This B10 congenic strain carries H1b, Tyrc, and Hbbd from 129/Rr.
Genetic Background | Generation |
---|---|
|
Allele Type | Gene Symbol | Gene Name |
---|---|---|
Spontaneous | Tyr | tyrosinase |
Allele Type | Gene Symbol | Gene Name |
---|---|---|
Not Applicable | Hbb | hemoglobin beta chain complex |
Marker Symbol | Marker Name | |
---|---|---|
H1 | histocompatibility 1 |
This strain is similar to B10.129P3-H1b Hbbd Tyrc Ea7a/(5M)oSnJ ((Stock No. 000409), but was backcrossed for the equivalent of 11 generations and does not carry Ea7a from the donor strain.
This B10 congenic strain carries H1b, Tyrc, and Hbbd from 129/Rr.
This is one of the “Congenic Resistant” strains of mice developed by George D. Snell in his studies of histocompatibility. [Snell, G.D. 1978. In Origins of Inbred Mice (H.C. Morse III, ed.). Academic Press, New York.]
Strain B10.129(5M)nSn was derived from an initial cross between C57BL/10ScSn and 129/Rr (antecedent of the current 129P3/J, Stock No. 000690) and developed into a congenic strain by a cross-intercross system resulting in the equivalent of 11 generations of backcross to C57BL/10ScSn before being maintained by sib matings. Embryos were cryopreserved in 1989 at generation NE11F63.
Allele Name | albino |
---|---|
Allele Type | Spontaneous |
Allele Synonym(s) | c |
Gene Symbol and Name | Tyr, tyrosinase |
Gene Synonym(s) | |
Site of Expression | Melanocytes. |
Strain of Origin | old mutant of the mouse fancy |
Chromosome | 7 |
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 pigment epithelium, 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 at position 103 or 85 (p.C103S for pre-protein, p.C85S for mature protein). This mutation introduces a DdeI enzyme restriction site. |
Marker Synonym(s) | |
---|---|
Chromosome(s) | 7 |
When using the B10.129(5M)/nSn mouse strain in a publication, please cite the originating article(s) and include JAX stock #000418 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
---|---|---|
Homozygous, 1 pair minimum |
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.
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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
What information were you hoping to find through your search?
How easy was it to find what you were looking for?
We may wish to follow up with you. Enter your email if you are happy for us to connect and reachout to you with more questions.
Please Enter a Valid Email Address
Thank you for sharing your feedback! We are working on improving the JAX Mice search. Come back soon for exciting changes.