Rna-seq transcriptome data for insulin-GFP+ cells differentiated from NEUROD1 knock out and NEUROD1+/+ control human embryonic stem cells.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA507177 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8247840.fastq.gz | Fastqsanger.gz | |||
| SRR8247841.fastq.gz | Fastqsanger.gz | |||
| SRR8247834.fastq.gz | Fastqsanger.gz | |||
| SRR8247835.fastq.gz | Fastqsanger.gz | |||
| SRR8247836.fastq.gz | Fastqsanger.gz |
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Project description:The purpose of this study was to identify genes regulated by NEUROD1 in insulin expressing cells differentiated from human embryonic stem cells.
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Project description:NeuroD1 encodes a basic helix-loop-helix transcription factor involved in the development of neural and endocrine structures. NeuroD1 mRNA is highly abundant in the adult mammalian pineal gland and exhibits a developmental expression pattern similar to the retina. This is consistent with the common evolutionary origin of pinealocytes and retinal photoreceptors. Pinealocytes and retinal photoreceptors express a shared set of phototransduction genes and submammalian pinealocytes are photosensitive. In contrast to the retina, the pineal gland is a relatively homogeneous structure, composed 95% of pinealocytes. This makes the pineal gland a particularly useful model for understanding photoreceptor cell biology. The loss of NeuroD1 in the retina results in progressive photoreceptor degeneration and the molecular mechanisms underlying this retinal degeneration phenotype remain unknown. Similarly, the role that NeuroD1 plays in the pineal gland is unknown. To determine the function of NeuroD1 in the pineal gland and retina, a Cre/loxP recombination strategy was used to selectively target a NeuroD1 floxed allele and generate NeuroD1 conditional knockout (cKO) mice. Tissue specificity was conferred using Cre recombinase expressed under the control of the promoter of Crx, a transcription factor selectively expressed in the pineal gland and retina. Pineal and retinal tissues from two-month-old NeuroD1 cKO and control animals were used in microarray studies to identify candidate genes responsible for the photoreceptor degeneration phenotype. The Cre/loxP recombination strategy was used to target a NeuroD1 floxed allele and generate NeuroD1 conditional knockout mice (NeuroD1floxed::Crx-Cre+/-). NeuroD1 floxed mice (NeuroD1floxed::Crx-Cre-/-) served as the controls. Pineal glands and retinas from two-month-old control and conditional knockout mice were collected at ZT6 and ZT20. 3 pools of 6 pineal glands per genotype and respective time of day were collected for each sample. Similarly, 3 pools of 6 retinas each were also collected. RNA from each pool was extracted and hybridized on the Affymetrix Mouse 430 2.0 array.
2012-07-25 | E-GEOD-35396 | biostudies-arrayexpress
Project description:RNAseq of GFP-sorted cells (Low-GFP vs. High-GFP, GFP-fed vs GFP+fed)
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Project description:We hypothesized that functional polymorphisms in NEUROD1 target genes may also affect the clinical outcomes of patients with SCLC, as NEUROD1 plays a crucial role in SCLC carcinogenesis. To test this hypothesis, we performed ChIP-seq of NeuroD1 and H3K4me3 in SCLC cells. Then we evaluated the association between putative functional polymorphisms in NEUROD1 target genes and the chemotherapy response and survival outcomes of patients with SCLC.
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Project description:NEUROD1 dependent gene regulation in murine pancreatic endocrine cells and human stem cell derived insulin producing cells
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Project description:Differentiation of INSGFP/w hESCs using published protocols demonstrated that all GFP+ cells co-expressed insulin, confirming the fidelity of the reporter gene. INS-GFP+ cells also co-expressed glucagon and somatostatin, confirming prior studies regarding the polyhormonal nature of early hESC derived insulin-expressing cells. INSGFP/w hESCs were employed to develop a 96 well format spin Embryoid Body (EB) differentiation protocol that utilized the recombinant protein based fully defined medium, APEL. Like INS-GFP+ cells generated with other methods, those derived using the spin EB protocol expressed a collection of pancreatic related transcription factors including ISL1, PAX6 and NKX2.2. However, in contrast to previous methods, the spin EB protocol yielded INS-GFP+ cells that also co-expressed the beta-cell transcription factor, NKX6.1 and comprised a substantial proportion of monohormonal insulin+ cells.
2012-02-02 | E-MEXP-3378 | biostudies-arrayexpress
Project description:Cell fate specification relies on the action of critical transcription factors that become available at distinct stages of embryonic development. One such factor is NeuroD1, which is essential for eliciting the neuronal development program and possesses the ability to reprogram other cell types into neurons. Given this capacity, it is important to understand its targets and the mechanism underlying neuronal specification. Here, we show that NeuroD1 directly binds regulatory elements of neuronal genes that are developmentally silenced by epigenetic mechanisms. This targeting is sufficient to initiate events that confer transcriptional competence, including reprogramming of transcription factor landscape, conversion of heterochromatin to euchromatin and increased chromatin accessibility, indicating potential pioneer factor ability of NeuroD1. The transcriptional induction of neuronal fate genes is maintained via epigenetic memory despite a transient NeuroD1 induction during neurogenesis. Our study not only reveals the NeuroD1-dependent gene regulatory program driving neurogenesis but also increases our understanding of how cell-fate specification during development involves a concerted action of transcription factors and epigenetic mechanisms. 1. Ectopic NeuroD1 was induced for 48 hours (+Dox) in ES cells for checking initiation of neuronal transcriptional program in comparison to uninduced condition (-Dox) 2. ChIP-seq was performed after 24 hours of NeuroD1 induction in ES cells.
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Project description:Cell-fate specification relies on a close cooperation of distinct transcription factors and their crosstalk with the epigenetic landscape during embryonic development. NeuroD1 is known to be essential for eliciting neurogenesis and is able to reprogram other cell types into neurons. Despite progress, its global impact on the epigenome and cooperativity with other transcription factors during neurogenesis remains unknown. Here we show that despite NeuroD1 binding and a gain of active chromatin, only sites that show high local density of adjacent bHLH motifs, higher minor groove width and propeller twist as well as enrichment of another novel bHLH motif were able to get transcriptionally induced. Transcription factor activity analysis on the epigenome timecourse following NeuroD1 induction further identified this bHLH factor among top factors that gained activity during this process. Importantly, this bHLH factor was induced simultaneously to NeuroD1 as cells transit from an apical to a basal progenitor state during cortical development. Moreover, this bHLH factor interacts with NeuroD1 and co-occupies NeuroD1 target distinct genomic regions. We further show that the loss of this bHLH factor during cortical development severely impairs neurogenesis. Our study not only reveals the mechanistic basis underlying a productive transcriptional response of NeuroD1 during neurogenesis but also identified a novel bHLH transcription factor that partners with NeuroD1 and plays a critical role during cortical development.
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Project description:Small cell lung carcinoma (SCLC) and large cell neuroendocrine carcinoma (LCNEC) are high-grade pulmonary neuroendocrine tumors. The neural basic helix-loop-helix (bHLH) transcription factors ASCL1 and NEUROD1 have been shown to play crucial roles in promoting the malignant behavior and survival of human SCLC cell lines. In this study, we find ASCL1 and NEUROD1 identify distinct neuroendocrine tumors, bind distinct genomic loci, and regulate mostly distinct genes. ASCL1 and NEUROD1 are often bound in super-enhancers that are associated with highly expressed genes in their respective SCLC cell lines suggesting different cell lineage of origin for these tumors. ASCL1 targets oncogenic genes such as MYCL1, RET, and NFIB, while NEUROD1 targets the oncogenic gene MYC. Although ASCL1 and NEUROD1 regulate different genes, many of these gene targets commonly contribute to neuroendocrine and cell migration function. ASCL1 in particular also regulates genes in the NOTCH pathway and genes important in cell-cycle dynamics. Finally, we demonstrate ASCL1 but not NEUROD1 is required for SCLC and LCNEC tumor formation in current in vivo genetic mouse models of pulmonary neuroendocrine tumors ChIP-seq analysis performed on three ASCL1high and two NEUROD1high human SCLC cell lines to identify ASCL1 and/or NEUROD1 binding sites in these two types of cells. Also, we performed ChIP-seq for Ascl1 binding sites in mouse neuroendocrine lung tumors obtained from Trp53;Rb1;Rbl2 triple knockout model mice treated with Adeno-CMVCRE intratracheally.
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Project description:Immunoprecipitation was performed on Cav1 WT and KO brain endothelial cells using Insulin receptor-beta (IR-b) antibody. Proteins that interact with IR-b were detected using Mass spectrometry.
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