Scaling_law_human_transcription
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB72056 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12529545_1.fastq.gz | Fastqsanger.gz | |||
| ERR12529545_2.fastq.gz | Fastqsanger.gz | |||
| ERR12529546_1.fastq.gz | Fastqsanger.gz | |||
| ERR12529546_2.fastq.gz | Fastqsanger.gz | |||
| ERR12529547_1.fastq.gz | Fastqsanger.gz |
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Project description:Synaptic scaling is a form of homeostatic plasticity which allows neurons to adjust their action potential firing rate in response to chronic alterations in neural activity. Synaptic scaling requires profound changes in gene expression, but the relative contribution of local and cell-wide mechanisms is controversial. Here we performed a comprehensive multi-omics characterization of the somatic and process compartments of primary rat hippocampal neurons during synaptic scaling. Thereby, we uncovered highly compartment-specific and correlated changes in the neuronal transcriptome and proteome. Specifically, we identified highly compartment-specific downregulation of crucial regulators of neuronal excitability and excitatory synapse structure. Motif analysis further suggests an important role for trans-acting post-transcriptional regulators, including RNA-binding proteins and microRNAs, in the local regulation of the corresponding mRNAs. Altogether, our study indicates that compartmentalized gene expression changes are widespread in synaptic scaling and might co-exist with neuron-wide mechanisms to allow synaptic computation and homeostasis
2021-07-09 | PXD020745 | Pride
Project description:Wu C, Tatavarty V, Jean-Beltran PM, Guerrero A, Keshishian H, Krug K, MacMullan M, de Arce KP, Carr SA, Cottrell J, Turrigiano GG. 2021
Homeostatic synaptic plasticity requires widespread remodeling of synaptic signaling and scaffolding networks, but the role of posttranslational modifications in this process has not been systematically studied. Here we analyzed changes in the phosphoproteome during synaptic scaling up and down and found wide-spread and temporally complex changes. These included 424 bidirectionally modulated phosphosites that were strongly enrichment for synapse-associated proteins, including the ASD-associated synaptic scaffold protein Shank3. Shank3 was dephosphorylated at two highly conserved sites (rat S1586 and S1615) during scaling up, and hyperphosphorylated during scaling down. These changes modified the synaptic localization of Shank3 during scaling, and phosphomimetic or deficient mutants of Shank3 prevented scaling up or down, respectively. Finally, we found that dephosphorylation of these sites via PP2A activity was essential for the maintenance of synaptic scaling up. Thus Shank3 undergoes an activity-dependent switch between hypo- and hyperphosphorylation at S1586/ S1615, that is necessary to enable scaling up or down, respectively. More broadly, our data suggest that widespread and bidirectional changes in the synaptic phosphoproteome are essential for the functional reconfiguration of synaptic scaffolds during homeostatic plasticity.
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Project description:Synaptic scaling is a form of homeostatic plasticity which allows neurons to reduce their action potential firing rate in response to chronic alterations in neural activity. Synaptic scaling requires profound changes in gene expression, but the relative contribution of local and cell-wide mechanisms to synaptic scaling is controversial. Here we performed a comprehensive multi-omics characterization of the somatic and process compartments of primary rat hippocampal neurons during synaptic scaling. Thereby, we uncovered highly compartment-specific and correlated changes in the neuronal transcriptome and proteome. Specifically, we identified highly compartment-specific downregulation of crucial regulators of neuronal excitability and excitatory synapse structure. Motif analysis further suggests an important role for trans-acting post-transcriptional regulators, including RNA-binding proteins and microRNAs, in the local regulation of the corresponding mRNAs. Altogether, our study indicates that compartmentalized gene expression changes are widespread in synaptic scaling and might co-exist with neuron-wide mechanism to allow synaptic computation and homeostasis.
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Project description:Homeostatic scaling allows neurons to maintain stable activity patterns by globally altering their synaptic strength in response to changing activity levels. Suppression of activity by blocking action potentials increases synaptic strength through an upregulation of surface AMPA receptors. Although this synaptic up-scaling was shown to require transcription, the molecular nature of the intrinsic transcription program underlying this process and its functional significance have been unclear. Using RNA-seq, we identified 73 genes that were specifically upregulated in response to activity suppression. In particular, Neuronal pentraxin-1 (Nptx1) increased within 6 h of activity blockade, and knockdown of this gene blocked the increase in synaptic strength. Notably, Nptx1 induction is mediated by calcium influx through the T-type Voltage-Gated Calcium Channel, as well as two transcription factors, SRF and ELK1. Taken together, these results uncover a transcriptional program that specifically operates when neuronal activity is suppressed, to globally coordinate the increase in synaptic strength.
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