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Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

ABSTRACT: Genome-wide Insm1 binding sites analysis revealed an overrepresentation of sequences predicted to bind bHLH and/or forkhead factors, and further analyses demonstrated that most Insm1 sites in the genome are co-occupied by Neurod1 and Foxa2. Binding regions co-occupied by all three factors but not single Insm1 sites explained a significant fraction of gene expression changes in Insm1 mutant β-cells. Together, our data provide evidence that an Insm1, Neurod1 and Foxa2 network maintains a mature gene expression program in β-cells. 6 samples include, replicates of Insm1 and Foxa2, IgG pull down as a control

ORGANISM(S): Mus musculus

SUBMITTER: Andranik Ivanov

PROVIDER: E-GEOD-54046 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

Project description:Genome-wide Insm1 binding sites analysis revealed an overrepresentation of sequences predicted to bind bHLH and/or forkhead factors, and further analyses demonstrated that most Insm1 sites in the genome are co-occupied by Neurod1 and Foxa2. Binding regions co-occupied by all three factors but not single Insm1 sites explained a significant fraction of gene expression changes in Insm1 mutant β-cells. Together, our data provide evidence that an Insm1, Neurod1 and Foxa2 network maintains a mature gene expression program in β-cells.

2015-03-31 | GSE54046 | GEO

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Expression data from islets of control and Insm1 conditional deleted adult pancreatic islets)

Project description:The zinc finger factor Insm1 is known to regulate differentiation of pancreatic β cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic β cells in mice. We used microarrays to analyse the global gene expression after deletion of insm1 in adult pancreatic β cells and identified functional important genes and immature islets releated genes deregulated in the mutatant islets.

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Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function.

Project description:Key transcription factors control the gene expression program in mature pancreatic β-cells, but their integration into regulatory networks is little understood. Here, we show that Insm1, Neurod1 and Foxa2 directly interact and together bind regulatory sequences in the genome of mature pancreatic β-cells. We used Insm1 ablation in mature β-cells in mice and found pronounced deficits in insulin secretion and gene expression. Insm1-dependent genes identified previously in developing β-cells markedly differ from the ones identified in the adult. In particular, adult mutant β-cells resemble immature β-cells of newborn mice in gene expression and functional properties. We defined Insm1, Neurod1 and Foxa2 binding sites associated with genes deregulated in Insm1 mutant β-cells. Remarkably, combinatorial binding of Insm1, Neurod1 and Foxa2 but not binding of Insm1 alone explained a significant fraction of gene expression changes. Human genomic sequences corresponding to the murine sites occupied by Insm1/Neurod1/Foxa2 were enriched in single nucleotide polymorphisms associated with glycolytic traits. Thus, our data explain part of the mechanisms by which β-cells maintain maturity: Combinatorial Insm1/Neurod1/Foxa2 binding identifies regulatory sequences that maintain the mature gene expression program in β-cells, and disruption of this network results in functional failure.

| S-EPMC4492000 | biostudies-literature

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic ?-cell function (Expression data from islets of control and Insm1 conditional deleted adult pancreatic islets)

Project description:The zinc finger factor Insm1 is known to regulate differentiation of pancreatic ? cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic ? cells in mice. We used microarrays to analyse the global gene expression after deletion of insm1 in adult pancreatic ? cells and identified functional important genes and immature islets releated genes deregulated in the mutatant islets. We used 8 mutant and 8 litter matched control mice for the islets preparation.

2015-03-31 | E-GEOD-54044 | biostudies-arrayexpress

RNA-Seq analysis of E15.5 mouse Insm1, Neurod1 and Pax6 knockouts vs Insm1GFP.Cre/+ controls

Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Insm1GFP.Cre/+ controls and Insm1 (Insm1GFP.Cre/GFP.Cre), Neurod1 (Insm1GFP.Cre/+; Neurod1LacZ/LacZ), or Pax6 (Insm1GFP.Cre/+; Pax6fl/fl) knockout FACS sorted pancreatic endocrine cells at E15.5. Comparison of Insm1GFP.Cre+/- and knockout animals revealed sets of differentially expressed genes that are required for endocrine cell specification and development.

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RNA-Seq analysis of E15.5 mouse Insm1, Neurod1 and Pax6 knockouts vs Insm1GFP.Cre/+ controls

Project description:RNA-Seq analysis of E15.5 mouse Insm1, Neurod1 and Pax6 knockouts vs Insm1GFP.Cre/+ controls

| PRJEB43866 | ENA

Mus musculus

Project description:Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

| PRJNA236026 | ENA

Chromatin immunopreciptiation of liver from wild type and Foxa2 knock out mice to identify Foxa2 binding sites

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Transcriptional regulation of endocrine cell differentiation by Insm1

Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Insm1^GFP/Pdx1^CFP HIGH [het/het] FACS sorted pancreatic cells (pre-beta cells) and Insm1^GFP/Pdx1^CFP LOW [het/het] cells (other endocrine progenitors) at E15.5 and E18.5. Comparison of Insm1 +/Pdx HIGH and Insm1 +/Pdx LOW cells revealed a set of differentially expressed genes that are required for beta cell specification.

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NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development

Project description:NEUROD1 is a transcription factor that helps maintain a mature phenotype of pancreatic β cells. Disruption of Neurod1 during pancreatic development causes severe neonatal diabetes; however, the exact role of NEUROD1 in the differentiation programs of endocrine cells is unknown. Here, we report a crucial role of the NEUROD1 regulatory network in endocrine lineage commitment and differentiation. Mechanistically, transcriptome and chromatin landscape analyses demonstrate that Neurod1 inactivation triggers a downregulation of endocrine differentiation transcription factors and upregulation of non-endocrine genes within the Neurod1-deficient endocrine cell population, disturbing endocrine identity acquisition. Neurod1 deficiency altered the H3K27me3 histone modification pattern in promoter regions of differentially expressed genes, which resulted in gene regulatory network changes in the differentiation pathway of endocrine cells, compromising endocrine cell potential, differentiation, and functional properties.

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