Search Criteria: Research Area is "Mouse/Human Gene Homologs: albinism, tyrosine negative"

JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
000058 B6(Cg)-Tyrc-2J/J
Level 2
Mice homozygous for Tyrc-2J are phenotypically identical to homozygotes for the classic albino allele. Pigment is completely absent from skin, hair and eyes. While Tyr mRNA levels of Tyrc-2J homozygotes are similar to those of wild-type mice, there is virtually no tyrosinase protein present (Le Fur et al. 1996). Both homozygote and heterozygote mice are highly resistant to light damage and exhibit retinal degeneration (increased photoreceptor death) into young adulthood. Degeneration does not continue in adult mice (Bravo-Nuevo et al. 2004).
002565 A.B6-Tyr+/J
Repository- Live
000578 B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J
Repository- Live
Mice homozygous for the Snell's waltzer spontaneous mutation (Myo6sv) show to a marked degree the typical circling, head-tossing, deafness, and hyperactivity of other mutant mice of this type. Homozygous mutant mice are recognizable by the age of 1 week. The abnormalities of the inner ear consist of degeneration of the entire neuroepithelium comprising the organ of Corti, the saccular and utricular maculae, and the cristae of all three semicircular canals. Although viability of homozygotes is nearly normal, breeding ability is reduced and males are more reliable breeders than females.

Specific cytoskeletal components are critical for specific cellular structures. The microvilli of intestinal brush border cells in Myo6sv homozygotes are shorter than normal. While myosin 6 is not critical for the development of hair cell stereocilia, it is essential for their maintenance. At birth the stereocilia appear nearly normal with only occasional stereocil .....
For more information please see the full descriiption on the strain data sheet

007484 B6.Cg-Tyrc-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ
Repository- Live
On an albino background Tg(Tyr)3412ARpw permits the identification of gender as early as embryonic day 10.5. This strain is segregating for Tg(Tyr)3412ARpw and homozygous for Tyrc-2J so the individuals not carrying Tg(Tyr3412)ARpw are albino. Because Tg(Tyr)3412ARpw inserted into the X Chromosome, breeding a carrier male with a noncarrier (wild-type) female results in embryos in which all XX individuals develop eye pigment, due to the Tg(Tyr)3412ARpw inherited from their father, while all XY individuals have non-pigmented eyes, having inherited a wild-type X Chromosome from their mother.

This strain is also homozygous for Tg(SryEGFP)92Ei. This reporter transgene consists of a 5 prime regulatory segment of the Sry gene driving EGFP. This transgene is expressed in the pre-support cell lineage (pre-sertoli and pre-granulosa cells) of the fetal genital ridge (Albrecht and Eicher, 2001) and in discrete areas the adult male but not female brain (Dewing et al., 20 .....
For more information please see the full descriiption on the strain data sheet

000899 C.B6-Tyr+ Hbbs/J
Repository- Live
004828 FVB.129P2-Pde6b+ Tyrc-ch/AntJ
Repository- Live
These mice are homozygous for the 129P2/OlaHsd wildtype Pde6b allele and do not suffer from blindness due to retinal degeneration. Mice from the colony of FVB.129P2-Fmr1tm1Cgr/J, Stock No. 004624, that no longer carried the mutant allele for Fmr1 were used to establish this line. Mice are pigmented as a result of the homozygosity of the Tyrc-ch allele. This mutant mouse strain may be useful in studies where a sighted mouse on the FVB background is an appropriate control, such as behavioral studies. This strain serves as the control for the FVB.129P2-Fmr1tm1Cgr/J strain, Stock No. 004624 .
000090 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J
Repository-Cryopreserved
The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a .....
For more information please see the full descriiption on the strain data sheet
000091 129T1/Sv-Oca2+ Tyrc-ch Dnd1Ter/J
Repository-Cryopreserved
001279 129T1/Sv-Oca2+ Tyrc-ch-Aft/J
Repository-Cryopreserved
Aft is a dominant mutation that causes increased postnatal lethality in heterozygotes and nearly 100% embryonic or perinatal lethality in homozygotes. Aft/+ mice can be identified by tail kinks near the tail tip and syndactyly of the third and fourth digits of the hind feet, a trait which is often unilateral. This syndactyly does not result from bone fusion, but rather from the persistence of the skin web that normally is removed via apoptosis during development. The tail kinks appear to result from cartilage overgrowth and fusion. Alopecia is found at six to eight months of age and can progress into bleeding ulcerations. Histology of Aft/+ skin shows fewer follicles, fibrosis, and an increase in the number of mast cells. The penetrance of this mutation is only approximately 65% on the 129/Sv and C57BL/6J backgrounds and the expressivity is variable. The most prevalent trait in Aft/+ mice is tail kinks, followed by syndactyly then skin lesions. The .....
For more information please see the full descriiption on the strain data sheet
005445 A.B6 Tyr+-Cybanmf333/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf333 entry.
005012 A.B6 Tyr+-Myo5ad-l31J/J
Repository-Cryopreserved
View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page.
001017 AKXD10/TyJ
Repository-Cryopreserved
000765 AKXD13/TyJ
Repository-Cryopreserved
000954 AKXD15/TyJ
Repository-Cryopreserved
000958 AKXD16/TyJ
Repository-Cryopreserved
001093 AKXD18/TyJ
Repository-Cryopreserved
001062 AKXD21/TyJ
Repository-Cryopreserved
000947 AKXD22/TyJ
Repository-Cryopreserved
000969 AKXD24/TyJ
Repository-Cryopreserved
000777 AKXD6/TyJ
Repository-Cryopreserved
000763 AKXD9/TyJ
Repository-Cryopreserved
000409 B10.129P-H1b Hbbd Tyrc Ea7a/(5M)oSnJ
Repository-Cryopreserved
000418 B10.129P-H1b Tyrc Hbbd/(5M)nSnJ
Repository-Cryopreserved
000432 B10.C-H1b Hbbd Tyrc/(41N)SnJ
Repository-Cryopreserved
000580 B10.D2/nSn-Tyrc-4J/J
Repository-Cryopreserved
000822 B6 x 129S1/SvEi Oca2+ Tyr+-Vsx2or-J/J
Repository-Cryopreserved
000383 B6.C-Tyrc H1b Hbbd/ByJ
Repository-Cryopreserved
000035 B6.Cg-Tyrc-J/J
Repository-Cryopreserved
000104 B6.Cg-Tyrc-h/J
Repository-Cryopreserved
000054 B6.D2-Tyrc-p/J
Repository-Cryopreserved
The coat color of mice homozygous for the platinum mutation is nearly albino, cream colored, and these mice have pink eyes and a sheen to their coat. These homozygotes are lighter in color than chinchilla homozygotes despite having more tyrosinase activity in their cells. This is due to the altered subcellular localization of platinum tyrosinase. (Dickie M., 1966.)
000339 C3H/HeJ-Tyrc-9J/J
Repository-Cryopreserved
001294 C3H/HeJ-Tyrc-a/J
Repository-Cryopreserved
001002 C57BL/10SnJ-Tyrc-11J/J
Repository-Cryopreserved
001006 CBA/J-Tyrc-10J/J
Repository-Cryopreserved
000619 FS/EiJ
Repository-Cryopreserved
The FS/Ei strain was originally used as a linkage testing stock for gene mapping. It is homozygous for several visible recessive mutations including brown (Tyrp1b), pink-eyed dilution (Oca2p), chinchilla (Tyrc-ch), frizzy (fr), and the neurological mutation shaker 1 (Myo7ash1). It is also homozygous for a couple allelic variants that can be easily typed (Mod2b and Hbbd). Mice homozygous for the shaker 1 show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist .....
For more information please see the full descriiption on the strain data sheet
000494 J.Cg-Oca2+ Tyr+ Lystbg/J
Repository-Cryopreserved
Mice homozygous for the beige spontaneous mutation (Lystbg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l .....
For more information please see the full descriiption on the strain data sheet
002281 NFS.C58-Tyr+/J
Repository-Cryopreserved
004304 NOD.CBALs-Tyr+/LtJ
Repository-Cryopreserved
This Chr 7 congenic strain in which the tyrosinase allele Tyr+ of the CBA/JLsLt strain is fixed on the NOD/Lt background, therefore making the strain agouti in color. This strain should be a good donor for blastocysts in which to microinject targeted NOD ES cells, and may alleviate unwanted genome integration experienced with use of the C57BL/6 blastocysts. The congenic segment on Chr 7 slightly supresses spontaneous T1D development which is an asset when these females are used as blastocyst recipients.
000271 SH1/LeJ
Repository-Cryopreserved
Mice homozygous for the shaker 1 spontaneous mutation (Myo7ash1) show circling, head-tossing, deafness, and hyperactivity characteristic of this type of mutant mice. Viability is normal, and breeding ability is high for a circling mutant. Homozygous mutant mice are most often deaf and swim well on the surface of water up to 4 weeks of age and more but lose the ability later. The degenerative changes of the labyrinth may occur a little later than in some of the other waltzing mutants. By light microscopy, the changes are seen to consist of degeneration of the organ of Corti, the spiral ganglion, and the stria vascularis in the cochlea, and of the saccular macula and the vestibular ganglion in the vestibular labyrinth.
001759 STOCK A Tyrc Sha/J
Repository-Cryopreserved
000306 STOCK Dll3pu + Tyrc-ch/+ Oca2p Tyrc-ch/J
Repository-Cryopreserved
000006 STOCK Hk Tyrc/J
Repository-Cryopreserved
While mice carrying the Hk mutation often have a hooked curl at the end of a shortened tail, this mutation may more consistently result in a displaced anus that is positioned posterior to the normal site and is more slit-shaped than circular. In some instances the anus has been located in the beginning of the tail and a depression was found to extend partway down the ventral side of the tail (Holman, 1951). The Hk mutation is semidominant with homozygotes often showing a shorter, more affected tail than heterozygotes (P.W. Lane Personal Communication).
000206 STOCK a/a Tyrc-h/J
Repository-Cryopreserved

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