These mice carry an ENU-induced mutation of the Reln gene and exhibit underdeveloped brains, characterized by disorganized cell layers in the cerebellum, hippocampus and cerebral cortex.
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 +
These mutants exhibit body tremor, intense hind limb spasms, and are unable to continuously work; mutants are unable to remain on their feet, fall over and struggle to regain balance. The on-set of the phenotype can be observed at 3.7 weeks of age (+/- 1.1 weeks; n=7). Since brain histology results of these mutants were similar to those observed in reeler mutants (see below), a complementation analysis with Reln was performed; the results of a heterozygote by heterozygote mating of nmf413 and Relnrl(Jax#0235), i.e. 3 mutants in a total of 7 progeny, confirmed that nmf413 indeed represents an allele of Reln. Standard pathology work-up performed on two mutants (17 or 44 days of age) revealed an underdeveloped brain, characterized by disorganized cell layers in the cerebellum, hippocampus and cerebral cortex. The colony has to be maintained through ovarian transplants.
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||reeler 6 Jackson|
|Allele Type||Chemically induced (ENU)|
|Allele Synonym(s)||neuroscience mutagenesis facility, 413; NMF413; Relnnmf413|
|Gene Symbol and Name||Reln, reelin|
|Strain of Origin||C57BL/6J|
|Molecular Note||This mutation, which was identified in an ENU mutagenesis screen, was shown to be an allele of Reln by complementation testing to the original reeler mutation.|