AKXD18/TyJ

Stock number: 001093
Research areas: Dermatology Research, Mouse/Human Gene Homologs, Research Tools

Detailed description

This is one of 20 cryopreserved recombinant inbred (RI) strains of mice derived from the progenitor strains AKR/J and DBA/2J.

The strain distribution pattern (SDP) for RI strains is available through the Mouse Genome Informatics Contributed Data Sets

Allele

Symbol: Emv3^a
Name: endogenous ecotropic MuLV 3, present
MGI accession ID: MGI:3579292
Generation method: Not Applicable
Marker symbol: Emv3
Marker name: endogenous ecotropic MuLV 3
Chromosome: 9
Strain of origin: Not Applicable
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: Rmcf^r
Name: MCF resistant
MGI accession ID: MGI:3798960
Generation method: Spontaneous
Marker symbol: Rmcf
Marker name: resistance to MCF virus
Chromosome: 5
Strain of origin: multiple strains
Molecular note: This locus controls resistance of cells to infection by mink cell focus-forming murine leukemia viruses. The dominant r (resistance) allele is found in strains DBA/1, DBA/2 and CBA/Ca.
General note:

This locus controls resistance and susceptibility of cells in tissue culture to infection by mink cell focus-forming murine leukemia viruses. The allele Rmcf^r determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcf^s determines susceptibility and occurs in strains AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB, 129/J, and many others. Heterozygotes are as resistant as the resistant parent or nearly so. Rmcf is different from and independent of Fv1, a locus that controls susceptibility to infection by ecotropic viruses. Rmcf is located on Chr 5 close to Hm near the centromeric end (J:7108). Rmcf^r protects (AKR x CBA/Ca)F1 and (AKR x DBA/2)F1 hybrids from development of spontaneous thymic lymphomas and reduces the incidence of MCF-induced thymic lymphomas (J:7175). It also reduces susceptibility of cells of Sxv^s/Sxv^r mice to exogenous xenotropic viruses (J:7951). In addition, in strains susceptible to Friend virus-induced erythroleukemia, a condition thought to be due to the replication of MCF virus, Rmcf^r increases resistance to the virus-induced erythroleukemia. It may cause resistance by coding for or regulating the production of an MCF-related envelope glycoprotein that blocks the receptor for MCF viruses (J:8074). This conclusion is reinforced by the findings of Buller et al. (J:8497), who showed that the Rmcf^r allele contains an endogenous MCF gp70 env gene and that the Rmcf^s allele, at least in some strains (C57BL/6, CBA/J, and A/WySn), contains a xenotropic gp70 env gene. Presumably the MCF gp70 inhibits exogenous MCF infection in vitro by a mechanism of viral interference.

Allele

Symbol: Tyr^c
Name: albino
MGI accession ID: MGI:1855976
Generation method: Spontaneous
Marker symbol: Tyr
Marker name: tyrosinase
Chromosome: 7
Strain of origin: old mutant of the mouse fancy
Site of expression: Melanocytes.
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.
General note: Tyr^c, 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).

Allele

Symbol: Myo5a^d
Name: dilute
MGI accession ID: MGI:1856004
Generation method: Spontaneous
Marker symbol: Myo5a
Marker name: myosin VA
Chromosome: 9
Strain of origin: old mutant of the mouse fancy
Molecular note: This mutation is the result of the integration of ecotropic murine leukemia virus Emv-3 into a noncoding region of the Myo5a^d gene. Reversions of Myo5a^d to wild-type are caused by excision of the virus leaving exactly one long terminal repeat in place.

Allele

MGI accession ID: MGI:95327
Marker symbol: Emv11
Marker name: endogenous ecotropic MuLV 11
Chromosome: 7

Allele

MGI accession ID: MGI:95330
Marker symbol: Emv14
Marker name: endogenous ecotropic MuLV 14
Chromosome: 11