These ENU induced mutant mice exhibit a hypercellular molecular layer of the cerebellum similar to Plxna2 and Sema6a knock-out mice, but the ENU mutation in the Plxna2 gene appears not to be null.
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 +
Due to aberrant migration of granule cells during development, mice homozygous for the nmf454 mutation have a hypercellular molecular layer of the cerebellum with many ectopic granule cells in the molecular layer.
The nmf454 mutation was chemically induced by treatment of a C57BL/6J male with N-ethyl-N-nutrosourea. This mutation was maintained purely on a C57BL/6J background and in 2006 sperm was cryopreserved from heterozygous males at generation N3F1.
|Allele Name||neuroscience mutagenesis facility 454|
|Allele Type||Chemically induced (ENU)|
|Gene Symbol and Name||Plxna2, plexin A2|
|Strain of Origin||C57BL/6J|
|Molecular Note||ENU mutagenesis was used to induce a nucleotide substitution that resulted in an amino acid substitution of glutamic acid for alanine at position 396 (A396E). This amino acid is involved in Sema6a binding to plexin-A2.|