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

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

PROVIDER: PRJNA622272 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11472175.fastq.gz	Fastqsanger.gz
	SRR11472176.fastq.gz	Fastqsanger.gz
	SRR11472177.fastq.gz	Fastqsanger.gz
	SRR11472178.fastq.gz	Fastqsanger.gz
	SRR11472179.fastq.gz	Fastqsanger.gz

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

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

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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.

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

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Amygdalostriatal transition zone neurons encode sustained valence to direct conditioned behaviors

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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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Project description:Astrotactin 2 (ASTN2) is a transmembrane neuronal protein highly expressed in the cerebellum that functions in receptor trafficking and modulates cerebellar Purkinje cell (PC) synaptic activity. Individuals with ASTN2 mutations exhibit neurodevelopmental disorders, including autism spectrum disorder (ASD), ADHD, learning difficulties and language delay. To provide a genetic model for the role of the cerebellum in ASD-related behaviors and study the role of ASTN2 in cerebellar circuit function, we generated global and PC-specific conditional Astn2 knockout (KO and cKO, respectively) mouse lines. Astn2 KO mice exhibited strong ASD-related behavioral phenotypes, including a marked decrease in separation-induced pup ultrasonic vocalization calls, hyperactivity, and repetitive behaviors, altered behavior in the three-chamber test, and impaired cerebellar-dependent eyeblink conditioning. Hyperactivity and repetitive behaviors were also prominent in Astn2 cKO animals but they did not show altered behavior in the three-chamber test. By Golgi staining, Astn2 KO PCs had region-specific changes in dendritic spine density and filopodia numbers. Proteomic analysis of Astn2 KO cerebellum revealed a marked upregulation of ASTN2 family member, ASTN1, a neuron-glial adhesion protein. Immunohistochemistry and electron microscopy demonstrated a significant increase in Bergmann glia volume in the molecular layer of Astn2 KO animals. Electrophysiological experiments indicated a reduced frequency of spontaneous excitatory postsynaptic currents (EPSCs), as well as increased amplitudes of both spontaneous EPSCs and inhibitory postsynaptic currents (IPSCs) in the Astn2 KO animals, suggesting that pre- and postsynaptic components of synaptic transmission were altered. Thus, ASTN2 regulates ASD-like behaviors and cerebellar circuit properties.

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