Expression data of immortlized GnRH neuron cell lines
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ABSTRACT:
PROVIDER: PRJNA731928 | ENA |
REPOSITORIES: ENA
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Project description:During development, gonadotropin releasing hormone (GnRH) neurons are born in the nasal placode and migrate to the hypothalamus, where they position to regulate sexual reproduction. Defective GnRH neuron development may lead to GnRH deficiency (GD) which is characterized by absent or delayed puberty. Several GD causative genes have been identified so far, but half of the cases are still idiopathic. The identification of candidate genes is also hampered by the difficulty in isolating and studying GnRH neurons, which are small in number, develop in a short developmental window and lack specific markers. Immortalized murine cell lines have been developed in past years. Of interest, GT1-7 represent hypothalamic post-migratory neurons, whereas GN11 cells represent GnRH neurons blocked at an early stage of their migration. Here, we obtained the transcriptomic profile of Gn11 abnd GT1-7 cells, representing GnRH neurons at an immature and mature developmental stage, respectively.
2023-02-28 | GSE174902 | GEO
Project description:During development, gonadotropin releasing hormone (GnRH) neurons are born in the nasal placode and migrate to the hypothalamus, where they position to regulate sexual reproduction. Defective GnRH neuron development may lead to GnRH deficiency (GD) which is characterized by absent or delayed puberty. Several GD causative genes have been identified so far, but half of the cases are still idiopathic. The identification of candidate genes is also hampered by the difficulty in isolating and studying GnRH neurons, which are small in number, develop in a short developmental window and lack specific markers. Gene expression profiles of GnRH neurons are lacking, as obtaining primary GnRH neurons is challenging and no reports on gene expression profiles during the whole developmental process of GnRH neurons are available. In this work, we obtained the transcriptomic profile of sorted GFP-positive and unsorted GFP-negative cells from Gnrh1-GFP rat embryos at three developmental stages, representing the initiation (embryonic day (E)14), the peak (E17) and the completion of GnRH neuronal migration (E20).
2023-02-28 | GSE174896 | GEO
Project description:Hypothalamic gonadotropin-releasing hormone (GnRH) neurons lays the foundation for human development and reproduction, however, the critical cell populations and the entangled mechanisms underlying the development of human GnRH neurons remain poorly understood. Here, by utilizing our established human pluripotent stem cells-derived GnRH neuron model, we decoded the cellular heterogeneity and differentiation trajectories at the single-cell level. We found that a glutamatergic neuron population, which generated together with GnRH neurons, showed similar transcriptomic properties with olfactory sensory neuron and provided the migratory path for GnRH neurons. Through trajectory analysis, we identified a specific gene module activated along the GnRH neuron differentiation lineage, and we examined one of the transcription factors, DLX5, expression in human fetal GnRH neurons. Furthermore, we found that Wnt inhibition could increase DLX5 expression, and improve the GnRH neuron differentiation efficiency through promoting neurogenesis and switching the differentiation fates of neural progenitors into glutamatergic neurons/GnRH neurons. Our research comprehensively reveals the dynamic cell population transition and gene regulatory network during GnRH neuron differentiation.
2022-10-04 | GSE212901 | GEO
Project description:Analysis of GT1-7 cells treated with GnRH. In this dataset, we include the expression data obtained from GT1-7 cells after treatment with GnRH. We confirmed that GT1-7 cells expressed DUSP5 and DUSP6 after GnRH treatment. Results provide insight into the effect of GnRH on MAP kinase pathway.
2018-05-31 | GSE112857 | GEO
Project description:Polycystic ovary syndrome (PCOS) is the most common form of infertility in women. The causes of PCOS are not yet understood and both genetics and early-life exposure have been considered as candidates. With regard to the latter, circulating androgens are elevated in mid-late gestation in women with PCOS, potentially exposing offspring to elevated androgens in utero; daughters of women with PCOS are at increased risk for developing this disorder. Consistent with these clinical observations, prenatal androgenization (PNA) of several species recapitulates many phenotypes observed in PCOS. There is increasing evidence that symptoms associated with PCOS, including elevated luteinizing hormone (LH) (and presumably gonadotropin-releasing hormone (GnRH)) pulse frequency emerge during the pubertal transition. We utilized translating ribosomal affinity purification coupled with RNA sequencing to examine GnRH neuron mRNAs from prepubertal (3wk) and adult female control and PNA mice. Prominent in GnRH neurons were transcripts associated with protein synthesis and cellular energetics, in particular oxidative phosphorylation. The GnRH neuron transcript profile was affected more by the transition from prepuberty to adulthood than by PNA treatment, however PNA did change the developmental trajectory of GnRH neurons. This included families of transcripts related to both protein synthesis and oxidative phosphorylation, which were more prevalent in adults than in prepubertal mice but were blunted in PNA adults. These findings suggest that prenatal androgen exposure can program alterations in the translatome of GnRH neurons, providing a mechanism independent of changes in the genetic code for altered expression.
2020-10-13 | GSE155314 | GEO
Project description:Translating Ribosome Affinity Purification results in non specific RNA binding to the immunoprecipitation matrix, even in mice not expressing cell specific GFP labelled ribosomal protein L10a. This creates false positive enriched transcripts in our datasets. To determine which RNA transcripts bind non specifically to the immunoprecipitation matrix, preoptic area punches were collected from young and adult mice that do not express L10a-GFP. Also, included was a positive control (GnRH CRE x floxed L10a-GFP mice) to ensure that the TRAP procedure was enriching for GnRH neuron specific transcripts as previously described. Four GnRH depleted supernatant RNA samples from the previous study were also included to aid comparison of the two sequencing runs.
2020-12-02 | GSE162558 | GEO
Project description:We utilized translating ribosome affinity purification (TRAP) coupled with RNA sequencing to examine mRNAs of GnRH neurons in adult intact and gonadectomized (GDX) male and female mice. TRAP produces one RNA fraction enhanced for GnRH neuron transcripts and one RNA fraction depleted. cDNA libraries were created from each fraction and 50-base, paired-end sequencing done and differential expression (enhanced fraction/depleted fraction) determined with a threshold of >1.5 or <0.66 fold (false discovery rate p≤0.05). A core of ~840 genes were differentially expressed in GnRH neurons in all treatments, including enrichment for Gnrh1 (~40 fold), and genes critical for GnRH neuron and/or gonadotrope development. In contrast, non-neuronal transcripts were not enriched or were de-enriched. Several epithelial markers were also enriched, consistent with the olfactory epithelial origins of GnRH neurons. Interestingly, many synaptic transmission pathways were de-enriched, in accordance with relatively low innervation of GnRH neurons. The most striking difference between intact and GDX mice of both sexes was a marked down regulation of genes associated with oxidative phosphorylation and upregulation of glucose transporters in GnRH neurons from GDX mice.
2018-04-18 | GSE110042 | GEO
Project description:Expression data of GFP-GnRH neurons during rat embryonic development
| PRJNA731929 | ENA
Project description:Expression data from GT1-7 cells after treatment with GnRH
| PRJNA449335 | ENA
Project description:The olfactory sensory system is formed by the coordinated morphogenesis and differentiation of the peripheral olfactory epithelium (OE) and the anterior forebrain. At early stages, immature olfactory receptor neurons (ORN) elongate their axons to penetrate the brain basement membrane, contact and form synapses with projection neurons of the olfactory bulb primordium. Axonal elongation is accompanied by migration of the GnRH+ neurons, followed by their ingression in the septo-hypothalamic area of the forebrain. This process is specifically impaired in the KallmannM-bM-^@M-^Ys syndrome (KS), a disorder characterized by anosmia and central hypogonadism. A set of transcription factors are master regulators of olfactory connectivity and GnRH neuron migration. We explored the transcriptional network underlying this process, by profiling the OE and adjacent mesenchyme at distinct embryonic ages. We also profiled the OE from embryos null for Dlx5, a homeogene essential for olfactory development, that causes a KS-like phenotype when deleted. We also applied analysis of conserved co-expression to integrate the obtained data with information on KS disease genes. The prevalent categories of genes differentially expressed during development are neuronal differentiation, extracellular remodelling and cell adhesion. From the analysis of Dlx5 mutant tissues we identify about 120 genes with a prevalence of intermediate filaments, cell signalling, epithelial and neuronal differentiation. Filtering for true OE expression and for the presence of Dlx5 binding sites, yielded twenty genes, of the following categories: 1) transmembrane adhesion/receptor molecules, 2) axon-glia interaction molecules, 3) synaptic proteins, 4) scaffold/adapter for signalling molecules. To functionally analyze these genes in vivo, we used three zebrafish fluorescent reporter zebrafish strains, in which we monitored early phases of olfactory/GnRH development upon gene downmodulation. The depletion of three (of five) Dlx5 targets affected axonal extension and targeting, while two (of two) altered GnRH neuron position and neurite organization. In one experiment we compare the olfactrory sensory epithelium from wild-type embryos, at three times of development, i.e. E11.5, E12.5 and E14.5. In a second experiment we compare the olfactory sensory epithelium from wild-type embryo with that from Dlx5 knock-out embryos, at the age E12.5
2014-01-31 | E-GEOD-52800 | biostudies-arrayexpress