Similar Datasets
Project description:Methylome assays of E14.5 pancreatic progenitor cells
| PRJNA488177 | ENA
Project description:RNA-seq of sorted pancreatic endocrine progenitor cells
| PRJNA630435 | ENA
Project description:Pancreatic endocrine cells arise from a NGN3+ population during pancreas organogenesis. To gain a more thorough understanding of this progenitor pool, we used a reporter mouse - NGN3-EGFP - and sorted EGFP+ cells from e15.5 pancreata of control animals. The data generated from this experiment will allow us to visualize gene expression levels in endocrine progenitors during normal development and can be used to compare against mutant animal gene expression.
2021-03-15 | GSE149889 | GEO
Project description:The pancreatic islet contains multiple hormone+ endocrine lineages (alpha, beta, delta, PP and epsilon cells), but the developmental processes that underlie endocrinogenesis are poorly understood. Here, we generated novel mouse lines and combined them with various genetic tools to enrich all types of hormone+ cells for well-based deep single-cell RNA sequencing (scRNA-seq), and gene coexpression networks were extracted from the generated data for the optimization of high-throughput droplet-based scRNA-seq analyses. These analyses defined an entire endocrinogenesis pathway in which different states of endocrine progenitor (EP) cells sequentially differentiate into specific endocrine lineages in mice. Subpopulations of the EP cells at the final stage (EP4-early and EP4-late) show different potentials for distinct endocrine lineages. epsilon cells and an intermediate cell population were identified as distinct progenitors that independently generate both alpha and PP cells. Single-cell analyses were also performed to delineate the human pancreatic endocrinogenesis process. Although the developmental trajectory of pancreatic lineages is generally conserved between humans and mice, clear interspecies differences, including differences in the proportions of cell types and the regulatory networks associated with the differentiation of specific lineages, have been detected. Our findings support a model in which sequential transient progenitor cell states determine the differentiation of multiple cell lineages and provide a blueprint for directing the generation of pancreatic islets in vitro.
2021-04-20 | GSE139627 | GEO
Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Ngn3^GFP/+ [het] FACS sorted pancreatic cells at E15.5 (commited endocrine progenitor cells) and in Ngn3^GFP/GFP [null] at E15.5 (defective endocrine progenitor cells). This experiment is designed to understand the gene expression alteration in the endocrine lineage at different embryonic days. The aim is to understand both Ngn3 dependent and independent gene expression profiles so as to reveal the instructive signals that specfy the collective endocrine islet cell fate or specific islet cell type.
2015-10-01 | E-MTAB-3352 | biostudies-arrayexpress
Project description:Endoderm cells undergo a sequence of fate choices to generate insulin-secreting M-NM-2 cells. Studies of chromatin transitions during this process have been limited to the pancreatic progenitor stage that can be reconstituted from stem cells in vitro, with a gap in understanding the induction of endocrine cells. To address this, we established conditions for isolating endoderm cells, pancreatic progenitors, and endocrine cells from different staged embryos and performed genome wide analysis of the H3K27me3 mark of the repressive Polycomb complex. During the transition from endoderm to pancreas progenitors and during the transition from pancreas progenitors to endocrine cells, genes that lose the H3K27me3 mark typically encode transcriptional regulators, whereas genes that acquire the mark typically are involved in cell biology morphogenesis. Precocious depletion of the EZH2, a H3K27 methylase, at the pancreas progenitor stage enhanced the production of endocrine cells, leading to a later increase in pancreatic beta cells. Similarly, pharmacologic inhibition of EZH2 in embryonic pancreatic tissue explants and human embryonic stem cell cultures led to an increase in endocrine progenitors in vitro. These findings reveal a repeating target gene pattern in H3K27me3 dynamics and provide a means to modulate M-NM-2 cell development from stem cells. Analyzed five FACS-sorted tissues in early mouse embryo; for each tissue we sequenced H3K27me3 and input; no replicates
2014-07-28 | E-GEOD-56617 | biostudies-arrayexpress
Project description:Patients with NEUROGENIN3 mutations have enteric endocrinopathy and diabetes mellitus. We generated pluripotent stem cells from a patient’s fibroblasts to investigate if gene editing restores endocrine differentiation. Corrected cell lines differentiated into all pancreatic lineages while native cell lines failed to activate pancreatic progenitor and lineage determination genes, suggesting that the mutation disrupts pancreatic organogenesis and results in endocrine and exocrine dysfunction. Clinical testing revealed the patient has exocrine pancreatic insufficiency. These results expose a novel role for NEUROGENIN3 in human pancreatic differentiation and illustrates how patient-specific stem cells can be used to interrogate disease etiology and affect patient care.
2022-06-01 | GSE176145 | GEO
Project description:During embryonic development, islet progenitors are specified from pancreatic duct cells by transient expression of Neurog3, a transcription factor necessary and sufficient for initiation of islet development. To understand the dynamics of Neurog3-dependent endocrine cell fate determination, in this study we used ATAC-Seq to identify accessible genomic regions of purified duct, endocrine progenitor, and endocrine cells isolated from mice with varying Neurog3 dosage
2020-04-01 | GSE65794 | GEO
Project description:Ptf1a was identified as the essential transcription factor which controls pancreatic exocrine enzyme expression. With lineage tracing eperiments Ptf1a was recognized as an important pancreatic progenitor transcription factor and Ptf1a null mice do not develop a pancreas. We used gene expression arrays to determine the global differeences in expression levels when pancreatic progenitor cells are expanding in Ptf1a heterozygote versus null mutants at E10.5. Ptf1a E10.5 dorsal pancreas total RNA from pools of 3 embryos was twice linear amplified and hybridized to Affymetrix GeneChip Mouse Genome 430 2.0 in triplicate for the Ptf1a KO and in duplicate for the Ptf1a heterozygote
2011-01-24 | E-GEOD-26816 | biostudies-arrayexpress
Project description:Fate commitment is a sum of unique intrinsic properties and extrinsic cues received by a progenitor/stem cell. The knowledge of intrinsic properties, such as transcription, is extensive, whereas much less is known about how they are regulated by extrinsic cues, such as cell-cell and cell-extracellular matrix (ECM) interactions. We demonstrated that differential cell-cell adhesion controls the fate of multipotent pancreatic progenitors by dictating their migration to the tip and trunk niches where they are exposed to specific fate-inducing cues. Within the trunk each Neurogenin 3+ (Neurog3+) endocrine progenitor can give rise to all five pancreatic islet hormone-producing endocrine cells. Forced exiting of Neurog3+ from the polarize luminal epithelium through conditional ablation of p120ctn or Ecad in Neurog3+ cells shift their differentiation towards alpha cells at the expense of beta cells. Based on these findings we hypothesized that cell adhesion and cell polarity might be linked to the fate decision of Neurog3+ cells into the alpha and beta cell lineages. Here, we show pancreatic endocrine progenitor cell-cell adhesion is linked to apical-basal polarity and cell fate, and disruption of apical-basal polarity in the developing mouse pancreas alters endocrine cell specification. Futhermore, apical-basally polarized human endocrine progenitors are primed to become beta cells. Finally, single-cell RNA sequencing reveals beta-like transcriptional signatures and differentiation propensities in polarized endocrine progenitors.
2025-01-01 | GSE224286 | GEO