| Time | 12:30-13:30, Aug 17, 2021 |
| Venue | E109, Biomedicine Hall, Tsinghua University |
| Host | Dr. Jun Yao |
| Speaker |
Yun Chen (陈运) |
| Topic | Revising the model of corticothalamic pathways in sensory system |
| Abstract | Synaptic vesicle (SV) docking is a dynamic multi-stage process that is required for efficient neurotransmitter release in response to nerve impulses. Although the steady-state SV docking likely involves the cooperation of Synaptotagmin-1 (Syt1) and SNAREs, where and how the docking process is initiated remains unknown. PI(4,5)P2 can interact with Syt1 and SNAREs to contribute to vesicle exocytosis. In the present study, using the CRISPRi-mediated multiplex gene knockdown and 3-D electron tomography approaches, we showed that in mouse hippocampal synapses, SV docking was initiated at ~12 nm to the active zone (AZ) by Syt1. Furthermore, we demonstrated that PI(4,5)P2 was the membrane partner of Syt1 to initiate SV docking, and disrupting their interaction could abolish the docking initiation. In contrast, the SNARE complex only contributed to the tight SV docking within 0-2 nm. Therefore, Syt1 interacted with PI(4,5)P2 to loosely dock SVs within 2-12 nm to the AZ in hippocampal neurons. |
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