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- Description
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- Genes & alleles
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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
Type Mutant Strain; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation N3 F50p Description
Testicular feminization (ArTfm) is a dominant spontaneous mutation on the X chromosome. Hemizygous male mice are outwardly female in appearance except that the vagina does not open until 3 months of age if at all. Male reproductive development is abnormal leading to very small testes, and the absense of vas deferens, the epididymis, and male accessory glands. Spermatogonia and Sertoli cells are present in the testes, but spermatogenesis does not proceed past meiotic prophase. Leydig cells, which normally produce androgen in males, fail to develop normally. This strain is also segregating for the tabby mutation (EdaTa) that affects both the coat color and hair pattern growth. The tabby mutation is maintained in repulsion with the testicular feminization mutation and is used as a coat color marker to assist in identifying resulting genotypes obtained from matings.
Control Information
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying Aw-J allele
View Strains carrying Aw-J (31 strains)
001809 B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J
000314 B6CBACa Aw-J/A-EdaTa/J-XO 000287 B6CBACa Aw-J/A-Plp1jp EdaTa/J 000583 STOCK T(X;16)16H +/+ EdaTa
002016 B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ 000552 B6-Aw-J-EdaTa-6J.Cg-Sxr 001730 B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J 000841 B6-Aw-J.CBy-EdaTa-By/J 001809 B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J 001232 C3H/HeJ-EdaTa-5J/J 000338 C57BL/6J Aw-J-EdaTa-6J/J 003112 STOCK EdaTa-5J/J
Additional Web Information
JAX® NOTES, January 1990, 440. Tabby Stocks Available from The Jackson Laboratory.
JAX® NOTES, Summer 1994; 458. Tfm Strains at The Jackson Laboratory.
Phenotype
Phenotype Information
Androgen Insensitivity Syndrome; AIS - Models with phenotypic similarity to human disease where etiologies involve orthologs.1 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).
assigned by genotype
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
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
ArTfm/Y
Background Not Specified
- reproductive system phenotype
- abnormal spermatogenesis (MGI Ref ID J:65900)
- germ cell development progressed to spermatocytes
- abnormal testis morphology (MGI Ref ID J:65900)
- an extra layer of parietal lymphatic cells was present, but these cells appeared to be normal; myoid cells were also normal
- peritubular fibrosis was observed, as indicated by a few extra layers of fibroblastic-like cells around the seminiferous tubules, although this fibrosis was not as severe as that seen in Dhhtm1Amc feminized males
- collagen and basal lamina material between Sertoli and myoid cells extended around the entire seminiferous tubule unlike that of the patchy basal lamina seen in Dhhtm1Amc feminized males
- abnormal Leydig cell morphology (MGI Ref ID J:65900)
- at 63 days of age, testes from adult male hemizygotes contained abundant adult-type Leydig cells which appeared relatively undifferentiated and lacked smooth endoplasmic reticulum
- endocrine/exocrine gland phenotype
- abnormal testis morphology (MGI Ref ID J:65900)
- an extra layer of parietal lymphatic cells was present, but these cells appeared to be normal; myoid cells were also normal
- peritubular fibrosis was observed, as indicated by a few extra layers of fibroblastic-like cells around the seminiferous tubules, although this fibrosis was not as severe as that seen in Dhhtm1Amc feminized males
- collagen and basal lamina material between Sertoli and myoid cells extended around the entire seminiferous tubule unlike that of the patchy basal lamina seen in Dhhtm1Amc feminized males
- abnormal Leydig cell morphology (MGI Ref ID J:65900)
- at 63 days of age, testes from adult male hemizygotes contained abundant adult-type Leydig cells which appeared relatively undifferentiated and lacked smooth endoplasmic reticulum
ArTfm/Y
involves: NMRI * STOCK EdaTa Atp7aMo-blo
- reproductive system phenotype
- abnormal seminiferous tubule morphology (MGI Ref ID J:140803)
- mice exhibit greater thickening and hyperplasia of peritubular myoid cells compared to ArTfm male mice on the original stock background
- Leydig cell hyperplasia (MGI Ref ID J:140803)
- unlike ArTfm male mice on the original stock background
- enlarged seminiferous tubules (MGI Ref ID J:140803)
- in 15 of 46 mice unlike ArTfm male mice on the original stock background
- arrest of male meiosis (MGI Ref ID J:140803)
- spermatogenesis does not proceed beyond meiosis prophase
- cryptorchism (MGI Ref ID J:140803)
- secondary sex reversal (MGI Ref ID J:140803)
- male mice have female genitals, a blind ending vagina, inguinal testes, no scrotum and lack derivatives of the Wolffian ducts
- tumorigenesis
- testis tumor (MGI Ref ID J:140803)
- 4 of 46 mice exhibit unilateral Leydig tumor unlike ArTfm male mice on the original stock background
- however, no germ cell tumors are observed
- endocrine/exocrine gland phenotype
- abnormal seminiferous tubule morphology (MGI Ref ID J:140803)
- mice exhibit greater thickening and hyperplasia of peritubular myoid cells compared to ArTfm male mice on the original stock background
- Leydig cell hyperplasia (MGI Ref ID J:140803)
- unlike ArTfm male mice on the original stock background
- enlarged seminiferous tubules (MGI Ref ID J:140803)
- in 15 of 46 mice unlike ArTfm male mice on the original stock background
- cryptorchism (MGI Ref ID J:140803)
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+
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)
- 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)
- 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
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
This mouse can be used to support research in many areas including:ArTfm related
EdaTa relatedEndocrine Deficiency Research
Gonad Defects
Mouse/Human Gene Homologs
testicular feminization
Reproductive Biology Research
Developmental Defects Affecting Gonads
Fertility Defects
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 | Aw-J | ||
|---|---|---|---|
| Allele Name | white bellied agouti Jackson | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | AWJ; | ||
| Strain of Origin | C57BL/6J | ||
| Gene Symbol and Name | a, nonagouti | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | AGSW; AGTI; AGTIL; ASP; As; MGC126092; MGC126093; SHEP9; agouti; agouti signal protein; agouti suppressor; | ||
| Allele Symbol | ArTfm | ||
| Allele Name | testicular feminization | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | Tfm; | ||
| Strain of Origin | (STOCK Eda | ||
| Gene Symbol and Name | Ar, androgen receptor | ||
| Chromosome | X | ||
| Gene Common Name(s) | AIS; AW320017; Andr; DHTR; HUMARA; HYSP1; KD; NR3C4; SBMA; SMAX1; TFM; Tfm; expressed sequence AW320017; testicular feminization; | ||
| General Note | ArTfm acts by causing insensitivity to androgens due to a defect in androgen-binding receptor present in cytosol and nucleus. Most responses to androgens are absent or defective in ArTfm/Y males and are not inducible by administration of androgens (J:5221, J:5532). Androgen receptor is found in kidney, submandibular gland (J:5667) and brain (J:5927). ArTfm/Y males have about 20-25 percent of normal testosterone-binding activity in brain (J:6096) and 10-20 percent in kidney. | ||
| Molecular Note | A frameshift mutation resulting from the deletion of a single cytosine residue generated a premature stop codon at residue 412. The nonsenes mutation is expected to preclude the translation of both the DNA- and steroid-binding domains. [MGI Ref ID J:11219] [MGI Ref ID J:1264] [MGI Ref ID J:19598] [MGI Ref ID J:30797] [MGI Ref ID J:712] | ||
| Allele Symbol | EdaTa | ||
| Allele Name | tabby | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | Ta; Ta3; TaFa; Taf; | ||
| Strain of Origin | stock 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] | ||
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
Additional References
Charest NJ; Zhou ZX; Lubahn DB; Olsen KL; Wilson EM; French FS. 1991. A frameshift mutation destabilizes androgen receptor messenger RNA in the Tfm mouse. Mol Endocrinol 5(4):573-81. [PubMed: 1681426] [MGI Ref ID J:712]
Gaspar ML; Bourgarel P; Meo T; Tosi M. 1991. [Structure of messenger RNA of androgen receptor in mice and molecular characterization in Tfm mutant] C R Seances Soc Biol Fil 185(6):510-9. [PubMed: 1822400] [MGI Ref ID J:1264]
Gaspar ML; Meo T; Bourgarel P; Guenet JL; Tosi M. 1991. A single base deletion in the Tfm androgen receptor gene creates a short-lived messenger RNA that directs internal translation initiation. Proc Natl Acad Sci U S A 88(19):8606-10. [PubMed: 1924321] [MGI Ref ID J:30797]
Lyon MF; Hawkes SG. 1970. X-linked gene for testicular feminization in the mouse. Nature 227(5264):1217-9. [PubMed: 5452809] [MGI Ref ID J:5173]
Murphy L; Jeffcoate IA; O'Shaughnessy PJ. 1994. Abnormal Leydig cell development at puberty in the androgen-resistant Tfm mouse. Endocrinology 135(4):1372-7. [PubMed: 7925099] [MGI Ref ID J:20980]
Aw-J relatedArTfm relatedAberg 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]
Barsh GS; Epstein CJ. 1989. Physical and genetic characterization of a 75-kilobase deletion associated with al, a recessive lethal allele at the mouse agouti locus. Genetics 121(4):811-8. [PubMed: 2566558] [MGI Ref ID J:9799]
Baurle J; Vogten H; Grusser-Cornehls U. 1998. Course and targets of the calbindin D-28k subpopulation of primary vestibular afferents. J Comp Neurol 402(1):111-28. [PubMed: 9831049] [MGI Ref ID J:118430]
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]
Chinta SJ; Rane A; Yadava N; Andersen JK; Nicholls DG; Polster BM. 2009. Reactive oxygen species regulation by AIF- and complex I-depleted brain mitochondria. Free Radic Biol Med 46(7):939-47. [PubMed: 19280713] [MGI Ref ID J:145908]
Cui CY; Hashimoto T; Grivennikov SI; Piao Y; Nedospasov SA; Schlessinger D. 2006. Ectodysplasin regulates the lymphotoxin-beta pathway for hair differentiation. Proc Natl Acad Sci U S A 103(24):9142-7. [PubMed: 16738056] [MGI Ref ID J:111051]
Cui CY; Kunisada M; Esibizione D; Grivennikov SI; Piao Y; Nedospasov SA; Schlessinger D. 2007. Lymphotoxin-beta regulates periderm differentiation during embryonic skin development. Hum Mol Genet 16(21):2583-90. [PubMed: 17673451] [MGI Ref ID J:129949]
Dickie MM. 1969. Mutations at the agouti locus in the mouse. J Hered 60(1):20-5. [PubMed: 5798139] [MGI Ref ID J:30922]
Esibizione D; Cui CY; Schlessinger D. 2008. Candidate EDA targets revealed by expression profiling of primary keratinocytes from Tabby mutant mice. Gene 427(1-2):42-6. [PubMed: 18848976] [MGI Ref ID J:143603]
Granholm DE; Reese RN; Granholm NH. 1996. Agouti alleles alter cysteine and glutathione concentrations in hair follicles and serum of mice (A y/a, A wJ/A wJ, and a/a). J Invest Dermatol 106(3):559-63. [PubMed: 8648194] [MGI Ref ID J:32132]
Granholm DE; Reese RN; Granholm NH. 1995. Agouti alleles influence thiol concentrations in hair follicles and extrafollicular tissues of mice (Ay/a, AwJ/AwJ, a/a). Pigment Cell Res 8(6):302-6. [PubMed: 8789738] [MGI Ref ID J:31403]
Jones JM; Huang JD; Mermall V; Hamilton BA; Mooseker MS; Escayg A; Copeland NG; Jenkins NA; Meisler MH. 2000. The mouse neurological mutant flailer expresses a novel hybrid gene derived by exon shuffling between Gnb5 and Myo5a. Hum Mol Genet 9(5):821-8. [PubMed: 10749990] [MGI Ref ID J:61324]
Kappenman KE; Dvoracek MA; Harvison GA; Fuller BB; Granholm NH. 1992. Tyrosinase abundance and activity in murine hairbulb melanocytes of agouti mutants (C57BL/6J-a/a, Ay/a, and AwJ/AwJ). Pigment Cell Res Suppl 2:79-83. [PubMed: 1409442] [MGI Ref ID J:1295]
Katoh A; Yoshida T; Himeshima Y; Mishina M; Hirano T. 2005. Defective control and adaptation of reflex eye movements in mutant mice deficient in either the glutamate receptor delta2 subunit or Purkinje cells. Eur J Neurosci 21(5):1315-26. [PubMed: 15813941] [MGI Ref ID J:101081]
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]
Lee M; Kim A; Chua SC Jr; Obici S; Wardlaw SL. 2007. Transgenic MSH overexpression attenuates the metabolic effects of a high-fat diet. Am J Physiol Endocrinol Metab 293(1):E121-31. [PubMed: 17374695] [MGI Ref ID J:126508]
Lu W; Tsirka SE. 2002. Partial rescue of neural apoptosis in the Lurcher mutant mouse through elimination of tissue plasminogen activator. Development 129(8):2043-50. [PubMed: 11934869] [MGI Ref ID J:111363]
Mayer TC; Fishbane JL. 1972. Mesoderm-ectoderm interaction in the production of the agouti pigmentation pattern in mice. Genetics 71(2):297-303. [PubMed: 4558326] [MGI Ref ID J:5288]
Mitsumori K; Yasuhara K; Mori I; Hayashi S; Shimo T; Onodera H; Nomura T; Hayashi Y. 1998. Pulmonary fibrosis caused by N-methyl-N-nitrosourethane inhibits lung tumorigenesis by urethane in transgenic mice carrying the human prototype c-Ha-ras gene. Cancer Lett 129(2):181-90. [PubMed: 9719460] [MGI Ref ID J:52138]
Monroe DG; Wipf LP; Diggins MR; Matthees DP; Granholm NH. 1998. Agouti-related maturation and tissue distribution of alpha-Melanocyte Stimulating Hormone in wild-type (AwJ/AwJ) and mutant (Ay/a,a/a) mice. Pigment Cell Res 11(5):310-3. [PubMed: 9877102] [MGI Ref ID J:52183]
Mullen RJ. 1974. A<w-J> - white-bellied agouti-J Mouse News Lett 50:38. [MGI Ref ID J:64104]
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]
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Health & husbandry
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Currently there no information available for this strain. This may be due to the supply level of this strain.
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Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 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.
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Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 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
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Supply Details
| Standard Supply | Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information. |
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Control Information
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| 000664 C57BL/6J | ||
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