Journal
EMBO JOURNAL
Volume 30, Issue 24, Pages 4955-4969Publisher
WILEY
DOI: 10.1038/emboj.2011.339
Keywords
membrane recruitment of dynamins; rod photoreceptor ribbon synapses; seizures with tonic-clonic convulsions; SV formation and recycling; F-BAR protein syndapin/PACSIN
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Funding
- Deutsche Forschungsgemeinschaft [QU116/2-1-4, 5-1, 6-1, 7-1, SFB TR3/B5, GL254/5-1, BO1718/3-1, SFB497/B8]
- EU [OT06/23, IDO06/004]
- KU Leuven fellowship
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Synaptic transmission relies on effective and accurate compensatory endocytosis. F-BAR proteins may serve as membrane curvature sensors and/or inducers and thereby support membrane remodelling processes; yet, their in vivo functions urgently await disclosure. We demonstrate that the F-BAR protein syndapin I is crucial for proper brain function. Syndapin I knockout (KO) mice suffer from seizures, a phenotype consistent with excessive hippocampal network activity. Loss of syndapin I causes defects in presynaptic membrane trafficking processes, which are especially evident under high-capacity retrieval conditions, accumulation of endocytic intermediates, loss of synaptic vesicle (SV) size control, impaired activity-dependent SV retrieval and defective synaptic activity. Detailed molecular analyses demonstrate that syndapin I plays an important role in the recruitment of all dynamin isoforms, central players in vesicle fission reactions, to the membrane. Consistently, syndapin I KO mice share phenotypes with dynamin I KO mice, whereas their seizure phenotype is very reminiscent of fitful mice expressing a mutant dynamin. Thus, syndapin I acts as pivotal membrane anchoring factor for dynamins during regeneration of SVs. The EMBO Journal (2011) 30, 4955-4969. doi: 10.1038/emboj.2011.339; Published online 16 September 2011
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