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A PDX1 cistrome and single-cell transcriptome resource of the developing pancreas

ABSTRACT: A PDX1 cistrome and single-cell transcriptome resource of the developing pancreas

PROVIDER: PRJNA830471 | ENA |

REPOSITORIES: ENA

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A PDX1 cistrome and single-cell transcriptome resource of the developing pancreas

Project description:Pancreatic and duodenal homeobox 1 (PDX1) is crucial for pancreas organogenesis, yet the dynamic changes in PDX1 binding in human or mouse developing pancreas have not been examined. To address this knowledge gap, we performed PDX1 ChIP-seq and single-cell RNA-seq using fetal human pancreata. We integrated our datasets with published datasets and revealed the dynamics of PDX1 binding and potential cell-lineage-specific PDX1 bound genes in the pancreas from fetal to adult stages. We identified a core set of developmentally conserved PDX1 bound genes that reveal the broad multifaceted role of PDX1 in pancreas development. Despite the well-known, dramatic changes in PDX1 function and expression, we found that PDX1 bound genes are largely conserved from embryonic to adult stages. This points towards a dual role of PDX1 in regulating the expression of its targets at different ages, dependent on other functionally-congruent or directly-interacting partners. We also showed that PDX1 binding is largely conserved in mouse pancreas. Together, our study reveals PDX1 targets in the developing pancreas in vivo and provides an essential resource for future studies on pancreas development.

2022-04-25 | GSE201230 | GEO

Identification of Sox9/Pdx1-coregulated Genes During Pancreas Organogenesis

Project description:Sox9/Pdx1 co-regulated target genes were identified by comparing gene expression in Sox9/Pdx1-double heterozygates versus Sox9- or Pdx1- heterozygates pancreata using microarray analysis. Pdx1LacZko (herein designated Pdx1-/+) (Offield et al. 1996) and one Sox9 allele was conditionally deleted in the developing pancreas via recombination of a Sox9-flox allele (Kist et al., 2002) using the Foxa3-Cre transgene (Lee et al., 2005). Total RNA was isolated and pooled from dorsal pancreatic epithelia of e12.5 Sox9fl/+; Foxa3-Cre (Sox9 het), Pdx1-/+ (Pdx1 het) versus Sox9fl/+; Foxa3-Cre; Pdx1-/+ (Sox9/Pdx1 double hets) littermates for three biological replicates

2015-08-07 | E-GEOD-62023 | biostudies-arrayexpress

The Pdx1 Cistrome of Pancreatic Islets

Project description:The Pdx1 Cistrome of Pancreatic Islets

| PRJEB3046 | ENA

Pdx1-Oc1 cooperatively drive the induction of the endocrine pancreatic program

Project description:We report the impact of heterozygous loss of either Pdx1 or Oc1 on the developing pancreas at e15.5

2016-06-09 | GSE77896 | GEO

RNA-seq of Pdx1-GFP+ sorted E10.5, wildtype and Hes1-/-. Neurog3-dependent Pancreas Dysgenesis Causes Ectopic Pancreas in Hes1 Mutants

Project description:RNA-seq of FACS Sorted E10.5 Pdx1-GFP+ of genotypes wildtype and Hes1-/-. Summary statement The developmental mechanisms that cause ectopic pancreas are poorly understood. We show that aberrant dorsal pancreas morphogenesis in Hes1 mutants leads to ectopic pancreas depending on the pro-endocrine gene Neurog3. Abstract Mutations in Hes1, a target gene of the Notch signalling pathway, lead to ectopic pancreas by a poorly described mechanism. Here we use genetic inactivation of Hes1 combined with lineage tracing in mouse embryos to reveal an endodermal requirement for Hes1 and that most ectopic pancreas tissue is derived from the E8.5 dorsal pancreas primordium. RNA-seq data from sorted E10.5 Pdx1-GFP+ cells from Hes1+/+ and Hes1−/− suggested that upregulation of endocrine lineage genes in Hes1−/− embryos was the major defect in the endoderm and accordingly early pancreas morphogenesis was normalised and the ectopic pancreas phenotype suppressed in Hes1−/−Neurog3−/− embryos. Analysis of other Notch pathway mutants uncovered a total depletion of progenitors in Mib1 deficient dorsal anlage, which was replaced by an anterior Gcg+ extension. Together, our results demonstrate that aberrant morphogenesis is the cause of ectopic pancreas and that a part of the endocrine differentiation program is mechanistically involved in the dysgenesis. Our results suggest that the ratio of endocrine lineage to progenitor cells is important for morphogenesis and that a strong endocrinogenic phenotype without complete progenitor depletion as seen in Hes1 mutants provokes an extreme dysgenesis that causes ectopic pancreas.

2018-08-20 | E-MTAB-6890 | biostudies-arrayexpress

Single-cell chromatin accessibility of developing murine pancreas identifies cell state-specific gene regulatory programs

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

The Pdx1 Cistrome of Pancreatic Islets

Project description:We performed global location analysis of Pdx1 occupancy in mouse and human islets.

2012-05-23 | E-MTAB-1143 | biostudies-arrayexpress

Identification of Sox9-Regulated Pathways During Early Pancreas Organogenesis

Project description:Sox9 target genes were identified by comparing gene expression in Sox9-ablated versus wild-type pancreata using microarray analysis. Sox9 was conditionally ablated in the developing pancreas via recombination of a Sox9-flox allele (Kist et al., 2002) using the Pdx1-Cre transgene (Gu et al., 2002). Total RNA was isolated and pooled from dorsal pancreatic epithelia of e12.5 Sox9fl/fl; Pdx1-Cre (mutant) versus Sox9fl/fl (wild-type) littermates for three biological replicates.

2012-08-01 | E-GEOD-28669 | biostudies-arrayexpress

Identification of Sox9/Pdx1-coregulated Genes During Pancreas Organogenesis

2015-08-07 | GSE62023 | GEO

Transcriptome profiling of e11.25 mouse pancreas: comparison between Ngn3-/- and Ngn3-/- ; Pdx1::Ngn3ER TM pancreatic epithelium

Project description:Individual pancreatic buds of crosses between Ngn3+/- and Ngn3+/- ; Pdx1::Ngn3ER TM -IRES-GFP were dissected. Pregnant females were injected intra-peritoneal with 2mg of Tamoxifen at e10.25 (9 am) and dissected at e11.25 (9 to 11 am). Most of the mesenchymal tissue was removed to reduce the tissue complexity of the sample and enrich in epithelial pancreas progenitors. Moreover, at that developmental stage, Pdx1 promoter exhibits strong and homogenous expression levels. Rescuing Ngn3 expression only 24 hours before dissection (12h before activity, due to the time to process tamoxifen into the active compound 4OH tamoxifen) enriches the gene list in direct targets of Ngn3.

2014-12-02 | E-MTAB-3139 | biostudies-arrayexpress

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