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Comparison of Hox6 mutant and control E12.5 mouse pancreas

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Deneen Wellik

PROVIDER: E-GEOD-68390 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2015-04-30 | GSE68390 | GEO

Neurog3-independant role of Notch signaling in pancreas explants. Microarray of pancreata of Wildtype or Neurog3tTA/tTA (Neurog3-Null) background at E12.5, explanted for 3d + treatment 24h with DAPT/vehicle.

Project description:Since loss of Hes1 and Notch signalling drives progenitors to the endocrine lineage, we set up a pancreas explant system with crosses of heterozygous Neurog3tTA/+, a knock-in allele which makes the homozygote Neurog3tTA/tTA embryos deficient in Neurog3 (hereafter Neurog3-null). Hereby endocrine differentiation is impeded and we can study the Neurog3-independent role of Notch signalling by DAPT inhibition of γ-secretase. E12.5 wildtype and Neurog3-null pancreata were explanted on fibronectin, grown for 3 days, and then treated with vehicle control (0.1% DMSO) or DAPT for 24h. RNA was isolated and subjected to Agilent microarray analysis

2022-02-27 | E-MTAB-6898 | 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.

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

Transcription profiling of mouse pancreas development in NMRI embryos on consecutive days from e12.5 to e16.5

Project description:Development of the pancreas from the endoderm is initiated at embryonic day 9 of mouse development and over the following days several different cell types develop from pancreas progenitor cells. A distinct phase of pancreas development, known as the secondary transition, is initiated at day 13 of development and one of the key features of this transition is a massive increase in the number of mature endocrine cells. To study gene expression in pancreas during the secondary transition we performed high-density oligonucleotide microarray experiments on dorsal pancreas tissue isolated from NMRI embryos on consecutive days from e12.5 to e16.5. Experiment Overall Design: Dorsal pancreata were isolated from embryos at embryonic day 12.5, 13.5, 14.5, 15.5, and 16.5 and pooled litter-wise prior to total RNA extraction. From each pool, two independent labelling reactions were made, and each sample was hybridized to the entire Murine Genome U74 version 2 chip set (A, B, and C).

2008-11-06 | E-GEOD-8070 | biostudies-arrayexpress

Expression analysis of neuronal differentiation of HOXA/B6 mutant cells

Project description:Transcriptome analysis of HOXB6 AND HOXA6 mutants during neuronal differentiation

2023-05-30 | E-MTAB-11943 | biostudies-arrayexpress

Expression analysis of neuronal differentiation of HOXA6/HOXB6/UBE3A mutants cells

Project description:Transcriptome analysis of HOXA6, HOXB6 and UBE3A mutants during neuronal differentiation

2024-04-30 | E-MTAB-13611 | biostudies-arrayexpress

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

2021-11-03 | PXD024161 | Pride

CUT&RUN of HOXA6 and HOXB6 in neuronal-derived human embryonic stem cells

Project description:CUT&RUN analysis of HOXA6 and HOXB6 binding sites in neuronal-derived human embryonic stem cells

2024-04-30 | E-MTAB-13627 | biostudies-arrayexpress

Sox4 null mice e12.5 pancreas

Project description:The purpose of this experiment was to assess global changes in gene expression pattern in the pancreas from Sox4-/- embryos vs. pancreas from Sox4 wild-type embryos at embryonic day 12.5. [Sox4 gene knock-out (Schilham, M. W. et al. (1996) Defects in cardiac outflow tract formation and pro-B-lymphocyte expansion in mice lacking Sox-4. Nature 380, 711-4.)] Embryonic pancreases from homozygous mutants and their wild-type littermates were harvested. Total RNA was isolated amplified using a linear amplification kit and used to prepare the hybridization samples through indirect labeling. Keywords = Pancreas Sox4 null e12.5 Keywords: parallel sample

2005-12-01 | GSE2539 | GEO

Transcription profiling by array of mouse E15.5 FACS sorted pancreas populations based on double fluorescent reporter (Hes1GFP and Neurog3-RFP), DBA staining and Ptf1a-YFP.

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.

2018-09-10 | E-MTAB-6891 | biostudies-arrayexpress

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