYON MF; SEARLE AG; FORD CE; OHNO S. 1964. A MOUSE TRANSLOCATION SUPPRESSING SEX-LINKED VARIEGATION. Cytogenetics 15:306-23. [PubMed: 14248461]  [MGI Ref ID J:149655]

Additional References

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]

Guidry G; Landis SC. 1998. Target-dependent development of the vesicular acetylcholine transporter in rodent sweat gland innervation. Dev Biol 199(2):175-84. [PubMed: 9698438]  [MGI Ref ID J:107703]

Hammerschmidt B; Schlake T. 2007. Localization of Shh expression by Wnt and Eda affects axial polarity and shape of hairs. Dev Biol 305(1):246-61. [PubMed: 17376426]  [MGI Ref ID J:121316]

Harsan L; Jalabi W; Grucker D; Ghandour MS. 2004. New insights on neuronal alterations in jimpy mutant brain. Neurochem Res 29(5):943-52. [PubMed: 15139292]  [MGI Ref ID J:106214]

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]

Jamieson RV; Zhou SX; Wheatley SC; Koopman P; Tam PP. 1998. Sertoli cell differentiation and Y-chromosome activity: a developmental study of X-linked transgene activity in sex-reversed X/XSxra mouse embryos. Dev Biol 199(2):235-44. [PubMed: 9698443]  [MGI Ref ID J:107693]

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]

Johnston DS; Russell LD; Friel PJ; Griswold MD. 2001. Murine germ cells do not require functional androgen receptors to complete spermatogenesis following spermatogonial stem cell transplantation. Endocrinology 142(6):2405-8. [PubMed: 11356688]  [MGI Ref ID J:109878]

Kangas AT; Evans AR; Thesleff I; Jernvall J. 2004. Nonindependence of mammalian dental characters. Nature 432(7014):211-4. [PubMed: 15538367]  [MGI Ref ID J:94561]

Kapalanga J; Blecher SR. 1990. Effect of the X-linked gene Tabby (Ta) on eyelid opening and incisor eruption in neonatal mice is opposite to that of epidermal growth factor. Development 108(2):349-55. [PubMed: 2351074]  [MGI Ref ID J:42661]

Knapp PE; Adjan VV; Hauser KF. 2009. Cell-specific loss of kappa-opioid receptors in oligodendrocytes of the dysmyelinating jimpy mouse. Neurosci Lett 451(2):114-8. [PubMed: 19110031]  [MGI Ref ID J:146365]

Knapp PE; Dutta S; Skoff RP. 1990. Differences in levels of neuroglial cell death in jimpy male mice and carrier females. Dev Neurosci 12(3):145-52. [PubMed: 2364893]  [MGI Ref ID J:116371]

Knapp PE; Skoff RP. 1993. Jimpy mutation affects astrocytes: lengthening of the cell cycle in vitro. Dev Neurosci 15(1):31-6. [PubMed: 8269866]  [MGI Ref ID J:116364]

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]

Kosaras B; Kirschner DA. 1990. Radial component of CNS myelin: junctional subunit structure and supramolecular assembly. J Neurocytol 19(2):187-99. [PubMed: 2113569]  [MGI Ref ID J:121320]

Kristenova P; Peterka M; Lisi S; Gendrault JL; Lesot H; Peterkova R. 2002. Different morphotypes of functional dentition in the lower molar region of tabby (EDA) mice. Orthod Craniofac Res 5(4):205-14. [PubMed: 12416535]  [MGI Ref ID J:103894]

Langton AK; Herrick SE; Headon DJ. 2008. An extended epidermal response heals cutaneous wounds in the absence of a hair follicle stem cell contribution. J Invest Dermatol 128(5):1311-8. [PubMed: 18037901]  [MGI Ref ID J:135502]

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]

Le Goascogne C; Eychenne B; Tonon MC; Lachapelle F; Baumann N; Robel P. 2000. Neurosteroid progesterone is up-regulated in the brain of jimpy and shiverer mice. Glia 29(1):14-24. [PubMed: 10594919]  [MGI Ref ID J:78788]

Le Goascogne C; Sannanes N; Gouezou M; Baulieu EE; Robel P. 1993. Suppressed expression of the cytochrome P45017 alpha protein in the testicular feminized (Tfm) mouse testes. J Endocrinol 139(1):127-30. [PubMed: 8254285]  [MGI Ref ID J:15718]

Lyon MF. 1963. Attempts to test the inactive-X theory of dosage compensation in mammals Genet Res 4:93-103.  [MGI Ref ID J:272]

Lyon MF. 1970. Genetic activity of sex chromosomes in somatic cells of mammals. Philos Trans R Soc Lond B Biol Sci 259(828):41-52. [PubMed: 4399067]  [MGI Ref ID J:5238]

Mayer TC; Green MC. 1978. Epidermis is the site of action of tabby (Ta) in the mouse. Genetics 90(1):125-31. [PubMed: 359407]  [MGI Ref ID J:6041]

Melnick M; Phair RD; Lapidot SA; Jaskoll T. 2009. Salivary gland branching morphogenesis: a quantitative systems analysis of the Eda/Edar/NFkappaB paradigm. BMC Dev Biol 9:32. [PubMed: 19500387]  [MGI Ref ID J:152818]

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]

Mou C; Jackson B; Schneider P; Overbeek PA; Headon DJ. 2006. Generation of the primary hair follicle pattern. Proc Natl Acad Sci U S A 103(24):9075-80. [PubMed: 16769906]  [MGI Ref ID J:111052]

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]

Pantalacci S; Prochazka J; Martin A; Rothova M; Lambert A; Bernard L; Charles C; Viriot L; Peterkova R; Laudet V. 2008. Patterning of palatal rugae through sequential addition reveals an anterior/posterior boundary in palatal development. BMC Dev Biol 8:116. [PubMed: 19087265]  [MGI Ref ID J:145173]

Pennycuik PR; Raphael KA. 1984. The tabby locus (Ta) in the mouse: its site of action in tail and body skin. Genet Res 43(1):51-63. [PubMed: 6373499]  [MGI Ref ID J:7450]

Peterkova R; Kristenova P; Lesot H; Lisi S; Vonesch JL; Gendrault JL; Peterka M. 2002. Different morphotypes of the tabby (EDA) dentition in the mouse mandible result from a defect in the mesio-distal segmentation of dental epithelium. Orthod Craniofac Res 5(4):215-26. [PubMed: 12416536]  [MGI Ref ID J:103893]

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]

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]

Rao MS; Jaszczak E; Landis SC. 1994. Innervation of footpads of normal and mutant mice lacking sweat glands. J Comp Neurol 346(4):613-25. [PubMed: 7983247]  [MGI Ref ID J:19910]

Rawlins EL; Hogan BL. 2005. Intercellular growth factor signaling and the development of mouse tracheal submucosal glands. Dev Dyn 233(4):1378-85. [PubMed: 15973734]  [MGI Ref ID J:119848]

Risnes S; Peterkova R; Lesot H. 2005. Distribution and structure of dental enamel in incisors of Tabby mice. Arch Oral Biol 50(2):181-4. [PubMed: 15721148]  [MGI Ref ID J:100300]

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]

Sofaer JA. 1979. Additive effects of the genes tabby and crinkled on tooth size in the mouse. Genet Res 33(2):169-74. [PubMed: 478295]  [MGI Ref ID J:151073]

Sofaer JA. 1969. Aspects of the tabby-crinkled-downless syndrome. I. The development of tabby teeth. J Embryol Exp Morphol 22(2):181-205. [PubMed: 5361554]  [MGI Ref ID J:5138]

Sofaer JA. 1969. Aspects of the tabby-crinkled-downless syndrome. II. Observations on the reaction to changes of genetic background. J Embryol Exp Morphol 22(2):207-27. [PubMed: 5361555]  [MGI Ref ID J:5139]

Sofaer JA. 1974. Differences between tabby and downless mouse epidermis and dermis in culture. Genet Res 23(2):219-25. [PubMed: 4420168]  [MGI Ref ID J:5489]

Sofaer JA; MacLean CJ. 1970. Dominance in threshold characters. A comparison of two tabby alleles in the mouse. Genetics 64(2):273-80. [PubMed: 5470481]  [MGI Ref ID J:5176]

Srivastava AK; Durmowicz MC; Hartung AJ; Hudson J; Ouzts LV; Donovan DM; Cui CY; Schlessinger D. 2001. Ectodysplasin-A1 is sufficient to rescue both hair growth and sweat glands in Tabby mice. Hum Mol Genet 10(26):2973-81. [PubMed: 11751679]  [MGI Ref ID J:73715]

Srivastava AK; Pispa J; Hartung AJ; Du Y; Ezer S; Jenks T; Shimada T; Pekkanen M; Mikkola ML; Ko MS; Thesleff I; Kere J; Schlessinger D. 1997. The Tabby phenotype is caused by mutation in a mouse homologue of the EDA gene that reveals novel mouse and human exons and encodes a protein (ectodysplasin-A) with collagenous domains. Proc Natl Acad Sci U S A 94(24):13069-74. [PubMed: 9371801]  [MGI Ref ID J:44605]

Sundberg JP (ed.). 1994. . In: Handbook of Mouse Mutations with Skin and Hair Abnormalities: Animal Models and Biomedical Tools. CRC Press, Boca Raton.  [MGI Ref ID J:30359]

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Tucker AS; Headon DJ; Courtney JM; Overbeek P; Sharpe PT. 2004. The activation level of the TNF family receptor, Edar, determines cusp number and tooth number during tooth development. Dev Biol 268(1):185-94. [PubMed: 15031115]  [MGI Ref ID J:92196]

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Vielkind U; Hardy MH. 1996. Changing patterns of cell adhesion molecules during mouse pelage hair follicle development. 2. Follicle morphogenesis in the hair mutants, Tabby and downy. Acta Anat (Basel) 157(3):183-94. [PubMed: 9226037]  [MGI Ref ID J:41386]

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Zhang Y; Tomann P; Andl T; Gallant NM; Huelsken J; Jerchow B; Birchmeier W; Paus R; Piccolo S; Mikkola ML; Morrisey EE; Overbeek PA; Scheidereit C; Millar SE; Schmidt-Ullrich R. 2009. Reciprocal requirements for EDA/EDAR/NF-kappaB and Wnt/beta-catenin signaling pathways in hair follicle induction. Dev Cell 17(1):49-61. [PubMed: 19619491]  [MGI Ref ID J:151982]

T(X;16)16H related

Carrel L; Hunt PA; Willard HF. 1996. Tissue and lineage-specific variation in inactive X chromosome expression of the murine Smcx gene. Hum Mol Genet 5(9):1361-6. [PubMed: 8872478]  [MGI Ref ID J:35234]

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Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Colony Maintenance

Breeding & HusbandryThe T(X;16)16H translocation chromosome (abbreviated T16H) is maintained in repulsion with EdaTa. T16H +/+ EdaTa females are bred to + EdaTa/Y males from the colony, which yields T16H +/Y and + EdaTa/Y males and T16H +/+ EdaTa and + EdaTa/EdaTa females. In the past, hybrid vigor was refreshed every few generations by crossing T16H +/+ EdaTa females to (C57BL/6J x CBA/J)F1 males; however, this has proven unnecessary and has been discontinued. Male mice having the T(X;16)16H translocation are sterile.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Pricing for USA, Canada and Mexico shipping destinations View International pricing
Price (US dollars $)
Cryorecovery Fee $1900.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Additional Supply Details

Pricing for International shipping destinations View USA Canada and Mexico pricing
Price (US dollars $)
Cryorecovery Fee $2470.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Additional Supply Details

Supply Details

Standard SupplyCryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
  • Cryorecovery - Standard.
    We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory 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.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

  • Genomic DNA is available for this strain from the Mouse DNA Resource.

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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.


See Terms of Use tab for General Terms and Conditions


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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In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

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In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. In purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

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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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