ArticleThe Journal of biological chemistry2010
Calmodulin suppresses synaptotagmin-2 transcription in cortical neurons.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Mutations of schizophrenia risk gene SETD1A dysregulate synaptic function in human neurons.Molecular psychiatry · 2025Article
- Analyses of the autism-associated neuroligin-3 R451C mutation in human neurons reveal a gain-of-function synaptic mechanism.Molecular psychiatry · 2024Article
- Proteins related to ictogenesis and seizure clustering in chronic epilepsy.Scientific reports · 2021Article
- The Role of Calmodulin vs. Synaptotagmin in Exocytosis.Frontiers in molecular neuroscience · 2021Review
- Inositol polyphosphate multikinase deficiency leads to aberrant induction of synaptotagmin-2 in the forebrain.Molecular brain · 2019Article
- The cell adhesion protein CAR is a negative regulator of synaptic transmission.Scientific reports · 2019Article
- Improved calcium sensor GCaMP-X overcomes the calcium channel perturbations induced by the calmodulin in GCaMP.Nature communications · 2018Article
- hsa-let-7c miRNA Regulates Synaptic and Neuronal Function in Human Neurons.Frontiers in synaptic neuroscience · 2018Article
- Calmodulin regulates CaThe Journal of biological chemistry · 2017Article
- Synaptotagmin2 (Syt2) Drives Fast Release Redundantly with Syt1 at the Output Synapses of Parvalbumin-Expressing Inhibitory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Calmodulin regulates KCNQ2 function in epilepsy.American journal of translational research · 2016Article
- Extended Synaptotagmin (ESyt) Triple Knock-Out Mice Are Viable and Fertile without Obvious Endoplasmic Reticulum Dysfunction.PloS one · 2016Article
- Human Neuropsychiatric Disease Modeling using Conditional Deletion Reveals Synaptic Transmission Defects Caused by Heterozygous Mutations in NRXN1.Cell stem cell · 2015Article
- Translating neuronal activity at the synapse: presynaptic calcium sensors in short-term plasticity.Frontiers in cellular neuroscience · 2014Review
- Lipid-anchored SNAREs lacking transmembrane regions fully support membrane fusion during neurotransmitter release.Neuron · 2013Article
- Membrane-tethered monomeric neurexin LNS-domain triggers synapse formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Complexin activates exocytosis of distinct secretory vesicles controlled by different synaptotagmins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- C-terminal complexin sequence is selectively required for clamping and priming but not for Ca2+ triggering of synaptic exocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Characterization and functional analysis of the calmodulin-binding domain of Rac1 GTPase.PloS one · 2012Article
- Decrease in calcium concentration triggers neuronal retinoic acid synthesis during homeostatic synaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Calmodulin (CaM) is a ubiquitous Ca(2+) sensor protein that plays a pivotal role in regulating innumerable neuronal functions, including synaptic transmission. In cortical neurons, most neurotransmitter release is triggered by Ca(2+) binding to synaptotagmin-1; however, a second delayed phase of release, referred to as asynchronous release, is triggered by Ca(2+) binding to an unidentified secondary Ca(2+) sensor. To test whether CaM could be the enigmatic Ca(2+) sensor for asynchronous release, we now use in cultured neurons short hairpin RNAs that suppress expression of ∼70% of all neuronal CaM isoforms. Surprisingly, we found that in synaptotagmin-1 knock-out neurons, the CaM knockdown caused a paradoxical rescue of synchronous release, instead of a block of asynchronous release. Gene and protein expression studies revealed that both in wild-type and in synaptotagmin-1 knock-out neurons, the CaM knockdown altered expression of >200 genes, including that encoding synaptotagmin-2. Synaptotagmin-2 expression was increased several-fold by the CaM knockdown, which accounted for the paradoxical rescue of synchronous release in synaptotagmin-1 knock-out neurons by the CaM knockdown. Interestingly, the CaM knockdown primarily activated genes that are preferentially expressed in caudal brain regions, whereas it repressed genes in rostral brain regions. Consistent with this correlation, quantifications of protein levels in adult mice uncovered an inverse relationship of CaM and synaptotagmin-2 levels in mouse forebrain, brain stem, and spinal cord. Finally, we employed molecular replacement experiments using a knockdown rescue approach to show that Ca(2+) binding to the C-lobe but not the N-lobe of CaM is required for suppression of synaptotagmin-2 expression in cortical neurons. Our data describe a previously unknown, Ca(2+)/CaM-dependent regulatory pathway that controls the expression of synaptic proteins in the rostral-caudal neuraxis.
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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.