GSE144953: Retinoic acid signaling within pancreatic endocrine progenitors regulates mouse and human pancreatic islet cell specification

Gene Expression Data Explorer
Info Gene counts are sourced from ARCHS4, which provides uniform alignment of GEO samples. You can learn more about ARCHS4 and its pipeline here.
Enter gene symbol:

Select conditions below to toggle them from the plot:

GROUP CONDITION SAMPLES
Pancreas
GSM4301403 GSM4301404 GSM4301405
GSM4301400 GSM4301401 GSM4301402
Description

Submission Date: Feb 07, 2020

Summary: 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.

GEO Accession ID: GSE144953

PMID: 32467243

Description

Submission Date: Feb 07, 2020

Summary: 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.

GEO Accession ID: GSE144953

PMID: 32467243

Visualize Samples

Info Visualizations are precomputed using the Python package scanpy on the top 5000 most variable genes.

Precomputed Differential Gene Expression

Info Differential expression signatures are automatically computed using the limma R package. More options for differential expression are available to compute below.

Signatures:

Select conditions:

Control Condition

Perturbation Condition

Only conditions with at least 1 replicate are available to select

Differential Gene Expression Analysis
Info Differential expression signatures can be computed using DESeq2 or characteristic direction.
Select differential expression analysis method:
Bulk RNA-seq Appyter

This pipeline enables you to analyze and visualize your bulk RNA sequencing datasets with an array of downstream analysis and visualization tools. The pipeline includes: PCA analysis, Clustergrammer interactive heatmap, library size analysis, differential gene expression analysis, enrichment analysis, and L1000 small molecule search.