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Npas4-regulated genes in mouse hippocampal neurons

ABSTRACT: we performed a DNA microarray experiment to identify activity-regulated genes that are misregulated in the absence of Npas4. Keywords: Primary neuron culture, depolarization, activity-dependent, Npas4

ORGANISM(S): Mus musculus

PROVIDER: GSE11258 | GEO | 2008/09/24

SECONDARY ACCESSION(S): PRJNA109195

REPOSITORIES: GEO

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RNAi profiling of mouse hippocampal neurons infected with lentivirus expressing Npas4-RNAi or control-RNAi to study Npas4-regulated genes

Project description:We performed a DNA microarray experiment to identify activity-regulated genes that are misregulated in the absence of Npas4. Experiment Overall Design: We infected mouse hippocampal neurons with lentivirus expressing Npas4-RNAi or control-RNAi @ 3 DIV and depolarized the neurons @ 8 DIV with 50 mM of KCl for 0, 1, 3 or 6 hours. Neurons were lysed, mRNA isolated and hybridized to Affymetrix arrays. Data were collected from 3 independent experiments.

2008-10-26 | E-GEOD-11258 | biostudies-arrayexpress

Genomic decoding of neuronal depolarization by stimulus-specific NPAS4 heterodimers, RNA sequencing

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2019-10-02 | GSE134203 | GEO

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.

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

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KCl depolarization-regulated genes in mouse cortical neurons

Project description:we used DNA microarray analysis to identify genes that are induced by neuronal activity in excitatory neurons at the time when inhibitory synapses are forming and maturing on them. Keywords: Primary neuron culture, depolarization, activity-dependent

2008-09-24 | GSE11256 | GEO

Transcription profiling of mouse primary cultured neurons to identify activity related gene expression

Project description:This SuperSeries is composed of the following subset Series:; GSE11256: KCl depolarization-regulated genes in mouse cortical neurons; GSE11258: Npas4-regulated genes in mouse hippocampal neurons Experiment Overall Design: Refer to individual Series

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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.

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NPAS4 regulates the transcriptional response of suprachiasmatic nucleus neurons to photic input

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2021-08-23 | GSE148252 | GEO

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

Project description:We evaluated genome-wide DNA binding of NPAS4, ARNT1, ARNT2, H3K27ac, and RNAPII by chromatin immunoprecipitation sequencing (ChIP-seq) in mature primary hippocampal neurons (rat, DIV 28) that were pharmacologically silenced (“–”; 24 hours in TTX, CPP, and NBQX) or silenced and then treated with PTX for two hours (“+”) to trigger the production of AP- and EPSP-induced NPAS4.

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