Homozygous synapsin II knockout mice exhibit seizures and retarded axon formation. These mice may be useful in studying the role of synapsin II in neurodevelopment.
Hung-Teh Kao, Nathan Kline Institute
Paul Greengard, Rockefeller University
TheSyn2 gene is a member of the synapsin family of neuronal phophsoproteins, which are associated with neurotransmitter release and synaptogenesis. Synapsin proteins are associated with autism. Synapsin II localizes to presynaptic terminals. The synapsin II knockout allele has a PGK-neo cassette replacing exon 1 of the Syn2 gene. Homozygous mice exhibit decreased brain weight, impaired lamellipodia formation, abnormal neurite formation, aberrant actin filament distribution, delayed axon differentiation, altered cytoskeletal formation, and to a lesser extent than the synapsin I KO, delayed synapse formation. Beginning at two months of age, mice experience spontaneous seizures. Homozygous mice are viable and fertile with no reported reproductive deficiency.
A targeting vector was designed by Dr. Paul Greengard (Rockefeller University) to
replace exon 1 of the synapsin II gene (Syn2) on chromosome 6 with a PGK-neomycin cassette. The construct was electroporated into 129-derived unspecified embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts, and chimeric males were bred with C57BL/6J females to establish the colony. The resulting mice were bred with C57BL/6 wildtype mice for at least ten generations prior to sending males to The Jackson Laboratory Repository in 2015.
|Allele Name||targeted mutation 1, Paul Greengard|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Syn2, synapsin II|
|Strain of Origin||129|
|Molecular Note||Exon1 was replaced with a neomycin cassette inserted by homologous recombination.|
While maintaining a live colony, these mice are bred as homozygotes.
When using the synapsin II KO mouse strain in a publication, please cite the originating article(s) and include MMRRC stock #41437 in your Materials and Methods section.