Strain Name: |
STOCK Hk Tyrc/J |
|---|---|
Stock Number: |
000006 |
Availability: | Repository-Cryopreserved |
Price and Supply Information | |
General Terms and Conditions |
| Genes & Alleles | Hk; Tyr; Tyrc; |
Type JAX® GEMM® Strain - Mutant Stock Additional information on JAX® GEMM® Strains. Type JAX® GEMM® Strain - Spontaneous Mutation Species laboratory mouse Generation F60p Appearance
white with hooked tail and displaced anus
Related Genotype: a/a Tyrc/Tyrc Hk/+ or a/a Tyrc/Tyrc Hk/HkStrain Description
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).Strain Development
The Hk mutation arose spontaneously. It was identified in 1949 in a piebald shaker stock and was sent from SP Holman to GD Snell in 1951. This was subsequently crossed once to a rex (Re) stock, crossed three times to C57BL/6, crossed once to AKR, crossed twice to A/Sn, and then crossed once to C57BL/6J before PW Lane inbred the line by sibling mating. This resulted in an inbred background homozygous for Tyrc and a and segregating for Hk. In 1978 embryos were generated for cryopreservation by breeding Hk/+ females with Hk/Hk males when the strain was at F59.
Mammalian Phenotype Terms assigned by genotype |
| Allele Symbol | Hk | ||
|---|---|---|---|
| Allele Name | hook | ||
| Strain of Origin | piebald shaker stock | ||
| Allele Symbol | Tyrc | ||
| Allele Name | albino | ||
| Common Name(s) | c; | ||
| Strain of Origin | old mutant of the mouse fancy | ||
| Gene Symbol and Name | Tyr, tyrosinase | ||
| Chromosome | 7 | ||
| Gene Common Name(s) | C; OCA1A; OCAIA; SHEP3; albino; c; skc35; skin/coat color 35; | ||
| General Note | Tyrc, albino. This very old mutant was already known in Greek and Roman times. Hair and eyes are completely devoid of pigment (J:5436, J:5001, J:30725). The albino mutation affects the amount of tyrosinase, and thus of melanin, in pigment cells, but does not interfere with the production of pigment cells themselves (J:12173, J:13092). Melanocytes with melanosomes showing normal fine structure occur in the retina and hair follicles. Pigment granules are smaller and fewer than normal and completely lack melanin (J:5346, J:5001, J:30725). Tyrosinase is almost absent (J:12173).Although Tyr is the structural gene for tyrosinase, some albino mutations may affect tyrosinase enzyme regulation rather than structure (J:6611), suggesting that these mutations affect tyrosinase inhibition (J:5346), presumably via control regions of the gene. All the mutant alleles are recessive to wild type in phenotype, but heterozygotes with wild type produce intermediate amounts of tyrosinase (J:12173).Albino-locus mutants with lightly pigmented eyes have a reduced number of fibers of the optic nerve going to the ipsilateral lateral geniculate nucleus of the brain. This is probably a secondary effect of reduced tyrosinase activity or amount of pigment in the pigmentepithelium, since genes at other loci that reduce eye pigmentation also cause the same anomaly (J:5436, J:6064).Abnormal retinal pathways disrupted at the optic chiasm that occur in albinism can be corrected with a Tyr normal transgene (J:22320).Lipofuscin is a terminal oxidation product pigment that accumulates with age. In a cross of C57BL/6J and BALB/cJ, which differ in cardiac deposition of the pigment, this trait segregated with albinism, and is controlled by the Tyr locus (J:15460).Tyrc homozygotes do not perform as well as normal in a number of behavioral tests. It is likely that this effect is mediated, at least in part, by defective vision resulting from lack of retinal pigment (J:5470, J:5360, J:5378). | ||
| Molecular Note | The specific mutation in the albino allele is a G to C transversion causing an amino acid change from cysteine to serine. This mutation introduces a DdeI enzyme restriction site. [MGI Ref ID J:10889] [MGI Ref ID J:40223] | ||
| Control | ||
|---|---|---|
| Heterozygote from the colony | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for JAX® GEMM® Strains | ||
Strains carrying Tyrc allele
001017 AKXD10/TyJ 000765 AKXD13/TyJ 000954 AKXD15/TyJ 000958 AKXD16/TyJ 001093 AKXD18/TyJ 001062 AKXD21/TyJ 000947 AKXD22/TyJ 000969 AKXD24/TyJ 000777 AKXD6/TyJ 000763 AKXD9/TyJ 000409 B10.129P-H1b Hbbd Tyrc Ea7a/(5M)oSnJ 000418 B10.129P-H1b Tyrc Hbbd/(5M)nSnJ 000432 B10.C-H1b Hbbd Tyrc/(41N)SnJ 000383 B6.C-Tyrc H1b Hbbd/ByJ 001759 STOCK A Tyrc Sha/J View Strains carrying Tyrc (15 strains)
Strains carrying other alleles of Tyr
000090 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J 000091 129T1/Sv-Oca2+ Tyrc-ch Dnd1Ter/J 001279 129T1/Sv-Oca2+ Tyrc-ch-Aft/J 005445 A.B6 Tyr+-Cybanmf333/J 005012 A.B6 Tyr+-Myo5ad-l31J/J 002565 A.B6-Tyr+/J 000580 B10.D2/nSn-Tyrc-4J/J 000822 B6 x 129S1/SvEi Oca2+ Tyr+-Vsx2or-J/J 000578 B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J 000058 B6(Cg)-Tyrc-2J/J 007484 B6.Cg-Tyrc-2J Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ 000035 B6.Cg-Tyrc-J/J 000104 B6.Cg-Tyrc-h/J 000054 B6.D2-Tyrc-p/J 000899 C.B6-Tyr+ Hbbs/J 000339 C3H/HeJ-Tyrc-9J/J 001294 C3H/HeJ-Tyrc-a/J 001002 C57BL/10SnJ-Tyrc-11J/J 001006 CBA/J-Tyrc-10J/J 000657 CE/J 000619 FS/EiJ 004828 FVB.129P2-Pde6b+ Tyrc-ch/AntJ 007483 FVB.Cg-Tg(Tyr)3412ARpw Tg(Sry-EGFP)92Ei/EiJ 000494 J.Cg-Oca2+ Tyr+ Lystbg/J 002281 NFS.C58-Tyr+/J 004304 NOD.CBALs-Tyr+/LtJ 005115 NOD.FVB-Tg(INS-MT2A,Tyr)1Pne/PneJ 005114 NOD.FVB-Tg(Ins1-Cat,Tyr)25Pne/PneJ 000271 SH1/LeJ 000306 STOCK Dll3pu + Tyrc-ch/+ Oca2p Tyrc-ch/J 000206 STOCK a/a Tyrc-h/J View Strains carrying other alleles of Tyr (31 strains)
Hk related
Tyrc relatedDevelopmental Biology Research
Skeletal Defects
Dermatology Research
Color and White Spotting Defects (oculocutaneous albinism, type I)
Mouse/Human Gene Homologs
albinism, tyrosine negative
| Strain Name: | STOCK Hk Tyrc/J |
| Stock Number: | 000006 |
IMPORTANT NOTE: Prices are based on shipping destination. The shipping destinations are:
| Price(s) in US dollars ($) | |||||
|---|---|---|---|---|---|
| Cryorecovery Fee | $2470.00 | ||||
| Standard Supply | Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
Cryorecovery - Standard. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. |
| Licensing | See General Terms and Conditions below |
| Control Information | View Control Information in Strain Details. View Control Pricing Information for JAX® Strains. |
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