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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)

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Andranik Ivanov

PROVIDER: E-GEOD-54044 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2015-03-31 | GSE54044 | GEO

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. 6 samples include, replicates of Insm1 and Foxa2, IgG pull down as a control

2015-03-31 | E-GEOD-54046 | biostudies-arrayexpress

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

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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.

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