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Identification of activity-induced Npas4-regulated genes in cortical inhibitory and excitatory neurons (array)

ABSTRACT: To identify the activity-induced gene expression programs in inhibitory and excitatory neurons, we analyzed RNA extracted from cultured E14 mouse MGE- and CTX-derived neurons (DIV 10) after these cultures were membrane-depolarized for 0, 1 and 6 hrs with 55mM extracellular KCl. To identify the gene programs regulated in these cells by the activity-induced early-response transcription factor Npas4, we repeated the same experiment in the MGE- and CTX-cultures lacking Npas4 (Npas4-KO).

ORGANISM(S): Mus musculus

PROVIDER: GSE55588 | GEO | 2015/06/04

SECONDARY ACCESSION(S): PRJNA240171

REPOSITORIES: GEO

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Identification of activity-induced Npas4-regulated genes in cortical inhibitory and excitatory neurons (array)

Project description:To identify the activity-induced gene expression programs in inhibitory and excitatory neurons, we analyzed RNA extracted from cultured E14 mouse MGE- and CTX-derived neurons (DIV 10) after these cultures were membrane-depolarized for 0, 1 and 6 hrs with 55mM extracellular KCl. To identify the gene programs regulated in these cells by the activity-induced early-response transcription factor Npas4, we repeated the same experiment in the MGE- and CTX-cultures lacking Npas4 (Npas4-KO). Littermate mouse E14 MGE- or CTX-derived neurons (WT or KO for Npas4) were cultured for 9 days, quieted overnight with TTX and AP-5 and then membrane-depolarized for 0, 1 or 6 hours by raising the extracellular KCl-concentration to 55mM. RNA was then extracted and analyzed using Affymetrix GeneChip Mouse Expression Set 430 2.0 microarray platform.

2015-06-04 | E-GEOD-55588 | biostudies-arrayexpress

Identification of activity-induced genes in cortical inhibitory neurons (RNA-Seq)

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Identification of activity-induced genes in cortical inhibitory neurons (RNA-Seq)

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Characterization of Npas4 and heterodimer DNA binding in stimulated and silenced rat neurons

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Genome-wide activity-dependent MeCP2 phosphorylation regulates nervous system development and function [cultured cortical neurons]

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shRNA profiling of rat neurons to identify MEF2 Regulated Genes

Project description:Expression profiling in hippocampal neurons to identify activity-regulated genes controlled by MEF2; Experiments were conducted to identify activity-regulated MEF2 target genes. Experiment Overall Design: Neurons were depolarized with 55mM extracellular KCl for one or six hours in the presence of control or MEF2-specific shRNAs

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An NPAS4:NuA4 complex couples synaptic activity to DNA repair

Project description:Neuronal activity is critical for adaptive circuit remodeling but poses an inherent risk to the stability of the genome across the long lifespan of post-mitotic neurons1-5. Whether neurons have acquired specialized genome protection mechanisms that enable them to withstand decades of potentially damaging stimuli during periods of heightened activity is not known. Here we identify an activity-dependent DNA repair mechanism via a new form of the NuA4/TIP60 chromatin modifier that assembles in activated neurons around the inducible, neuronal-specific transcription factor NPAS4. We purify this complex directly from the brain and demonstrate its functions in eliciting activity-dependent changes to neuronal transcriptomes and circuitry. By identifying the landscape of activity-induced DNA double-strand breaks in the brain, we show that the NPAS4:NuA4 complex binds to recurrently damaged regulatory elements and recruits additional DNA repair machinery to stimulate their repair. Gene regulatory elements bound by the NPAS4:NuA4 complex are partially protected from age-dependent accumulation of somatic mutations. Impaired NPAS4:NuA4 signaling leads to a cascade of cellular defects including dysregulated transcriptional responses to activity, loss of control over neuronal inhibition, and genome instability, culminating in reduced organismal lifespan. In addition, mutations in several components of the NuA4 complex are reported to lead to neurodevelopmental disorders and autism. Together, these findings identify a neuronal-specific complex that couples neuronal activity directly to genome preservation and whose disruption may contribute to developmental disorders, neurodegeneration and aging.

2023-02-15 | PXD038718 | Pride

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