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Activity-dependent transcriptional changes in human neurons

ABSTRACT: Activity-dependent transcriptional changes in human neurons

PROVIDER: PRJNA313218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3189480.fastq.gz	Fastqsanger.gz
	SRR3189480_1.fastq.gz	Fastqsanger.gz
	SRR3189480_2.fastq.gz	Fastqsanger.gz
	SRR3189490.fastq.gz	Fastqsanger.gz
	SRR3189490_1.fastq.gz	Fastqsanger.gz

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Activity-dependent transcriptional changes in human neurons

Project description:We used genome-wide sequencing methods to identify activity-regulated gene expression and regulatory elements in human neurons. Sensory stimuli drive the maturation and function of the mammalian nervous system in part through the activation of gene expression networks that regulate synapse development and plasticity. These programs of gene transcription have primarily been studied in mice, and it is not known if there are neuronal activity-regulated genes that control features of brain development and function that are unique to humans. In this study, we used genome-wide sequencing methods to identify activity-regulated gene expression and regulatory elements in human neurons.

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Project description:We generated human-induced pluripotent stem cell (hiPSC) derived neurons isolated from six childhood-onset schizophrenia (COS) cases and five healthy controls. To measured the transcriptional and epigenomic changes following neuronal activation with KCl, we harvested these cells one and six hours after stimulation with 50mM KCl and under non-stimulating conditions, followed by RNA-seq and ATAC-seq profiling. We comprehensively characterized activity-dependent changes in gene expression and gene regulatory element activity (chromatin accessibility) in hiPSC-derived neurons. After one hour of KCl induced depolarization, neurons invoked substantial activity-dependent changes in the expression of genes regulating synaptic functions, some of which are known to be perturbed in neuropsychiatric diseases, including schizophrenia and autism spectrum disorder. By capturing changes in chromatin accessibility, we extended our analysis to activity-dependent gene regulatory elements, captured by changes in chromatin accessibility, and also found significant heritability enrichment for schizophrenia variants in the activity-induced enhancers. Our framework not only offers an alternative approach to study the mechanisms of COS but also adds to converging evidence that activity-induced expression changes mediated by the activity of regulatory elements might contribute to schizophrenia risk.

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Project description:Activity-dependent gene expression is critical for synapse development and plasticity. To elucidate novel mechanisms linking neuronal activity to changes in transcription, we compared the nuclear proteomes of tetrodotoxin-silenced and bicuculline-stimulated cultured neurons using nuclear-localized APEX2 proximity biotinylation and mass spectrometry. The tumor suppressor protein PDCD4 was enriched in the nuclear proteome of silenced neurons, and PDCD4 levels rapidly decreased in the nucleus and cytoplasm of stimulated neurons. The activity-dependent decrease of PDCD4 was prevented by inhibitors of both PKC and proteasome activity and by a phospho-incompetent mutation of Ser71 in the βTRCP ubiquitin ligase-binding motif of PDCD4. We compared the activity-dependent transcriptomes of neurons expressing wildtype or degradation-resistant (S71A) PDCD4. We identified 91 genes as PDCD4 targets at the transcriptional level, including genes encoding proteins critical for synapse formation, remodeling, and transmission. Our findings indicate that regulated degradation of nuclear PDCD4 facilitates activity-dependent transcription in neurons.

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Project description:Neurons express numerous genes in response to environmental stimuli. This activity-dependent transcription is vital for neurons to function and hence for the brain to exert its complex processes. Post translational modifications of core histones have been implicated in the regulation of neuronal activity-dependent transcription. On the other hand, transcription and repair also involves the exchange of core histones, which regulates histone metabolism, but its involvement in neural activity-dependent transcription is currently well unknown. Here, in mature postmitotic neurons derived from mouse hippocampus, a Hist1h3f gene, which encodes replication-dependent histone H3.2, is expressed upon stimulation to glutamine receptors. Salt extraction and metabolic labeling of newly synthesized proteins in neurons revealed that core histone proteins are increased at protein levels in response to glutamine receptor stimulation. These results suggest that newly synthesized replication-dependent histone play a role in post-mitotic neurons. We performed microarrays to investigte the global transcriptional profiles of activity-dependent gene expression and identified two class of up-regulated genes during this process.

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