Strain Name: |
AKXD13/TyJ |
|---|---|
Stock Number: |
000765 |
Availability: | Repository-Cryopreserved |
General Terms and Conditions |
| Former Name |
AKXD-13/TyJ (Changed: 15-DEC-04
) |
| Genes & Alleles | Emv14; Emv3; Emv3a; Myo5a; Myo5ad; Rmcf; Rmcfr; Tyr; Tyrc; ; |
Product Information
Strain Details
Type Recombinant Inbred (Ri) Additional information on Recombinant Inbred Mice. Species laboratory mouse RI progenitor AKR/J DBA/2J H2 Haplotype d Generation F32p Appearance
albino
Related Genotype: Tyrc/Tyrc
Mammalian Phenotype Terms assigned by genotype |
Gene & Allele Details
| Allele Symbol | Emv3a | ||
|---|---|---|---|
| Allele Name | endogenous ecotropic MuLV 3, present | ||
| Gene Symbol and Name | Emv3, endogenous ecotropic MuLV 3 | ||
| Chromosome | 9 | ||
| Gene Common Name(s) | Emv-3; Sev-1; | ||
| General Note | The provirus is present in the following strains: BDP/J, DBA/1J, DBA/2DeJ, DBA/2J, HRS/J, I/LnJ, P/J, and SEA/GnJ. | ||
| Allele Symbol | Myo5ad | ||
| Allele Name | dilute | ||
| Common Name(s) | d; dv; maltese dilution; | ||
| Strain of Origin | old mutant of the mouse fancy | ||
| Gene Symbol and Name | Myo5a, myosin Va | ||
| Chromosome | 9 | ||
| Gene Common Name(s) | 9630007J19Rik; AI413174; AI661011; D; Dbv; Dop; GS1; MVa; MYH12; MYO5; MYR12; Myo5; MyoVA; RIKEN cDNA 9630007J19 gene; d; dilute; expressed sequence AI413174; expressed sequence AI661011; flail; flailer; flr; myosin V; nmf244; | ||
| General Note |
Mutations at the Myo5a locus lighten coat color through an abnormal morphology of melanocytes that causes uneven pigmentation of the hair shaft (J:11005). Most of these mutations also cause severe neurological defects; in some mutant forms, these defectslead to early death (J:12978), while in others life span is normal, but convulsions and loss of equilibrium occur after about four months of age (J:16915). Maltese dilution, as this mutation was originally called, is an old mutation of the mouse fancy. The blue-gray color of the hair produced by this mutation in nonagouti (a/a) mice is caused by clumping of the melanin pigment into a few large masses (J:12958). The melanocytes are misshapen, with fewer and thinner dendritic processes than wild-type melanocytes, and melanin granules are largely clumped around the nucleus (J:12970). Incorporation of tyrosine into melanin proceeds at a normal rate (J:12173), and the fine structure of the melanin granules is normal (J:5346). Cultured primary melanocytesfrom dilute homozygotes are normal in morphology but display clustering of melanosomes (J:37976). Griscelli disease (Chediak-Higashi-like syndrome, OMIM 214450) is a human autosomal recessive disorder whose symptoms include pigment dilution, immunodeficiency, and acute lethal lymphocyte and macrophage activation. Melanocyte malformation is characteristic of the pigment abnormality. The immunological abnormality includes absence of cutaneous hypersensitivity and impaired function of natural-killer cells. Griscelli disease resembles the dilute-lethal mouse mutant, except for the neurological disorder in the mouse. The locus for Griscelli disease colocalizes with the locus for myosin Va, which is mutated in at least some Griscelli patients. Griscelli disease is thus the homolog of mouse Maltese dilution (J:41253). The original Myo5ad mutation which identified the locuswas caused by insertion of an ecotropic murine leukemia virus (see Emv3) (J:6844, J:6587). All other mutations examined lack the virus. Reversions of Myo5ad to wild-type, which have been reported frequently, are caused by excision of the virusleaving exactly one long terminal repeat in place (J:7092). The virus is integrated into a noncoding region of the DNA (J:7751). | ||
| Allele Symbol | Rmcfr | ||
| Allele Name | MCF resistant | ||
| Gene Symbol and Name | Rmcf, resistance to MCF virus | ||
| Chromosome | 5 | ||
| 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] | ||
| Gene Symbol and Name | Emv14, endogenous ecotropic MuLV 14 | ||
| Chromosome | 11 | ||
| Gene Common Name(s) | AKR leukemia virus inducer 4; Akv-2J; Akv-4; Emv-14; | ||
Related Strains
AKXD Strains
001005 AKXD1/TyJ 001017 AKXD10/TyJ 001003 AKXD11/TyJ 000779 AKXD14/TyJ 000954 AKXD15/TyJ 000958 AKXD16/TyJ 001093 AKXD18/TyJ 000776 AKXD2/TyJ 001001 AKXD20/TyJ 001062 AKXD21/TyJ 000947 AKXD22/TyJ 000780 AKXD23/TyJ 000969 AKXD24/TyJ 000949 AKXD25/TyJ 000764 AKXD27/TyJ 000957 AKXD28/TyJ 000959 AKXD3/TyJ 000777 AKXD6/TyJ 000763 AKXD9/TyJ View AKXD Strains (19 strains)
000779 AKXD14/TyJ 000954 AKXD15/TyJ 001093 AKXD18/TyJ 000947 AKXD22/TyJ 000764 AKXD27/TyJ 000959 AKXD3/TyJ
001005 AKXD1/TyJ 001003 AKXD11/TyJ 000779 AKXD14/TyJ 000954 AKXD15/TyJ 001093 AKXD18/TyJ 000776 AKXD2/TyJ 001062 AKXD21/TyJ 000947 AKXD22/TyJ 000949 AKXD25/TyJ 000764 AKXD27/TyJ 000959 AKXD3/TyJ 000285 B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J 000652 BDP/J 000036 BXD1/TyJ 000013 BXD16/TyJ 000015 BXD18/TyJ 000010 BXD19/TyJ 000077 BXD21/TyJ 000043 BXD22/TyJ 000081 BXD25/TyJ 006255 BXD25/TyJRwwJ 000029 BXD29/TyJ 000037 BXD5/TyJ 000007 BXD6/TyJ 000084 BXD8/TyJ 000105 BXD9/TyJ 000284 CWD/LeJ 000670 DBA/1J 000671 DBA/2J 000963 DBA/2J-Myo5ad+17J/Myo5ad/J 000964 DBA/2J-Myo5ad+18J/Myo5ad/J 000067 DBA/2J-Myo5ad+2J/Myo5ad/J 000673 HRS/J 000674 I/LnJ 001850 MEV-Q/TyJ 001855 MEV-V/TyJ 003345 MEV/2Ty-Emv64/J 000679 P/J 000644 SEA/GnJ 000390 STOCK Myo5ad Ds/J 000994 STOCK a Myo5ad Mregdsu/J 000286 STOCK a/a Myo5ad fd/+ +/J
000690 129P3/J 000954 AKXD15/TyJ 001093 AKXD18/TyJ 000947 AKXD22/TyJ 000763 AKXD9/TyJ 000654 CBA/CaJ 000670 DBA/1J
001017 AKXD10/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 000006 STOCK Hk Tyrc/J
Phenotypic Data
Mouse Phenome Database
Wellcome Trust Centre for Human Genetics: Mouse Recombinant Inbred Line (RIL) Genotype Data for AKXD RI Line
Research Applications
This mouse can be used to support research in many areas including:
Myo5ad relatedResearch Tools
Cancer Research (genes regulating lymphoma development)
Genetics Research (Gene Mapping: Tools for QTL Mapping, Segregation and Linkage Analysis)
Tyrc relatedDermatology Research
Color and White Spotting Defects
Mouse/Human Gene Homologs
Griscelli Syndrome
Dermatology Research
Color and White Spotting Defects (oculocutaneous albinism, type I)
Mouse/Human Gene Homologs
albinism, tyrosine negative
References
Selected Reference(s)
Additional ReferencesMucenski ML; Taylor BA; Jenkins NA; Copeland NG. 1986. AKXD recombinant inbred strains: models for studying the molecular genetic basis of murine lymphomas. Mol Cell Biol 6(12):4236-43. [PubMed: 3025647] [MGI Ref ID J:20300]
Price and Supply Information
| Strain Name: | AKXD13/TyJ |
| Stock Number: | 000765 |
Price Details
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Supply Details
| 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 |
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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.Ordering and Purchasing Information
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