These mice carry an ENU-induced mutation characterized by thinning of the peripheral retina in the eyes and an increase in the rate of retinal degeneration.
The Jackson Laboratory cannot guarantee that cryorecovery of strains from the discontinued NIH-funded Neuroscience Mutagenesis Facility (NMF) will be successful or that the anticipated phenotype or genotype will be obtained. The cryorecovery fee for this effort will not be refunded or prorated if the recovery is unsuccessful or is in any way unsatisfactory. Genotyping will be the responsibility of the Purchaser.Read More +
Single mutant found at 13 weeks of age with retinal patch in left eye. The original mutant was non-productive and ovarian transplants of mutant ovaries also produced no offspring. However, matings of presumed heterozygotes have produced additional offspring. Standard pathology work-up on 3 mutants (266, 325 or 360 days of age) showed thinning of the peripheral retina in both eyes. One eye also showed a small area in which the outer nuclear layer was very thin.
This phenotypic deviant was generated by ethylnitrosourea (ENU) mutagenesis in C57BL/6J males (Stock No. 000664), in the Neuroscience Mutagenesis facility at The Jackson Laboratory. Mutagenized males were crossed to C57BL/6J females; G3 descendants of the mutagenized males were selected for neurological impairment.
|Allele Name||neuroscience mutagenesis facility, 12|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||Mertk, c-mer proto-oncogene tyrosine kinase|
|Strain of Origin||C57BL/6J|
|Molecular Note||ENU induced a A to G missense mutation at base pair 2147 resulting in a histidine to arginine substitution at amino acid position 716.|