ArticleProceedings of the National Academy of Sciences of the United States of America2008
Genetic analysis of synaptotagmin-7 function in synaptic vesicle exocytosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 102 citations in OpenAlex.
- Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Synaptotagmin 7 docks synaptic vesicles to support facilitation and Doc2α-triggered asynchronous release.eLife · 2024Article
- Synaptotagmin 7 Sculpts Short-Term Plasticity at a High Probability Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Synaptotagmin-7 outperforms synaptotagmin-1 to promote the formation of large, stable fusion pores via robust membrane penetration.Nature communications · 2023Article
- Synaptotagmin-1-dependent phasic axonal dopamine release is dispensable for basic motor behaviors in mice.Nature communications · 2023Article
- Phorbolester-activated Munc13-1 and ubMunc13-2 exert opposing effects on dense-core vesicle secretion.eLife · 2022Article
- Synaptotagmins 1 and 7 Play Complementary Roles in Somatodendritic Dopamine Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Deconstructing Synaptotagmin-1's Distinct Roles in Synaptic Vesicle Priming and Neurotransmitter Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
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- Synaptic Vesicle Recycling and the Endolysosomal System: A Reappraisal of Form and Function.Frontiers in synaptic neuroscience · 2022Review
- Article
- Neuromodulator release in neurons requires two functionally redundant calcium sensors.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A novel dual Ca2+ sensor system regulates Ca2+-dependent neurotransmitter release.The Journal of cell biology · 2021Article
- Synaptotagmin-7 places dense-core vesicles at the cell membrane to promote Munc13-2- and CaeLife · 2021Article
- Neurotransmitter Release Site Replenishment and Presynaptic Plasticity.International journal of molecular sciences · 2020Review
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- Article
- Cytotoxic Granule Trafficking and Fusion in Synaptotagmin7-Deficient Cytotoxic T Lymphocytes.Frontiers in immunology · 2020Article
- Presynaptic Calcium Channels.International journal of molecular sciences · 2019Review
- The Ever-Growing Puzzle of Asynchronous Release.Frontiers in cellular neuroscience · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Synaptotagmin-7 is a candidate Ca(2+) sensor for exocytosis that is at least partly localized to synapses. Similar to synaptotagmin-1, which functions as a Ca(2+) sensor for fast synaptic vesicle (SV) exocytosis, synaptotagmin-7 contains C(2)A and C(2)B domains that exhibit Ca(2+)-dependent phospholipid binding. However, synaptotagmin-7 cannot replace synaptotagmin-1 as a Ca(2+) sensor for fast SV exocytosis, raising questions about the physiological significance of its Ca(2+)-binding properties. Here, we examine how synaptotagmin-7 binds Ca(2+) and test whether this Ca(2+) binding regulates Ca(2+)-triggered SV exocytosis. We show that the synaptotagmin-7 C(2)A domain exhibits a Ca(2+)-binding mode similar to that of the synaptotagmin-1 C(2)A domain, suggesting that the synaptotagmin-1 and -7 C(2) domains generally employ comparable Ca(2+)-binding mechanisms. We then generated mutant mice that lack synaptotagmin-7 or contain point mutations inactivating Ca(2+) binding either to both C(2) domains of synaptotagmin-7 or only to its C(2)B domain. Synaptotagmin-7-mutant mice were viable and fertile. Inactivation of Ca(2+) binding to both C(2) domains caused an approximately 70% reduction in synaptotagmin-7 levels, whereas inactivation of Ca(2+) binding to only the C(2)B domain did not alter synaptotagmin-7 levels. The synaptotagmin-7 deletion did not change fast synchronous release, slow asynchronous release, or short-term synaptic plasticity of release of neurotransmitters. Thus, our results show that Ca(2+) binding to the synaptotagmin-7 C(2) domains is physiologically important for stabilizing synaptotagmin-7, but that Ca(2+) binding by synaptotagmin-7 likely does not regulate SV exocytosis, consistent with a role for synaptotagmin-7 in other forms of Ca(2+)-dependent synaptic exocytosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.