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Role of transcription factors ONECUT1 (HNF6), GATA6 and NKX6.1 during in vitro pancreatic differentiation of human pluripotent stem cells.

ABSTRACT: We have identified HNF6 as an essential transcription factor for endocrine pancreatic development. HNF6 binds to and possibly regulates other isletogenesis transcription factors, driving endocrine differentiation. ChIP sequencing of HNF6 as well as GATA6 and NKX6.1 during in vitro pancreatic differentiation will help to understand the regulatory mechanisms during cell fate decisions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE131812 | GEO | 2021/10/27

REPOSITORIES: GEO

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Role of transcription factor ONECUT1 (HNF6) during in vitro pancreatic differentiation of human pluripotent stem cells [RNA-seq]

Project description:We have identified HNF6 as an essential transcription factor for endocrine pancreatic development. HNF6 binds to and possibly regulates other isletogenesis transcription factors, driving endocrine differentiation. RNA sequencing of control and HNF6-depleted hESC during in vitro pancreatic differentiation will help to understand the regulatory mechanisms during cell fate decisions.

2021-10-27 | GSE135416 | GEO

Role of transcription factor ONECUT1 (HNF6) during in vitro pancreatic differentiation of human pluripotent stem cells [ATAC-seq]

Project description:We have identified HNF6 as an essential transcription factor for endocrine pancreatic development. HNF6 binds to and possibly regulates other isletogenesis transcription factors, driving endocrine differentiation. ATAC sequencing of control and HNF6-depleted hESC during in vitro pancreatic differentiation will help to understand the regulatory mechanisms during cell fate decisions.

2021-10-27 | GSE131816 | GEO

Role of transcription factors ONECUT1 (HNF6), GATA6 and NKX6.1 during in vitro pancreatic differentiation of human pluripotent stem cells.

Project description:Role of transcription factors ONECUT1 (HNF6), GATA6 and NKX6.1 during in vitro pancreatic differentiation of human pluripotent stem cells.

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Mutations and variants of ONECUT1 in diabetes

Project description:Genes involved in distinct diabetes types suggest shared disease mechanisms. We show that rare ONECUT1 coding variants cause monogenic recessive diabetes (neonatal or very early-onset, syndromic) in two unrelated patients, and monogenic dominant diabetes (early adult-onset) in heterozygous relatives of these and 13 additional unrelated cases. Patients heterozygous for rare ONECUT1 coding variants define a subgroup of T2D with early-onset diabetes and other features. In addition, common regulatory ONECUT1 variants are associated with multifactorial T2D. Directed differentiation of human pluripotent stem cells to the pancreatic lineage revealed that loss of ONECUT1 impairs pancreatic progenitor formation and a subsequent endocrine program. We uncovered that ONECUT1 activates the pro-endocrine genes NKX6.1 and NKX2.2 through binding to their cis-regulatory elements. Globally, ONECUT1-directed gene transcription occurs in association with major islet transcription factors, at clusters of pancreas- and endocrine-specific enhancers within open chromatin. ONECUT1 regulates a transcriptional and epigenetic machinery critical for proper endocrine pancreatic development, involved in a spectrum of diabetes, monogenic recessive and dominant, and multifactorial.

2021-11-03 | PXD018887 | Pride

Identification of Nkx6.1 regulated genes in mature pancreatic islets.

2013-09-12 | GSE40470 | GEO

Identification of Nkx6.1 regulated genes in mature pancreatic islets.

Project description:Nkx6.1 target genes were identified in mature pancreatic islets by comparing gene expression in conditional Nkx6.1-ablated islets versus control islets using microarray analysis. Nkx6.1 was conditionally ablated in mature pancreatic islets by recombination of a Nkx6.1-flox allele using the tamoxifen-inducible Pdx1-CreERTM allele (Gu et al 2002). Mice were injected with 2 mg/25 g tamoxifen in corn oil four times between 4 and 6 weeks of age. Islets were isolated after the final tamoxifen injection. Total RNA was isolated and pooled from pancreata of 6 week old Nkx6.1fl/-;Pdx1-CreERTM (mutant) versus Nkx6.1fl/+;Pdx1-CreERTM (control) littermates for 3 biological replicates.

2013-09-12 | E-GEOD-40470 | biostudies-arrayexpress

Genome-wide map of Gata6 DNA binding in mouse pancreas

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GATA6-AS1 Regulates GATA6 Expression to Modulate Human Endoderm Differentiation

Project description:Transcriptome analysis has uncovered a series of long noncoding RNAs (lncRNAs) transcribed during cell differentiation. Here, we uncovered lncRNA GATA6-AS1 is a functional lncRNA in definitive endoderm (DE) differentiation. We found GATA6-AS1 positively regulated the expression of endoderm key factor GATA6, which was different from previous reports in other biological contexts. Further investigation showed GATA6-AS1 interacted with SMAD2/3 and recruited SMAD2/3 to the promoter region of the GATA6 gene locus. In addition, overexpression of GATA6 was able to rescue the defect of DE differentiation due to the absence of GATA6-AS1, suggesting GATA6 was the functional target of GATA6-AS1 during endoderm differentiation. Ultimately, our study uncovers GATA6-AS1 is necessary for DE and pancreas differentiation, and reveals the detailed regulation mechanism between GATA6-AS1 and DE differentiation.

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Project description:Loss of functional beta-cell mass is a hallmark of Type 1 and Type 2 diabetes, and methods for restoring these cells are needed. We have previously reported that overexpression of the homeodomain transcription factor Nkx6.1 in rat pancreatic islets induces beta-cell proliferation and enhances glucose-stimulated insulin secretion, but the pathway by which Nkx6.1 activates beta-cell expansion has not been defined. Here we demonstrate that Nkx6.1 induces expression of the Nr4a1 and Nr4a3 orphan nuclear receptors, and that these factors are both necessary and sufficient for Nkx6.1-mediated beta-cell proliferation. Consistent with this finding, global knockout of Nr4a1 results in a decrease in beta-cell area in neonatal and young mice. Overexpression of Nkx6.1 and the Nr4a receptors results in increased expression of key cell cycle inducers E2F1 and cyclin E1. Furthermore, Nkx6.1 and Nr4a receptors induce components of the anaphase-promoting complex, including Ube2c, resulting in degradation of the cell cycle inhibitor p21CIP1. These studies identify a new bipartite pathway for activation of beta-cell proliferation, suggesting several new targets for expansion of functional beta-cell mass. We set up a microarray using primary rat islets that were left untreated or transduced with adenoviruses overexpressing betagal or Nkx6.1 for 48 h.

2014-02-18 | E-GEOD-55077 | biostudies-arrayexpress

Genome-wide map of GATA6 DNA binding in human PDAC cells

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2015-02-03 | E-GEOD-47535 | biostudies-arrayexpress

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