Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA392311 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5766304_1.fastq.gz | Fastqsanger.gz | |||
| SRR5766304_2.fastq.gz | Fastqsanger.gz | |||
| SRR5766305_1.fastq.gz | Fastqsanger.gz | |||
| SRR5766305_2.fastq.gz | Fastqsanger.gz | |||
| SRR5766306_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:High-Resolution temporal profiling of developing pancreas uncovers the mechanisms of endocrine cell fate determination
| PRJNA392308 | ENA
Project description:High-Resolution temporal profiling of developing pancreas uncovers the mechanisms of endocrine cell fate determination [ATAC-Seq]
| PRJNA392309 | ENA
Project description:High-Resolution temporal profiling of developing pancreas uncovers the mechanisms of endocrine cell fate determination [MATQ-seq]
| PRJNA392310 | ENA
Project description:To define genetic pathways that regulate development of the endocrine pancreas, we generated transcriptional profiles of enriched cells isolated from four biologically significant stages of endocrine pancreas development: endoderm before pancreas specification, early pancreatic progenitor cells, endocrine progenitor cells and adult islets of Langerhans. These analyses implicate new signaling pathways in endocrine pancreas development, and identified sets of known and novel genes that are temporally regulated, as well as genes that spatially define developing endocrine cells from their neighbors. The differential expression of several genes from each time point was verified by RT-PCR and in situ hybridization. Moreover, we present preliminary functional evidence suggesting that one transcription factor encoding gene (Myt1), which was identified in our screen, is expressed in endocrine progenitors and may regulate alpha, beta and delta cell development. In addition to identifying new genes that regulate endocrine cell fate, this global gene expression analysis has uncovered informative biological trends that occur during endocrine differentiation.
2006-06-30 | E-CBIL-14 | biostudies-arrayexpress
Project description:deBack2012 - Lineage Specification in Pancreas Development
This model of two neighbouring pancreas precursor cells, describes the exocrine versus endocrine lineage specification process. To account for the tissue scale patterns, this couplet model has been extended to hundreds of coupled cells.
This model is described in the article:
On the role of lateral stabilization during early patterning in the pancreas
de Back W., Zhou JX, Brusch L
J. R. Soc. Interface 6 February 2013 vol. 10 no. 79 20120766
Abstract:
The cell fate decision of multi-potent pancreatic progenitor cells between the exocrine and endocrine lineages is regulated by Notch signalling, mediated by cell–cell interactions. However, canonical models of Notch-mediated lateral inhibition cannot explain the scattered spatial distribution of endocrine cells and the cell-type ratio in the developing pancreas. Based on evidence from acinar-to-islet cell transdifferentiation in vitro, we propose that lateral stabilization, i.e. positive feedback between adjacent progenitor cells, acts in parallel with lateral inhibition to regulate pattern formation in the pancreas. A simple mathematical model of transcriptional regulation and cell–cell interaction reveals the existence of multi-stability of spatial patterns whose simultaneous occurrence causes scattering of endocrine cells in the presence of noise. The scattering pattern allows for control of the endocrine-to-exocrine cell-type ratio by modulation of lateral stabilization strength. These theoretical results suggest a previously unrecognized role for lateral stabilization in lineage specification, spatial patterning and cell-type ratio control in organ development.
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2024-09-02 | BIOMD0000000435 | BioModels
Project description:A number of studies have reported cell heterogeneity within the developing mouse pancreas, as well as the transcriptional profiles corresponding to various cell states. The upstream mechanisms that initiate and maintain gene expression programs across cell states, however, remain largely unknown. Here, we applied single-nucleus ATAC-Seq to developing mouse pancreas to generate an atlas of chromatin accessibility, at single-cell resolution. Our goals were first, to generate an atlas of chromatin accessibility of embryonic mouse pancreas, at single-cell resolution, that can serve as a resource for the field. We aimed to provide such a resource not only for epithelial cells within the pancreas, but for non-epithelial (e.g., mesenchymal) as well. Our second goal was to identify gene regulatory networks governing cell fate transitions through integration of single-cell chromatin accessibility and gene expression data.
2023-05-18 | GSE210569 | GEO
Project description:The expansion procedure strengthened the pancreas progenitor identity while efficiently repressed endocrine differentiation and liver fate as well as acinar and duct differentiation programs
2023-12-07 | GSE216266 | GEO
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
Project description:The basic helix-loop-helix transcription factor Neurogenin3 (Ngn3/Neurog3) is expressed in endocrine progenitor cells in the embryonic mouse pancreas. Ngn3 controls endocrine cell fate decisions. Ngn3 deficient mice do not develop any pancreatic endocrine cells, including insulin producing beta cells, and die postnatally from diabetes. Therefore, the characterization of gene expression in Ngn3-expressing cells and their progeny is of particular interest for the development of novel strategies for cell replacement therapies in type-1 diabetes. Here we describe two studies. In the first study (8 assays) we used mice where the EYFP (Enhanced Yellow fluorescent Protein) is expressed under the control of Ngn3 regulatory elements (knock add on strategy). EYFP-positive, Ngn3-expressing cells, were FACS sorted from embryonic pancreas at day 15.5 (E15.5), as well as EYFP-negative cells. In the second study (6 assays) we compared wild-type and Ngn3 mutant pancreas at E15.5. All samples were hybridized to Affymetrix GeneChip Mouse Genome 430.2.0 array.
2009-12-03 | E-CBIL-48 | biostudies-arrayexpress
Project description:Retinoic acid (RA) signaling is essential for multiple developmental processes, including appropriate pancreas formation from the foregut endoderm. RA is also required to generate pancreatic progenitors from human pluripotent stem cells. However, the role of RA during the later stages of pancreas development is not well understood. In this study, we generated an inducible system to block RA signaling and demonstrate that disruption of the RA pathway within the Neurog3-expressing endocrine progenitor population is required for appropriate mouse b cell differentiation and repression of critical d cell genes, including Somatostatin. In addition, inhibition of the RA pathway in hESC-derived pancreatic progenitors downstream of NEUROG3 induction impairs INSULIN expression. We further determined that RA-regulation of endocrine cell differentiation is mediated through Wnt pathway components. Together, these data demonstrate the importance of RA signaling in endocrine specification and identify conserved mechanisms by which RA signaling directs endocrine cell fate.
2020-06-02 | GSE144953 | GEO