Clarinet, a novel C. elegans active zone protein with homology to vertebrate Piccolo and Rim, uses its different isoforms for diverse functions, including synaptic vesicle clustering, vesicle release and synaptogenesis.
Synaptophysins and gyrins dampen synaptic strength selectively at low frequencies, hinting that synaptic transmission may play a frequency filtering role in biological computation that is more general than currently envisioned.
Experiments in C. elegans reveal how synaptotagmin and Rab3, the 'yin and yang' of synapses, control whether transmitter vesicles remain docked at the presynaptic membrane or release their contents into the synapse.
Drosophila synaptotagmin 7 functions to restrict SV availability and release, but does not act as the Ca2+ sensor mediating the asynchronous release and facilitation remaining in synaptotagmin 1 mutants.
In mammals, the vesicular glutamate transporter 1 acquired a proline-rich sequence that negatively regulates the spontaneous release of glutamate by reducing the exchange of synaptic vesicles along the axon.
RIM binding UNC-13L C2A domain releases UNC-13L from an autoinhibitory homodimeric complex to become fusion-competent, and regulates probability of synaptic vesicle release in the post-priming process.
Building on previous work (Diao et al., 2012), we show that the mechanism by which complexin suppresses spontaneous fusion is distinct from the mechanism by which it synchronizes Ca2+-triggered fusion.