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Transcriptional changes in specifc subsets of Drosophila neurons following inhibition of the serotonin transporter

ABSTRACT: Transcriptional changes in specifc subsets of Drosophila neurons following inhibition of the serotonin transporter

PROVIDER: PRJNA947532 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23932406.fastq.gz	Fastqsanger.gz
	SRR23932407.fastq.gz	Fastqsanger.gz
	SRR23932408.fastq.gz	Fastqsanger.gz
	SRR23932409.fastq.gz	Fastqsanger.gz
	SRR23933579_1.fastq.gz	Fastqsanger.gz

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Transcriptional changes in specifc subsets of Drosophila neurons following inhibition of the serotonin transporter

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

2023-06-26 | GSE227935 | GEO

Hyperactive Mouse Serotonin Transporter Interacting Proteins LC-MSMS

Project description:The serotonin (5-HT) transporter (SERT) is a key determinant of the concentration of 5-HT available for synaptic signaling and is the target of the antidepressant-selective 5-HT reuptake inhibitors (SSRIs). In addition to the role of SERT in mediating the actions of antidepressant medications, multiple, rare gain of function coding variants in SERT have been identified in subjects with autism spectrum disorder (ASD). The Blakely lab has extensively characterized the structural and functional impact of one of these variants, SERT Ala56, in vitro and in vivo, revealing a constitutively-imposed, biased conformation that enhances transporter function and that perturbs transporter regulation. We hypothesize that SERT Ala56 disrupts the interactions of molecular networks that normally ensure proper transporter structure, localization and regulation, and whose elucidation may reveal new determinants of serotonergic dysfunction in ASD. Here, we pursue an unbiased proteomic analysis of changes in SERT interacting protein (SIPs) imposed by the SERT Ala56 variant, expressed in transgenic mice. Further investigation of the SIPs and associated networks nominated through our studies may provide new opportunities to detect and modulate brain networks that contribute to the underlying complexity of ASD.

2020-05-29 | PXD018695 | Pride

Transcriptional changes in specific subsets of Drosophila neurons following inhibition of the serotonin transporter.

Project description:The transcriptional effects of SSRIs and other serotonergic drugs remain unclear, in part due to the heterogeneity of postsynaptic cells, which may respond differently to changes in serotonergic signaling. Relatively simple model systems such as Drosophila afford more tractable microcircuits in which to investigate these changes in specific cell types. Here, we focus on the mushroom body, an insect brain structure heavily innervated by serotonin and comprised of multiple different but related subtypes of Kenyon cells. We use fluorescence-activated cell sorting of Kenyon cells, followed by either bulk or single-cell RNA sequencing to explore the transcriptomic response of these cells to SERT inhibition. We compared the effects of two different Drosophila Serotonin Transporter (dSERT) mutant alleles as well as feeding the SSRI citalopram to adult flies. We find that the genetic architecture associated with one of the mutants contributed to significant artefactual changes in expression. Comparison of differential expression caused by loss of SERT during development versus aged, adult flies, suggests that changes in serotonergic signaling may have relatively stronger effects during development, consistent with behavioral studies in mice. Overall, our experiments revealed limited transcriptomic changes in Kenyon cells, but suggest that different subtypes may respond differently to SERT loss-of-function. Further work exploring the effects of SERT loss-of-function in other circuits may be used help to elucidate how SSRIs differentially affect a variety of different neuronal subtypes both during development and in adults.

| S-EPMC10290657 | biostudies-literature

The serotonin transporter is a regulator of neurodegeneration and axon regeneration after retinal injury

Project description:Loss of specialized neurons in neurodegenerative diseases and after nerve injury is mediated in a neuronal subtype- and region-specific fashion. However, little is known about what molecular contexts define selective vulnerability. Here, we demonstrate that retinal ganglion cells (RGCs) in the mouse peripheral ventrotemporal (VT) retina are the most susceptible to optic nerve injury. Mechanistically, we show that the ventral-specific molecule, the serotonin transporter (SERT) is upregulated on VT axons within one day after injury and loss of SERT attenuates VT RGC death and promotes axon regeneration. From RNA-seq analysis, the transmembrane protein Gpnmb has been identified as a target downregulated by SERT. Moreover, GPNMB is involved in RGC protection and axon regeneration. Together, our studies reveal the serotonin transporter as a determinant of selective vulnerability.

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Project description:To unravel the effect of increased extracellular serotonin levels on brain development, RNA-seq was performed in the medial prefrontal cortex of serotonin transporter knockout and wildtype rats at five time points from early life to adulthood (postnatal day (PND) 8, 14, 21, 35 and 70). Differential expression of protein-coding genes was analyzed and we demonstrate that a lack of functional 5-HTT especially affects gene expression in early postnatal life (PND8).

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Conformational dynamics of the human serotonin transporter during substrate and drug binding

Project description:The serotonin transporter (SERT), a member of the neurotransmitter:sodium symporter family, is responsible for termination of serotonergic signaling by re-uptake of serotonin (5-HT) into the presynaptic neuron. Its key role in synaptic transmission makes it a major drug target, e.g. for the treatment of depression, anxiety and post-traumatic stress. Here, we apply hydrogen-deuterium exchange mass spectrometry to probe the conformational dynamics of human SERT in the absence and presence of known substrates and targeted drugs. Our results reveal significant changes in dynamics in regions TM1, EL3, EL4, and TM12 upon binding co-transported ions (Na+/K+) and ligand-mediated changes in TM1, EL3 and EL4 upon binding 5-HT, the drugs S-citalopram, cocaine and ibogaine. Our results provide a comprehensive direct view of the conformational response of SERT upon binding both biologically relevant substrate/ions and ligands of pharmaceutical interest, thus advancing our understanding of the structure-function relationship in SERT.

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Project description:We performed a comprehensive survey of DR and MR serotonin neurons in the adult mouse brain by scRNA-seq. To specifically label serotonin neurons, we crossed Sert-Cre mice (Gong et al., 2007) with the tdTomato Cre reporter mouse, Ai14 (Madisen et al., 2010). (Serotonin transporter, or Sert, is a marker for serotonin neurons; see more details below.) We collected serotonin neurons acutely dissociated from brain slices by fluorescence-activated cell sorting (FACS) and used Smart-seq2 (Picelli et al., 2013) to generate scRNA-seq libraries.

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Project description:The rhesus embryonic stem cell line 366.4 differentiates into serotonin neurons. RNA was extracted from ESC colonies, embryoid body (Ebs), Neurospheres in selection (N1), Proliferating serotonin neurons (N2) and differentiating serotonin neurons (N3). RNA was labeled with Enzo biotin labelling kit and hybridized to Rhesus chip from Affymetrix. single sample represent each stages and total 5 rhesus chip were hybridized

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Serotonin transporter-dependent histone serotonylation in placenta contributes to the neurodevelopmental transcriptome

Project description:Serotonin transporter-dependent histone serotonylation in placenta contributes to the neurodevelopmental transcriptome

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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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