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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE127793 | GEO | 2019/10/02

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.

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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.

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

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Arnt2 tunes activity-dependent gene expression through NCoR2-mediated repression and Npas4-mediated activation

Project description:ChIP-, ATAC-, and RNA-seq data Neuronal activity-dependent transcription is tuned to ensure precise gene induction during periods of heightened synaptic activity, allowing for appropriate responses of activated neurons within neural circuits. The consequences of aberrant induction of activity-dependent genes on neuronal physiology are not yet clear. Here, we demonstrate that, in the absence of synaptic excitation, the basic-helix-loop-helix (bHLH)-PAS family transcription factor ARNT2 recruits the NCoR2 co-repressor complex to suppress neuronal activity-dependent regulatory elements and maintain low basal levels of inducible genes. This restricts inhibition of excitatory neurons, maintaining them in a state that is receptive to future sensory stimuli. By contrast, in response to heightened neuronal activity, ARNT2 recruits the neuronal-specific bHLH-PAS factor NPAS4 to activity-dependent regulatory elements to induce transcription and thereby increase somatic inhibitory input. Thus, the interplay of bHLH-PAS complexes at activity-dependent regulatory elements maintains temporal control of activity-dependent gene expression and scales somatic inhibition with circuit activity.

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Arnt2 tunes activity-dependent gene expression through NCoR2-mediated repression and Npas4-mediated activation

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