Faculty mentor: Erik Jorgensen
Here, we use CRISPR/Cas9 to develop disease models of epilepsy-causing human mutations in C. elegans. We use these models to determine how each mutation changes the rates of neurotransmission. We postulate that snt-1 binds SNAP-25 at these regions to perform a repressive role in synaptic vesicle fusion. The findings presented here will 1) help physicians make more informed decisions regarding patient therapies and 2) increase the basic scientific understanding of SNAP-25 and snt-1 binding.
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