Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neuronal activation modulates enhancer activity of genes for excitatory synaptogenesis through de novo DNA methylation

ABSTRACT: Neuronal activation modulates enhancer activity of genes for excitatory synaptogenesis through de novo DNA methylation

PROVIDER: PRJNA628066 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11608334.fastq.gz	Fastqsanger.gz
	SRR11608335.fastq.gz	Fastqsanger.gz
	SRR11608336.fastq.gz	Fastqsanger.gz
	SRR11608337.fastq.gz	Fastqsanger.gz
	SRR11608338.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 45

Similar Datasets

Neuronal activation modulates enhancer activity of genes for excitatory synaptogenesis through de novo DNA methylation

Project description:Post-mitotic neurons exhibit DNA methylation changes, contrary to the longstanding belief that the epigenetic pattern in terminally differentiated cells is essentially unchanging. While the mechanism and physiological significance of DNA demethylation in neurons have been extensively elucidated, occurrence of de novo DNA methylation and its impacts have been much less investigated. Here we show that neuronal activation induces global de novo DNA methylation at enhancer regions that can repress target genes in primary cultured hippocampal neurons. The functional significance of this de novo DNA methylation was underpinned by the demonstration that inhibition of DNA methyltransferase (DNMT) activity decreased neuronal activity-induced excitatory synaptogenesis. Overexpression of WW and C2 Domain containing 1 (Wwc1), a representative target gene of de novo DNA methylation, could phenocopy this DNMT inhibition-induced decrease in the synaptogenesis. We found that both DNMT1 and DNMT3a were required for the neuronal activity-induced de novo DNA methylation of Wwc1 enhancer. Taking these findings altogether, we concluded that activity-induced de novo DNA methylation affecting gene expression has impacts on neuronal physiology comparable to those of DNA demethylation.

2020-04-26 | GSE149342 | GEO

Neuronal activation modulates enhancer activity of genes for excitatory synaptogenesis through de novo DNA methylation.

Project description:Post-mitotic neurons do exhibit DNA methylation changes, contrary to the longstanding belief that the epigenetic pattern in terminally differentiated cells is essentially unchanged. While the mechanism and physiological significance of DNA demethylation in neurons have been extensively elucidated, the occurrence of de novo DNA methylation and its impacts have been much less investigated. In the present study, we showed that neuronal activation induces de novo DNA methylation at enhancer regions, which can repress target genes in primary cultured hippocampal neurons. The functional significance of this de novo DNA methylation was underpinned by the demonstration that inhibition of DNA methyltransferase (DNMT) activity decreased neuronal activity-induced excitatory synaptogenesis. Overexpression of WW and C2 domain-containing 1 (Wwc1), a representative target gene of de novo DNA methylation, could phenocopy this DNMT inhibition-induced decrease in synaptogenesis. We found that both DNMT1 and DNMT3a were required for neuronal activity-induced de novo DNA methylation of the Wwc1 enhancer. Taken together, we concluded that neuronal activity-induced de novo DNA methylation that affects gene expression has an impact on neuronal physiology that is comparable to that of DNA demethylation. Since the different requirements of DNMTs for germ cell and embryonic development are known, our findings also have considerable implications for future studies on epigenomics in the field of reproductive biology.

| S-EPMC8668374 | biostudies-literature

A human-specific microRNA controls the timing of excitatory synaptogenesis

Project description:The development of neural circuits in the human cortex is considerably prolonged in comparison to non-human primates, a trait which contributes to the remarkable cognitive capacity of modern humans. In contrast to protein-coding genes, non-coding genes underwent a dramatic expansion during evolution, suggesting their involvement in human-specific aspects of brain development. Here, using a glial free human-induced pluripotent stem-cell derived neuron model (“igNeurons”), we show widespread expression and dynamic regulation of various non-coding RNA classes, including microRNAs, during human excitatory synapse development. The expression of a human-specific microRNA, miR-1229-3p, strongly correlates with the neuromorphological trajectory of igNeurons. miR-1229-3p inhibition promotes the formation of excitatory synaptic co-clusters at early stages but reduces dendritic arborization in more mature neurons, consistent with accelerated neuronal maturation. Morphological alterations are accompanied by enhanced calcium spike activity and excitatory synaptic transmission. Mechanistically, miR-1229-3p controls mitochondrial homeostasis by directly targeting important regulators of mitochondrial autophagy and fission, such as Pink1. Stimulation of mitochondrial metabolism rescues the enhanced calcium spike activity in miR-1229-3p depleted neurons, demonstrating a causal involvement of mitochondrial homeostasis. Thus, our findings reveal an important function of human-specific miR-1229-3p in developmental timing of human synaptogenesis and generally implicate non-coding RNAs in the control of human connectivity and cognition.

2025-11-03 | PXD045809 | Pride

A human-specific microRNA controls the timing of excitatory synaptogenesis

Project description:A human-specific microRNA controls the timing of excitatory synaptogenesis

| PRJNA1023169 | ENA

A human-specific microRNA controls the timing of excitatory synaptogenesis (pLNA dataset)

Project description:Neural circuit development in the human cortex is considerably prolonged in comparison to non-human primates, a trait that contributes to the remarkable cognitive capacity of modern humans. Here, we explore the regulatory role of non-coding RNAs, which dramatically expanded during brain evolution, in synapse development of human-induced pluripotent stem-cell derived neurons. We found that inhibition of a human-specific microRNA, miR-1229-3p, alters the trajectory of human neuronal maturation and enhances excitatory synaptic transmission. Transcriptome analysis following miR-1229 knockdown revealed a downregulation of mitochondrial DNA (mtDNA) encoded genes. We further show that miR-1229 regulates mitochondrial morphology, mtDNA abundance and matrix calcium concentration, and that stimulation of mitochondrial metabolism rescues decreased calcium buffering in miR-1229-3p depleted neurons. Accordingly, miR-1229 directly targets an entire network of genes involved in mitochondrial function and ER-associated protein homeostasis. Our findings reveal an important function of human-specific miR-1229-3p in developmental timing of human synaptogenesis and generally implicate non-coding RNAs in the control of human connectivity and cognition.

2025-10-30 | GSE244441 | GEO

A human-specific microRNA controls the timing of excitatory synaptogenesis (pLNA dataset)

Project description:A human-specific microRNA controls the timing of excitatory synaptogenesis (pLNA dataset)

| PRJNA1023177 | ENA

A human-specific microRNA controls the timing of excitatory synaptogenesis (time course ribozero)

2025-10-30 | GSE244440 | GEO

A human-specific microRNA controls the timing of excitatory synaptogenesis (time course smallRNA)

2025-10-30 | GSE244443 | GEO

A human-specific microRNA controls the timing of excitatory synaptogenesis (time course smallRNA)

Project description:A human-specific microRNA controls the timing of excitatory synaptogenesis (time course smallRNA)

| PRJNA1023178 | ENA

A human-specific microRNA controls the timing of excitatory synaptogenesis (time course ribozero)