These Cdk knock-out mice exhibit unique lesions in the central nervous system associated with perinatal mortality. They are suitable for use in applications related to the study of brain development, neuronal differentiation, and neuronal cytoskeleton structure and organization.
Ashok B Kulkarni, NIDCR NIH
Cdk5 is an important molecule for brain development and neuronal differentiation. Cdk null mice exhibit unique lesions in the central nervous system associated with perinatal mortality. The brains of mutant mice lack cortical laminar structure and cerebellar foliation. The large neurons in the brain stem and in the spinal cord show chromatolytic changes with accumulation of neurofilament immunoreactivity. They also exhibit neuronal migration abnormalities, cerebellar defoliation, NF accumulation neuronal bodies, and degenerated motor neurons.
Genomic clones of the mouse Cdk5 gene were isolated from a 129/SvJ mouse genomic library. Genomic fragments were used to construct the targeting vector, which carried a 0.8kb deletion including a part of exon III, and exons IV and V. The deletion was replaced by a neomycin resistance gene.
|Allele Name||targeted mutation 1, Ashok B Kulkarni|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Cdk5 (-)|
|Gene Symbol and Name||Cdk5, cyclin-dependent kinase 5|
|Strain of Origin||129S4/SvJae|
|Molecular Note||Replacement of part of exon III, exons IV and V with a neomycin cassette.|
|Mutations Made By|| |
Ashok Kulkarni, NIDCR NIH
The strain is on a mixed B6;129 background. Heterozygous mice appear normal; homozygous mice either die in utero or within 12 hours after birth. Expected coat color from breeding:Black,Agouti
When using the Cdk5- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003536 in your Materials and Methods section.