RNA-seq of manually sorted transgenically labeled sNPFr-Gal4 and TRH-Gal4 drosphila neurons
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE131405 | GEO | 2019/05/18
REPOSITORIES: GEO
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Project description:RNA-seq of manually sorted transgenically labeled sNPFr-Gal4 and TRH-Gal4 drosphila neurons
| PRJNA543486 | ENA
Project description:In this study, we performed single-cell RNA-sequencing (scRNA-seq) on 24 hours post-fertilization (hpf) mnx1:GFP zebrafish embryos to characterize the transcriptional diversity of developing spinal motor neurons. Our goal was to identify molecularly distinct subtypes within the motor neuron population. This dataset provides evidence for the existence of at least three transcriptionally distinct motor neuron subtypes.
2025-11-11 | E-MTAB-15160 | biostudies-arrayexpress
Project description:Modulation of action choices according to the environmental context is crucial for animal survival and reproductive success1. Aggression, despite its general importance as a social behavior2, can become detrimental if uncontrolled3,4. However, the genetic and neural basis for aggression control through active suppression remains largely unknown. Here we found nvy, a Drosophila homolog of vertebrate myeloid translocation gene (MTG)5 involved in transcriptional regulation6-8, suppresses aggression through a specific subset of neurons. Mutation of the nvy gene resulted in hyper-aggressiveness, which was rescued by neuronal expression of human MTGs as well as Drosophila nvy. The mutant exhibited persistent aggression under various contexts in which wild-type flies switch their behavioral patterns. Knockdown of nvy in octopaminergic/tyraminergic (OA/TA) neurons increased aggression, phenocopying the nvy deletion. Cell-type specific transcriptomics on OA/TA neurons derived from the nvy mutants revealed aggression-controlling genes that are likely downstream of nvy. Moreover, we found that the nvy-expressing OA/TA neuronal subpopulations specifically suppress aggression. Our results presents a powerful genetic model to unravel not only the neuronal systems that modulate aggression in a social context-dependent manner, but also the conserved molecular mechanism underlying the tumorigenesis caused by the MTG mutations.
2022-06-22 | GSE148630 | GEO
Project description:During murine hypothalamic development, different neuroendocrine cell phenotypes are generated in overlapping periods; this suggests that cell-type specific developmental programs operate to achieve complete maturation. A balance between programs that include cell proliferation, cell cycle withdrawal as well as epigenetic regulation of gene expression characterizes neurogenesis. Thyrotropin releasing hormone (TRH) is a peptide that regulates energy homeostasis and autonomic responses. To better understand the molecular mechanisms underlying TRH neuron development, we performed a genome wide study of its transcriptome during fetal hypothalamic development. In primary cultures, TRH cells constitute 2% of the total fetal hypothalamic cell population. To purify these cells, we took advantage of the fact that the segment spanning –774 to +84 bp of the Trh gene regulatory region confers specific expression of the green fluorescent protein (GFP) in the TRH cells. Transfected TRH cells were purified by fluorescence activated cell sorting, various cell preparations pooled, and their transcriptome compared to that of GFP- hypothalamic cells. TRH cells undergoing the terminal phase of differentiation, expressed genes implicated in protein biosynthesis, intracellular signaling and transcriptional control. Among the transcription-associated transcripts, we identified the transcription factors Klf4, Klf10 and Atf3, which were previously uncharacterized within the hypothalamus. To our knowledge, this is the first report identifying transcripts with a potentially important role during the development of a specific hypothalamic neuronal phenotype. This genome-scale study forms a rational foundation for identifying genes that might participate in the development and function of hypothalamic TRH neurons.
2011-05-27 | GSE28441 | GEO
Project description:During murine hypothalamic development, different neuroendocrine cell phenotypes are generated in overlapping periods; this suggests that cell-type specific developmental programs operate to achieve complete maturation. A balance between programs that include cell proliferation, cell cycle withdrawal as well as epigenetic regulation of gene expression characterizes neurogenesis. Thyrotropin releasing hormone (TRH) is a peptide that regulates energy homeostasis and autonomic responses. To better understand the molecular mechanisms underlying TRH neuron development, we performed a genome wide study of its transcriptome during fetal hypothalamic development. In primary cultures, TRH cells constitute 2% of the total fetal hypothalamic cell population. To purify these cells, we took advantage of the fact that the segment spanning –774 to +84 bp of the Trh gene regulatory region confers specific expression of the green fluorescent protein (GFP) in the TRH cells. Transfected TRH cells were purified by fluorescence activated cell sorting, various cell preparations pooled, and their transcriptome compared to that of GFP- hypothalamic cells. TRH cells undergoing the terminal phase of differentiation, expressed genes implicated in protein biosynthesis, intracellular signaling and transcriptional control. Among the transcription-associated transcripts, we identified the transcription factors Klf4, Klf10 and Atf3, which were previously uncharacterized within the hypothalamus. To our knowledge, this is the first report identifying transcripts with a potentially important role during the development of a specific hypothalamic neuronal phenotype. This genome-scale study forms a rational foundation for identifying genes that might participate in the development and function of hypothalamic TRH neurons. Hypothalamic primary cultures were prepared from E17 rat embryos. Twenty-four hours after seeding, cells were transfected using the minimal Trh promoter (-776/+84 bp) upstream of the GFP. Forty-eight hours after transfection, cells were trypsinized and subjected to FACS. TRH+ cells were purified from a pool of five 60-mm dishes using the FACS Vantage (Becton Dickinson, San Jose, CA) and the exclusion method at high speed (60 µl/min). In general, 20,000 GFP+ cells were purified from 5 X 106 cells. The microarray analysis was performed as described in the Affymetrix expression analysis technical manual (http://www.affymetrix.com). Total RNA (10 µg) was extracted from three different cell populations: i) sorted TRH-GFP+ cells (GFP+); ii) TRH-GFP+ and GFP- mixed cells (GFP+/-) passed through the FACS but not sorted, and iii) non transfected cells (NT). To obtain a sufficient amount of RNA for each cell population, the number of independent experiments pooled for the GFP+ sample was higher than for the other samples. Therefore, a pool of six independent experiments was used to prepare total RNA from the GFP+ and three independent experiments for GFP+/- or NT cells.
2011-05-27 | E-GEOD-28441 | biostudies-arrayexpress
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2025-05-01 | E-MTAB-12940 | biostudies-arrayexpress
Project description:Most cancers including pancreatic ductal adenocarcinoma (PDAC) are infiltrated by PNS neurons participating in their complex tumor microenvironment. However, their cell bodies and nuclei are located in the para- and pre-vertebral PNS ganglia located far from the tumor mass itself. Thus, molecular information on healthy organ- vs. cancer-infiltrating neurons is currently lacking in any sequencing dataset of healthy or tumor tissue. To specifically identify and molecularly characterize the identity and transcriptomes of PDAC-infiltrating neurons at single cell resolution, we developed “Trace-n-seq”. This method is based on retrograd tracing of axons from target tissues to their respective ganglia, followed by individual FACS-isolation and transcriptomic analysis. We characterized >2000 sympathetic and sensory neurons that infiltrate PDAC, healthy pancreas, or other abdominal organs.
2025-02-28 | E-MTAB-12941 | biostudies-arrayexpress
Project description:Molecular mechanisms controlling specification and differentiation of distinct neuron subtypes in the cerebral cortex are not well understood. Corticothalamic projection neurons (CThPN) are a diverse set of neurons, critical for function of the neocortex, but little is known about the molecular mechansims controlling their development. We used microarrays to detail CThPN gene expression at 3 developmental time points. We then compared CThPN gene expression, with the gene expression of other neuron subtypes in the cerebral cortex at the same stages (previously described in Arlotta et a., 2005) CThPN were retrogradely label with fluorescent microespheres injected into the thalamus, and were FACS purified at 3 developmental stages for RNA extraction and hybridization on Affymetrix microarrays.
2016-06-28 | E-GEOD-61711 | biostudies-arrayexpress
Project description:To explore the molecular basis of the distinct intrinsic membrane properties and other dstinguishing features of functionally defined DRG neuron subtypes, we bulk-sequenced RNA at high depth of genetically-labeled DRG neurons to generate transcriptome profiles of eight major DRG neuron subtypes. The trancriptome profiles revealed differentially expressed and functionally relevant genes, including voltage-gated ion channels. Guided by the transcriptome pofiles, electrophysiological analyses using pharmacological and genetic manipulations as well as computational modeling of DRG neuron subtypes were undertaken to assess the functions of select voltage-gated potassium channels (Kv1, Kv2, Kv3, and Kv4) in shaping action potential (AP) waveforms and firing patterns of the DRG neuron subtypes. Our findings show that the transcriptome profiles have predictive value for defining ion channel contributions to sensory neuron subtype-specific intrinsic physiological properties.
2019-05-16 | GSE131230 | GEO
Project description:Sensorimotor reflex circuits engage distinct neuronal subtypes, defined by precise connectivity, to transform sensation into compensatory behavior. Whether and how motor partner populations shape the subtype fate and connectivity of their pre-motor counterparts remains controversial. Here, we discovered that motor partners are dispensable for proper connectivity across an entire vestibular reflex circuit that stabilizes gaze. We first measured activity following vestibular sensation in pre-motor projection neurons after constitutive loss of their extraocular motor neuron partners.We observed normal responses and topography consistent with unchanged functional connectivity between sensory neurons and projection neurons. Next, we show that projection neurons remain anatomically and molecularly poised to connect appropriately with their motor partners. Lastly, we show that the transcriptional signatures of projection neuron subtypes develop independently of motor partners. Our findings comprehensively overturn a long-standing model: that connectivity in the circuit for gaze stabilization is retrogradely determined by motor partner-derived signals. By defining the contribution of motor neurons to canonical sensorimotor circuit assembly, our work speaks to comparable processes in spinal circuits and advances our understanding of general principles of neural development.
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