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Transcriptomic analyses of embryonic pancreata from pancreas-specific Groucho mutants

ABSTRACT: Transcriptomic analyses of embryonic pancreata from pancreas-specific Groucho mutants

PROVIDER: PRJNA630434 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11688232_1.fastq.gz	Fastqsanger.gz
	SRR11688232_2.fastq.gz	Fastqsanger.gz
	SRR11688233_1.fastq.gz	Fastqsanger.gz
	SRR11688233_2.fastq.gz	Fastqsanger.gz
	SRR11688234_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analyses of embryonic pancreata from pancreas-specific Groucho mutants

Project description:A large number of studies have identified and characterized the many transcription factors and cofactors that regulate pancreas organogenesis. Groucho-related genes/Transducin-like Enhancer of Split (Grgs/TLEs) are one such family of cofactors that act as transcriptional co-repressors and are critical for many developmental processes. Several essential pancreatic transcription factors are capable of interacting with GRGs; however, the role of GRG-mediated transcriptional repression in pancreas development is only partially characterized. In this study, we used phenotypic and transcriptomic analyses to determine that GRG3 is essential for β cell development, and in the absence of Grg3 there is compensatory upregulation of Grg4. In Grg3/4 double mutants, mice have severe dysregulation of the pancreas gene program with ectopic expression of liver genes and Foxa1, a master regulator of the liver program. Neurod1, an essential β cell transcription factor and predicted target of Foxa1, becomes downregulated in Grg3/4 mutants, resulting in a loss of β cell proliferation, hyperglycemia, and early lethality. These findings uncover a novel function of GRG-mediated repression in pancreas development.

2021-03-15 | GSE149891 | GEO

Analysis of donor pancreata defines the transcriptomic signature and microenvironment of early neoplastic lesions.

Project description:The adult healthy human pancreas has been poorly studied given lack of indication to obtain tissue from the pancreas in the absence of disease and rapid postmortem degradation. We obtained pancreata from brain dead donors thus avoiding any warm ischemia time. We found that neoplastic lesions occur frequently in healthy organs, in donors as young as in their 3rd decade of life. Using the 10X Genomics Platform, we performed single cell RNA sequencing on 6 donor pancreata, 5 of which we separately sequenced tissue from the pancreas head and tail, for a total of 11 sequencing runs. This is a robust single-cell dataset of healthy, nonpathologic pancreas tissue and includes acinar, ductal, and non-epithelial cells (myeloid cells, fibroblasts, endothelial cells, lymphocytes). We compared this dataset of normal pancreata to single cell sequencing of tumor samples previously published in Steele, et al, Nature Cancer 2020, (raw fastq in dbGap phs002071) realigned to GRCh38 reference genome (CellRanger 6.0). This GEO series contains the raw and filtered feature matrices for the donor pancreata as well as the realigned tumor samples. Supplementary files contain the aggregate feature matrices and the metadata of the donor pancreata samples and the tumor samples.

2023-05-01 | GSE229413 | GEO

Analysis of donor pancreata defines the transcriptomic signature and microenvironment of early pre-neoplastic pancreatic lesions

Project description:The adult healthy human pancreas has been poorly studied given lack of indication to obtain tissue from the pancreas in the absence of disease and rapid postmortem degradation. We obtained pancreata from brain dead donors thus avoiding any warm ischemia time. The 30 donors were diverse in age and race and had no known pancreas disease. Histopathological analysis of the samples revealed PanIN lesions in most individuals irrespective of age. Using a combination of multiplex immunohistochemistry, single cell RNA sequencing, and spatial transcriptomics, we provide the first ever characterization of the unique microenvironment of the adult human pancreas and of sporadic PanIN lesions. We compared healthy pancreata to pancreatic cancer and peritumoral tissue and observed distinct transcriptomic signatures in fibroblasts, and, to a lesser extent, macrophages. PanIN epithelial cells from healthy pancreata were remarkably transcriptionally similar to cancer cells, suggesting that neoplastic pathways are initiated early in tumorigenesis.

2023-03-08 | GSE226829 | GEO

Peptidomics of pancreas in wild type and neuronatin deficien mice

Project description:Pancreata of wild type and a neuronatin deficient mouse strain were homogenised and the peptidome characterised. Particular attention was paid to the processing of insulin, to assess if neuronatin deficiency causes changes in the processing efficiency of insulin and other bioactive peptides produced in the pancreas

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Identification of Sox9-Regulated Pathways During the Secondary Transition Stage of Pancreas Development

Project description:Sox9 target genes were identified during the secondary transition stage of pancreas development by comparing gene expression in Sox9-ablated versus wild-type pancreata using microarray analysis. Sox9 was conditionally ablated during the secondary transition in the developing pancreas via recombination of a Sox9-flox allele (Kist et al., 2002) using the tamoxifen-inducible Rosa26-CreER allele (Vooijs et al., 2001). Dams were injected with 6 mg/40 g tamoxifen in corn oil at e12.5. Pancreata were manually microdissected at e15.5. Total RNA was isolated and pooled from pancreata of e15.5 Sox9fl/fl; Rosa26-CreER (mutant) versus Rosa26-CreER (wild-type) littermates for four biological replicates.

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Project description:In order to generate a comprehensive map of differentially expressed genes in embryonic mouse pancreas cell types on which to map results from later analyses, we first performed microarray-based gene expression profiling of purified E15.5 pancreas cell populations. We isolated GFP+RFP−DBA+, GFP+RFP+DBA+, and GFP+RFP+DBA− cells from dissociated E15.5 Neurog3-RFP; Hes1-GFP pancreata subsequently labelled with Dolichos Biflorus Agglutinin (DBA) and YFP+ cells from dissociated E15.5 Ptf1aYfp/+ pancreata. This sorting strategy allowed us to isolate bipotent trunk progenitors (GFP+RFP−DBA+), early (GFP+ RFP+DBA+) and late (GFP+RFP+DBA−) endocrine precursors, as well as tip progenitors/acinar precursors (YFP+) and subject all four populations to gene expression analysis by microarray.

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Comparison of Hox6 mutant and control E12.5 mouse pancreas

Project description:Hox genes are critical developmental transcription factor. We found that in mice with disrupted expression of Hoxa6, Hoxb6 and Hoxc6 there is significantly disrupted endocrine pancreas development. We used microarray analysis to probe for possible molecular mechanisms involed in Hox6 signaling in pancreas development. We dissected pancreata from E12.5 control and Hox6 null embryos and extracted total RNA.

2015-04-30 | E-GEOD-68390 | biostudies-arrayexpress

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.

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Pancreas-specific deletion of Ikba and RelA.

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Identification of Sox9-Regulated Pathways During the Secondary Transition Stage of Pancreas Development

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