Regulation of spontaneous neurotransmission and homeostatic synaptic plasticity by synaptotagmin-1 disease variants at the SNARE primary interface.
This study demonstrates that the severe neurodevelopmental disorder-causing synaptotagmin-1 mutation p.N341S disrupts spontaneous neurotransmission and homeostatic plasticity by introducing a novel phosphorylation site that alters the protein's critical interaction interface with SNAP-25.