Ena-DATASET-WTCHG-16-11-2017-17:13:35:582-1047 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001003807 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:To characterize the epigenetic programs that underlie pancreas differentiation, we have generated genome-scale maps of H3K4me and H3K27me3 patterns by ChIP-seq and determined expression profiles by RNA-seq from undifferentiated human ESCs, four intermediate differentiated stages (definitive endoderm, primitive gut tube, posterior foregut, and pancreatic endoderm), and in vitro-differentiated polyhormonal cells. Antibodies against CD142 and CD200 were used to select for targeted pancreatic and endocrine populations at the end of the culture. Cells at the end of culture were implanted into mice for further differentiation into mature insulin-producing beta-cells and compared to sorted polyhormonal cells by RNA-seq and ChIP-seq analysis. For the experimental factor values the time points are along a differentiation protocol from stem cells to tissue. Values in the CD antibody column refer to antibodies used for cell sorting. In this column 'not applicable' refers to samples that were not sorted. 'none' refers to samples that were sorted, but did not bind to either of the two antibodies, CD200 and CD142. Values in the histone antibody column are about the ChIP process.
2013-02-08 | E-MTAB-1086 | biostudies-arrayexpress
Project description:The definitive endoderm germ layer is the provenance of multiple internal organs, including the lungs, liver, pancreas and intestines. Molecular events driving initial endoderm germ layer specification and subsequent anterior-posterior patterning of endoderm into distinct organ primordia remain largely cryptic. Through microarray analyses, we captured genome-wide transcriptional dynamics driving successive stages of endoderm development with the intent of identifying novel regulatory genes or diagnostic markers that respectively drive or mark endoderm committment. HES3 human embryonic stem cells (hESCs) were differentiated into highly homogeneous endodermal progenitor populations, and microarray analyses were conducted of six different populations at different tiers of the endodermal lineage hierarchy: undifferentiated hESCs, anterior primitive streak (day 1 of in vitro differentiation), definitive endoderm (day 3) and anterior foregut, posterior foregut or midgut/hindgut patterned endoderm populations (day 7). Additionally, we compared hESCs differentiated using two alternative endoderm induction protocols, serum-based or AFBLy-based differentiation (both day 3 of differentiation).
2013-11-07 | E-GEOD-52158 | biostudies-arrayexpress
Project description:Microarray analysis of chick embryo tissues: Hamburger Hamilton (HH) stage 3+/4 and HH6 Hensenâs node, HH 3+/4 posterior primitive streak, notochord with ventral neural tube at HH10-11, dorsal neural tube at HH10-11 and anterior and posterior thirds of the wing bud at stages HH20-21 and HH24.
2016-08-23 | E-MTAB-4048 | biostudies-arrayexpress
Project description:A small molecule, AT7867, is a proliferation-promoting factor of human iPS cell-derived pancreatic progenitor cells; yet how it promotes cell proliferation is not known. AT7867 induces proliferation of pancreatic progenitor cells, but not that of definitive endoderm cells or primitive gut tube cells suggesting a cell type-specific effect. Our aim is to perform RNA-seq of cells obtained during a three stage differentiation of hiPS cells to the endodermal cell lineage in addition to pancreatic progenitor cells treated with AT7867, and analyze signaling pathways altered by the compound treatment.
2020-07-06 | GSE153806 | GEO
Project description:The definitive endoderm germ layer is the provenance of multiple internal organs, including the lungs, liver, pancreas and intestines. Molecular events driving initial endoderm germ layer specification and subsequent anterior-posterior patterning of endoderm into distinct organ primordia remain largely cryptic. Through microarray analyses, we captured genome-wide transcriptional dynamics driving successive stages of endoderm development with the intent of identifying novel regulatory genes or diagnostic markers that respectively drive or mark endoderm committment.
2013-11-07 | GSE52158 | GEO
Project description:To comprehensively delineate the ontogeny of an organ system, we generated 112,217 single- cell transcriptomes representing all endoderm populations within the mouse embryo until midgestation. We employed graph-based approaches to model differentiating cells for spatio- temporal characterization of developmental trajectories. Our analysis reveals the detailed architecture of the emergence of the first (primitive or extra-embryonic) endodermal population and pluripotent epiblast. We uncover an unappreciated relationship between descendants of these lineages, before the onset of gastrulation, suggesting that mixing of extra-embryonic and embryonic endoderm cells occurs more than once during mammalian development. We map the trajectories of endoderm cells as they acquire embryonic versus extra-embryonic fates, and their spatial convergence within the gut endoderm; revealing them to be globally similar but retaining aspects of their lineage history. We observe the regionalized localization of cells along the forming gut tube, reflecting their extra-embryonic or embryonic origin, and their coordinate patterning into organ-specific territories along the anterior-posterior axis.
2019-04-10 | GSE123046 | GEO
Project description:To comprehensively delineate the ontogeny of an organ system, we generated 112,217 single- cell transcriptomes representing all endoderm populations within the mouse embryo until midgestation. We employed graph-based approaches to model differentiating cells for spatio- temporal characterization of developmental trajectories. Our analysis reveals the detailed architecture of the emergence of the first (primitive or extra-embryonic) endodermal population and pluripotent epiblast. We uncover an unappreciated relationship between descendants of these lineages, before the onset of gastrulation, suggesting that mixing of extra-embryonic and embryonic endoderm cells occurs more than once during mammalian development. We map the trajectories of endoderm cells as they acquire embryonic versus extra-embryonic fates, and their spatial convergence within the gut endoderm; revealing them to be globally similar but retaining aspects of their lineage history. We observe the regionalized localization of cells along the forming gut tube, reflecting their extra-embryonic or embryonic origin, and their coordinate patterning into organ-specific territories along the anterior-posterior axis.
2019-04-10 | GSE123124 | GEO
Project description:In vertebrates the endoderm which gives rise to the epithelial lining of the digestive tract becomes regionalized along its antero-posterior axis after gastrulation. The molecular basis of the initial step of this regionalization has largely remained unclear. Using chick model, we generated high-quality transcriptomic datasets of different stages/regions of the endoderm and analyzed their molecular heterogeneity. Total RNA from HH stage 4-5 entire definitive endoderm, HH stages 10-11 foregut endoderm and HH stages 8-10 mid/hindgut endoderm were purified. 5 M-NM-<g of RNA from each sample were used to screen Affymetrix Chicken Genome Array without an amplification step.
2013-06-08 | E-GEOD-22222 | biostudies-arrayexpress
Project description:To better understand the mechanism by which HES1 regulates pancreas development we took advantage of recent developments in directed differentiation of human embryonic stem cells (hESCs) to the pancreatic endocrine lineage via a series of progenitor stages (Figure 1 and (Rezania et al., 2014). Using the iCRISPR platform (González et al., 2014), we introduced indels in the HES1 and NEUROG3 genes, either singly or in combination in iCRISPR H1 cells. Using previously described gRNAs (Zhu et al., 2016) to target exon2 of the NEUROG3 gene and exon2 of the HES1 gene we detected by Sanger and RNA-sequencing a 2 bp insertion and a T insertion, respectively, resulting in premature STOP codons in two/multiple clonal cell lines carrying the introduced mutation and the loss of NEUROG3 by immunostaining We then subjected two or more clonal lines of H1-iCRISPR (wildtype), HES1−/−, NEUROG3−/− and HES1−/−NEUROG3−/− (abbreviated H1N3-dKO or H1−/−N3−/−) to differentiation to β-like cells using a modified version of the protocol from Rezania et al. (2014). Marker analysis showed that all cell lines maintained pluripotency (OCT4+) as hESC and were able to differentiate to FOXA2+ and SOX17+ co-positive definitive endoderm (DE, Day 3), PDX1+ cells at the posterior foregut stage (PF, Day 7), to bipotent progenitors marked by PDX1+ and NKX6-1+ at the Pancreatic Endoderm stage (PE, Day 10), and the Endocrine Precursor stage (EP, Day 13)
2020-09-30 | E-MTAB-7185 | biostudies-arrayexpress
Project description:Lineage segregation in the mouse embryo is a finely controlled process dependent upon coordination of signalling pathways and transcriptional responses. We employed conditional deletion of Oct4 to investigate consequences of interference with embryonic patterning and lineage specification. Nanog becomes upregulated in the first epiblast cells to lose Oct4, leading to an expanded Nanog-positive domain. The primitive streak forms in the presumptive proximal posterior region, but epithelial to mesenchymal transition is impeded by dramatic increase of E-cadherin, leading to complete disorganisation and failure to generate germ layers. Formerly, expression domains of lineage markers were disrupted. Specifically, definitive endoderm expanded, the boundaries between presumptive anterior and posterior domains blurred and an ectopic posterior-like region appeared anteriorly, suggesting a role for Oct4 in maintaining the embryonic axis. Despite intermixing of lineage marker domains in mutants, cells co-expressing distinct lineage genes were not observed, suggesting that Oct4 deletion does not alter the connectivity of the transcription networks which underlie cell fate decisions in vivo. Molecular profiling corroborated genome-wide posteriorisation of mutants and disrupted expression of genes involved in gastrulation. Lastly, we confirmed a requirement for Oct4 in self-renewal of post-implantation epiblast ex vivo
2018-06-11 | GSE103403 | GEO