| Annotated protein: | Synaptotagmin-17 (Protein B/K) (Synaptotagmin XVII) (SytXVII). Gene symbol: SYT17. Taxonomy: Homo sapiens (Human). Uniprot ID: Q9BSW7 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ SYT17 |
| Ontology domain: | Biological Process |
| SynGO term: | regulation of postsynaptic neurotransmitter receptor endocytosis (GO:0099149) |
| Synapse type(s): | hippocampus, glutamatergic |
| Annotated paper: | Ruhl DA, et al. "Synaptotagmin 17 controls neurite outgrowth and synaptic physiology via distinct cellular pathways" Nat Commun. 2019 Aug 6;10(1):3532 PMID:31387992 |
| Figure(s): | Figure 6, 7 |
| Annotation description: | Figure 6, 7, S8: Synaptotagmin 17 (SYT17) knockout resulted in increased postsynaptic responsiveness of hippocampal neurons (higher evoked and spontaneous EPSC amplitudes). Further, these knockouts exhibited an increased number of AMPA receptors at the postsynaptic surface. "These data demonstrate an upregulation of surface GluR2 in syt-17 KO synapses which results in a dramatic increase in synaptic strength." "If syt-17 in fact controls synaptic strength by regulating endosomal recycling of AMPARs, then LTD, but not LTP, should be disrupted in KO animals. We measured LTD along the Shaffer collateral pathway in acute hippocampal slices prepared from WT or syt-17 KO mice, and found that this form of synaptic plasticity was abolished in slices prepared from syt-17 KO mice (Fig. 7g, h), confirming the defect in AMPAR internalization. In addition, we observed an increase in basal synaptic responses (Supplementary Fig. 8D) without an alteration in paired-pulse facilitation (Supplementary Fig. 8E), validating in slices our observation that syt-17 KOs exhibit an augmentation of synaptic strength via a postsynaptic mechanism. This alteration in synaptic plasticity is specific to LTD, as LTP was unaffected using multiple induction paradigms (Supplementary Fig. 8F-G), consistent with a role for syt-17 in the endocytosis, but not exocytosis, of AMPARs. These data collectively document a defect in endosomal recycling of AMPARs in syt-17 KO animals, leading to abnormally strong synapses, and an inability to downscale said synapses in response to circuit activity." |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Whole-cell patch clamp Confocal |
| Annotator(s): | Frank Koopmans (ORCID:0000-0002-4973-5732) Guus Smit (ORCID:0000-0002-2286-1587) Matthijs Verhage (ORCID:0000-0002-2514-0216) |
| Lab: | Department of Functional Genomics, Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands |
| SynGO annotation ID: | 5244 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |