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DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors

ABSTRACT: DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors

PROVIDER: PRJNA622271 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11459675_1.fastq.gz	Fastqsanger.gz
	SRR11459675_2.fastq.gz	Fastqsanger.gz
	SRR11472175.fastq.gz	Fastqsanger.gz
	SRR11459676_1.fastq.gz	Fastqsanger.gz
	SRR11459676_2.fastq.gz	Fastqsanger.gz

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DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RRBS]

Project description:DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RRBS]

| PRJNA622272 | ENA

DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RNA-seq]

Project description:DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RNA-seq]

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DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RRBS]

Project description:Emerging evidence suggests that epigenetic mechanisms regulate aberrant gene transcription in stress-associated mental disorders. However, it remains to be elucidated about the role of DNA methylation and its catalyzing enzymes, DNA methyltransferases (DNMTs), in this process. Here we found that rats exposed to chronic (2-week) unpredictable stress exhibited a substantial reduction of Dnmt3a after stress cessation in the prefrontal cortex (PFC), a key target region of stress. Treatment of unstressed control rats with DNMT inhibitors recapitulated the effect of chronic unpredictable stress on decreased AMPAR expression and function in PFC. In contrast, overexpression of Dnmt3a in PFC of stressed animals prevented the loss of glutamatergic responses. Moreover, the stress-induced behavioral abnormalities, including the impaired recognition memory and aggressive behaviors, were ameliorated by Dnmt3a expression in PFC of stressed animals. Lastly, we found genome-wide DNA methylation changes in PFC of stressed rats are selectively enriched at several pathways, such as axon guidance, Wnt signaling and neurotransmission. These findings have therefore recognized the role of DNA epigenetic modification in stress-induced disturbance of synaptic functions and cognitive & emotional processes.

2020-12-31 | GSE147846 | GEO

DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RNA-seq]

2020-12-31 | GSE147845 | GEO

DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-31 | GSE147847 | GEO

DNA Methyltransferase 3A Is Involved in the Sustained Effects of Chronic Stress on Synaptic Functions and Behaviors.

Project description:Emerging evidence suggests that epigenetic mechanisms regulate aberrant gene transcription in stress-associated mental disorders. However, it remains to be elucidated about the role of DNA methylation and its catalyzing enzymes, DNA methyltransferases (DNMTs), in this process. Here, we found that male rats exposed to chronic (2-week) unpredictable stress exhibited a substantial reduction of Dnmt3a after stress cessation in the prefrontal cortex (PFC), a key target region of stress. Treatment of unstressed control rats with DNMT inhibitors recapitulated the effect of chronic unpredictable stress on decreased AMPAR expression and function in PFC. In contrast, overexpression of Dnmt3a in PFC of stressed animals prevented the loss of glutamatergic responses. Moreover, the stress-induced behavioral abnormalities, including the impaired recognition memory, heightened aggression, and hyperlocomotion, were partially attenuated by Dnmt3a expression in PFC of stressed animals. Finally, we found that there were genome-wide DNA methylation changes and transcriptome alterations in PFC of stressed rats, both of which were enriched at several neural pathways, including glutamatergic synapse and microtubule-associated protein kinase signaling. These results have therefore recognized the potential role of DNA epigenetic modification in stress-induced disturbance of synaptic functions and cognitive and emotional processes.

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The Wilms' tumour 1 transcription factor regulates epigenetic states via DNA methyltransferase 3A

Project description:The Wilms' tumour 1 transcription factor regulates epigenetic states via DNA methyltransferase 3A.

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The Wilms' tumour 1 transcription factor regulates epigenetic states via DNA methyltransferase 3A

Project description:The Wilms' tumour 1 transcription factor regulates epigenetic states via DNA methyltransferase 3A. The data consists of two Nimblegen promoter/CpG island microarrays hybridized with MCIP DNA immunoprecipitated from either a HEK293-derived cell line expressing a heterologous WT1 cDNA (W210) or a control cell line containing the expression vector (IP100), both hybridized against input DNA.

2012-11-05 | E-GEOD-39713 | biostudies-arrayexpress

Amygdalostriatal transition zone neurons encode sustained valence to direct conditioned behaviors

Project description:Amygdalostriatal transition zone neurons encode sustained valence to direct conditioned behaviors

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m6A/YTHDF1 modulates CAP1-mediated actin turnover and synaptic function to regulate anxiodepressive-like behaviors

Project description:Neuroplasticity and synaptic dysfunction are central to depression, yet the underlying mechanisms remain poorly understood. While m6A and its reader YTHDF1 regulate mRNA translation, neuroplasticity and learning behaviors, their role in affective disorders such as depression remains unexplored. This study identifies YTHDF1 as a key regulator of depression pathogenesis. Genetic deletion of YTHDF1 in mice caused anterior cingulate cortex (ACC) hyperactivity, heightened social stress sensitivity, and anxiodepressive-like behaviors after acute social stress. Using multi-omic approaches, we uncovered a critical role for actin cytoskeleton dynamics and identified cyclase-associated protein 1 (CAP1) as a downstream effector of YTHDF1. Loss of YTHDF1 reduced CAP1 expression from early postnatal stages, resulting in F-actin accumulation, impaired synaptic function, and behavioral deficits. Strikingly, early postnatal YTHDF1 re-expression in the ACC restored CAP1 levels, synaptic integrity, and reversed depressive-like phenotypes. These findings establish the m6A/YTHDF1/CAP1 axis as a critical pathway regulating synaptic function and depression.

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