Effect of SERT LOF on Drosophila Kenyon Cells postsynaptic to serotonin [bulkRNA-seq]
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ABSTRACT:
PROVIDER: PRJNA947203 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23933579_1.fastq.gz | Fastqsanger.gz | |||
| SRR23933579_2.fastq.gz | Fastqsanger.gz | |||
| SRR23933580_1.fastq.gz | Fastqsanger.gz | |||
| SRR23933580_2.fastq.gz | Fastqsanger.gz | |||
| SRR23933581_1.fastq.gz | Fastqsanger.gz |
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Project description:to investigate the transcriptional effects on postsynaptic cells following SSRI-like SERT LOF, we used Drosophila mutants for SERT and compared to controls, isolating and profiling Kenyon Cells of the mushroom body
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Project description:to investigate the transcriptional effects on postsynaptic cells following SSRI-like SERT LOF, we used Drosophila mutants for SERT and compared to controls, isolating and profiling Kenyon Cells of the mushroom body
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Project description:Effect of SERT LOF on Drosophila Kenyon Cell subtypes postsynaptic to serotonin [scRNA-seq]
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Project description:Identifying new immune checkpoint molecules hindering antitumor T cell responses and devising new therapeutic blockades are key to the development of next-generation cancer immunotherapies. Here, we report the induction of the serotonin transporter (SERT) in solid tumor-infiltrating cytotoxic CD8 T cells, a molecule best known for its role in regulating serotonin neurotransmission in the brain. In solid tumors, CD8 T cells secrete serotonin, which stimulates their antitumor reactivities, while SERT functions as a negative regulator by depleting intratumoral serotonin. Inhibition of SERT using clinically approved selective serotonin reuptake inhibitors (SSRIs), a popular class of antidepressants, significantly suppressed tumor growth and enhanced CD8 T cell-mediated antitumor responses in various preclinical mouse syngeneic and human xenograft tumor models. Importantly, SSRI treatment exhibited significant therapeutic synergy with anti-PD-1 therapy, and clinical data correlation studies negatively associated intratumoral SERT expression with patient survival in a range of cancers. These findings highlight the significance of the intratumoral serotonin axis and identify SERT as a novel immune checkpoint, positioning SSRIs as promising candidates for next-generation combination cancer therapies.
2025-05-27 | GSE262781 | GEO
Project description:Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed drugs to pregnant women experiencing depression. While such drugs might be beneficial in combating depression by competitively binding to serotonin transporter (SERT), they can adversely affect the placenta and fetal brain development. Parietal trophoblast giant cells (pTGCs) in the mouse placenta are postulated to internalize maternal serotonin (5-HT) via transport through SERT, encoded by Slc6a4. The placenta provides the initial source of 5-HT to the emerging brain via the placental-brain axis. Disruption of 5-HT acquisition by pTGCs due to genetic deletion of Slc6a4 is hypothesized to impact placental and fetal brain development. A transgenic mouse line with the SERT transporter selectively deleted was created by pairing mice with Cre-recombinase linked to proliferin (Prl2c2) with LoxP sites flanking the Slc6a4 gene. Proliferin is solely expressed by pTGCs and other giant cells of the placenta. To compare placental and fetal brain development in selective Sl6a4 KO and WT mice, 5-HT content in the placenta and fetal brains of the mice was measured. No significant differences in 5-HT content were evident between knockout (KO) and wild-type (WT) placenta and fetal brain. However, there was significantly lower average number of pTGCs in KO placentas compared to WT (p ≤ 0.05). Sexually dimorphic differences in gene expression were evident in the placenta and fetal brain between KO and WT counterparts with female conceptuses showing the most dramatic responses. Findings suggest that ablation of SERT in pTGC disrupts the placenta-brain axis in a sex-dependent manner. These results might have important clinical ramifications for pregnant women being treated with SSRIs.
2025-08-02 | GSE304347 | GEO
Project description:The serotonin transporter (SERT, SLC6A4), belonging to Na+ and Cl- dependent transporters, functions to regulate the availability of serotonin (5-HT) in various tissues including brain, platelets, and intestine. Alterations in 5-HT levels and/or SERT expression have been implicated in pathophysiological conditions including anxiety-like behavior, obesity, cardiovascular disorders and GI disorders such as IBD, IBS, and diarrhea. Accordingly, SERT deficiency in mice is pleiotropic with many different phenotypic traits. Transgenic mice with global deletion of SERT exhibit increased anxiety, abnormal GI motility, and obesity associated with hyperglycemia. Additionally, these mice are more susceptible to intestinal inflammation. The mechanism by which SERT deficiency underlies GI related disturbances and exacerbates the severity of gut inflammation is not known. Thus, we evaluated the ileal mRNA expression to identify potential intestinal targets that contribute to disease pathogenesis when the SERT gene is non-functional. For these studies, RNA was extracted from ileum mucosa from age matched (9-10 wk) control and SERT KO mice by Trizol and was subjected to Mouse mRNA and OneArray Profiling. Our microarray data revealed 492 significantly upregulated and 293 downregulated genes in SERT KO ileum. Pathway analysis revealed significant enrichment in cell cycle, signaling, chemotaxis, and epithelial transporters. Genes of interest were validated by RT-PCR, which included CYP1A1 (~20 fold decrease, p < 0.05), CLDN8 (~30% decrease, p < 0.05), and HMGCS2 (~7 fold increase, p < 0.05). Similar changes were found in colon. A remarkable decrease in expression of Cyp1a1, which encodes a cytochrome P450 enzyme, provides a novel role of serotonergic pathways in drug and xenobiotic detoxification. CLDN8 encodes for claudin 8, which is downregulated in patients with Crohn’s disease. Deficiency of HMGCS2, the mitochondrial 3-hydroxy-3-methylglutaryl CoA synthase, is linked to hypoglycemia. Our data provides novel clues for differential expression of genes affected by 5-HT and/or SERT deficiency in the intestine.
2017-11-08 | GSE93534 | GEO
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
Project description:Genome-wide gene expression profiling was performed in pulmonary arteries from 32 mice. Four mice in 8 different groups; Normoxic: wild type female/male, Sert female/male; Hypoxic: wild type female/male and Sert female/male.
2010-12-16 | E-MTAB-455 | biostudies-arrayexpress