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Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation (ChIP-Seq)

ABSTRACT: Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation (ChIP-Seq)

PROVIDER: PRJNA955207 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24154320.fastq.gz	Fastqsanger.gz
	SRR24154321.fastq.gz	Fastqsanger.gz
	SRR24154322.fastq.gz	Fastqsanger.gz
	SRR24154323.fastq.gz	Fastqsanger.gz
	SRR24154324.fastq.gz	Fastqsanger.gz

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Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation

Project description:Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation

| PRJNA955204 | ENA

Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation (RNA-Seq)

Project description:Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation (RNA-Seq)

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Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation (ChIP-Seq)

Project description:To profile Sox2 and Sox9 binding sites in Gq-DREADD expressing CNO treated brains in comparison to control. Furthermore, we also aimed to profile Sox9 binding sites in odor treated vs. control olfactory bulbs. An additional goal of this study was to profile histone serotonylation mark in Slc22a3-cKO olfactory bulb in comparison to control.

2023-04-17 | GSE229644 | GEO

Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation.

Project description:Neuronal activity drives alterations in gene expression within neurons, yet how it directs transcriptional and epigenomic changes in neighboring astrocytes in functioning circuits is unknown. We found that neuronal activity induces widespread transcriptional up-regulation and down-regulation in astrocytes, highlighted by the identification of Slc22a3 as an activity-inducible astrocyte gene that encodes neuromodulator transporter Slc22a3 and regulates sensory processing in the mouse olfactory bulb. Loss of astrocytic Slc22a3 reduced serotonin levels in astrocytes, leading to alterations in histone serotonylation. Inhibition of histone serotonylation in astrocytes reduced the expression of γ-aminobutyric acid (GABA) biosynthetic genes and GABA release, culminating in olfactory deficits. Our study reveals that neuronal activity orchestrates transcriptional and epigenomic responses in astrocytes while illustrating new mechanisms for how astrocytes process neuromodulatory input to gate neurotransmitter release for sensory processing.

| S-EPMC10874521 | biostudies-literature

Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation

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

2023-04-17 | GSE229645 | GEO

Induction of astrocytic Slc22a3 regulates sensory processing through histone serotonylation (RNA-Seq)

Project description:To profile gene expression differences in astrocytes after chemogenetic neuronal activation in different mouse brain regions. Furthermore, we also sought to profile gene expression differences between control and Slc22a3 conditional knockout astrocytes in the mouse olfactory bulb.

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Serotonin transporter-dependent histone serotonylation in placenta contributes to the neurodevelopmental transcriptome [RNA-seq]

Project description:Brain development requires appropriate regulation of serotonin (5-HT) signaling from distinct tissue sources across embryogenesis. At the maternal-fetal interface, the placenta is thought to be an important contributor of offspring brain 5-HT and is critical to overall fetal health. Yet, how placental 5-HT is acquired, and the mechanisms through which 5-HT influences placental functions, are not well understood. Recently, our group identified a novel epigenetic role for 5-HT, in which 5-HT can be added to histone proteins to regulate transcription, a process called H3 serotonylation. Here, we show that H3 serotonylation undergoes dynamic regulation during placental development, corresponding to gene expression changes that are known to influence key metabolic processes. Using transgenic mice, we demonstrate that placental H3 serotonylation largely depends on 5-HT uptake by the serotonin transporter (Sert/Slc6a4). Sert deletion robustly reduces enrichment of H3 serotonylation across the placental genome, and disrupts neurodevelopmental gene networks in offspring brain tissues. Thus, these findings suggest a novel role for H3 serotonylation in coordinating placental transcription at the intersection of maternal physiology and offspring brain development.

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Serotonin transporter-dependent histone serotonylation in placenta contributes to the neurodevelopmental transcriptome [ChIP-seq]

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Epigenetic reprogramming of cell identity in the rat primary neuron-glia cultures involves histone serotonylation

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Single genomic enhancers drive experience-dependent GABAergic plasticity to maintain sensory processing in the adult cortex

Project description:Experience-dependent plasticity of synapses modulates information processing in neural circuits and is essential for cognitive functions. The genome, via non-coding enhancers, was proposed to control information processing and circuit plasticity by regulating experience-induced transcription of genes that modulate specific sets of synapses. To test this idea, we analyze here the cellular and circuit functions of the genomic mechanisms that control the experience-induced transcription of Igf1 (insulin-like growth factor 1) in vasoactive intestinal peptide (VIP) interneurons (INs) in the visual cortex of adult mice. We find that two sensory-induced enhancers selectively and cooperatively drive the activity-induced transcription of Igf1 to thereby promote GABAergic inputs onto VIP INs and to homeostatically control the ratio between excitation and inhibition (E/I ratio)—in turn, this restricts neural activity in VIP INs and principal excitatory neurons and maintains spatial frequency tuning. Thus, enhancer-mediated activity-induced transcription maintains sensory processing in the adult cortex via homeostatic modulation of E/I ratio.

2023-06-27 | GSE210658 | GEO

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