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Genome-wide characterization of Zac1 target genes reveals its role as a broad regulator of the imprinted gene network including extracellular matrix genes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE76032 | GEO | 2017/11/24

SECONDARY ACCESSION(S): PRJNA306039

REPOSITORIES: GEO

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Genome-wide characterization of Zac1 target genes reveals its role as a broad regulator of the imprinted gene network including extracellular matrix genes.

Project description:In order to determine the imprinted transcription factor Zac1 targets, we overexpressed Zac1 in a neuroblastoma cell line and measured both the regulated expressed genes by Differential Gene Expressed analysis and Zac1 binding sites throughout the mouse genome by ChIP-seq. We have shown that Zac1 regulates and binds closed to many genes belonging to the Imprinted Gene Network.

2017-11-24 | GSE75943 | GEO

Plagl1/Zac1 regulates extracellular matrix genes and the imprinted gene network

Project description:In order to determine the targets of the imprinted transcription factor Zac1, we compared wild type and Zac1-mutant MEFs and measured the differentially expressed genes by RNA-seq. Genes deregulated in the absence of Zac1 include genes belonging to the Imprinted Gene Network and genes coding for the extra-cellular matrix.

2017-11-24 | GSE99409 | GEO

Identification of Plagl1/Zac1 binding sites and target genes establishes its role in the regulation of extracellular matrix genes and the imprinted gene network.

Project description:PLAGL1/ZAC1 undergoes parental genomic imprinting, is paternally expressed, and is a member of the imprinted gene network (IGN). It encodes a zinc finger transcription factor with anti-proliferative activity and is a candidate tumor suppressor gene on 6q24 whose expression is frequently lost in various neoplasms. Conversely, gain of PLAGL1 function is responsible for transient neonatal diabetes mellitus, a rare genetic disease that results from defective pancreas development. In the present work, we showed that Plagl1 up-regulation was not associated with DNA damage-induced cell cycle arrest. It was rather associated with physiological cell cycle exit that occurred with contact inhibition, growth factor withdrawal, or cell differentiation. To gain insights into Plagl1 mechanism of action, we identified Plagl1 target genes by combining chromatin immunoprecipitation and genome-wide transcriptomics in transfected cell lines. Plagl1-elicited gene regulation correlated with multiple binding to the proximal promoter region through a GC-rich motif. Plagl1 target genes included numerous genes involved in signaling, cell adhesion, and extracellular matrix composition, including collagens. Plagl1 targets also included 22% of the 409 genes that make up the IGN. Altogether, this work identified Plagl1 as a transcription factor that coordinated the regulation of a subset of IGN genes and controlled extracellular matrix composition.

| S-EPMC5737700 | biostudies-literature

Genome-wide characterization of Zac1 target genes reveals its role as a broad regulator of the imprinted gene network including extracellular matrix genes

Project description:Genome-wide characterization of Zac1 target genes reveals its role as a broad regulator of the imprinted gene network including extracellular matrix genes

| PRJNA306039 | ENA

Zac1 is a regulator of the imprinted gene network (ChIP-seq)

2017-11-24 | GSE75942 | GEO

Zac1 is a regulator of the imprinted gene network (RNA-seq)

Project description:In order to determine the imprinted transcription factor Zac1 targets, we overexpressed Zac1 in a mouse insulinoma cell line and measured the regulated expressed genes by RNA-seq. We have shown that Zac1 regulates many genes belonging to the Imprinted Gene Network, including genes coding for the extra-cellular matrix.

2017-11-24 | GSE84914 | GEO

Imprinted Zac1 in neural stem cells.

Project description:Neural stem cells (NSCs) and imprinted genes play an important role in brain development. On historical grounds, these two determinants have been largely studied independently of each other. Recent evidence suggests, however, that NSCs can reset select genomic imprints to prevent precocious depletion of the stem cell reservoir. Moreover, imprinted genes like the transcriptional regulator Zac1 can fine tune neuronal vs astroglial differentiation of NSCs. Zac1 binds in a sequence-specific manner to pro-neuronal and imprinted genes to confer transcriptional regulation and furthermore coregulates members of the p53-family in NSCs. At the genome scale, Zac1 is a central hub of an imprinted gene network comprising genes with an important role for NSC quiescence, proliferation and differentiation. Overall, transcriptional, epigenomic, and genomic mechanisms seem to coordinate the functional relationships of NSCs and imprinted genes from development to maturation, and possibly aging.

| S-EPMC4369488 | biostudies-literature

A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation.

Project description:Genomic imprinting is an epigenetic mechanism that restrains the expression of ∼ 100 eutherian genes in a parent-of-origin-specific manner. The reason for this selective targeting of genes with seemingly disparate molecular functions is unclear. In the present work, we show that imprinted genes are coexpressed in a network that is regulated at the transition from proliferation to quiescence and differentiation during fibroblast cell cycle withdrawal, adipogenesis in vitro, and muscle regeneration in vivo. Imprinted gene regulation is not linked to alteration of DNA methylation or to perturbation of monoallelic, parent-of-origin-dependent expression. Overexpression and knockdown of imprinted gene expression alters the sensitivity of preadipocytes to contact inhibition and adipogenic differentiation. In silico and in cellulo experiments showed that the imprinted gene network includes biallelically expressed, nonimprinted genes. These control the extracellular matrix composition, cell adhesion, cell junction, and extracellular matrix-activated and growth factor-activated signaling. These observations show that imprinted genes share a common biological process that may account for their seemingly diverse roles in embryonic development, obesity, diabetes, muscle physiology, and neoplasm.

| S-EPMC4352888 | biostudies-literature

A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation

Project description:We used the 3T3-L1 preadipocyte cell line (Green and Kehinde. Cell 5:19-25, 1974; ATCC CL-173), in which adipogenic differentiation is experimentally induced when quiescent 3T3-L1 cells are incubated with serum and IDX (insulin, dexamethasone, isobutylmethylxanthine). Following IDX addition, the cells retract and re-enter the cell cycle in the so-called clonal expansion phase. Two to three days later the cells definitively exit the cell cycle, express adipocyte-specific genes, and accumulate lipids to form lipid droplets. 3T3-L1 cells were grown in DMEM/FBS 10% until they reached confluence and entred quiescence following contact inhibition. The cells were kept confluent in the same medium for 2 days. The medium was renewed and supplemented with IDX for 48 hours. The medium was supplemented with insulin and renewed every 2 days until the adipogenic differentiation was completed.

2015-01-01 | E-GEOD-50612 | biostudies-arrayexpress

Zac1 and the Imprinted Gene Network program juvenile NAFLD in response to maternal metabolic syndrome

Project description:Background and Aims Within the next decade, non-alcoholic fatty liver disease (NAFLD) is predicted to become the most prevalent cause of childhood liver failure in developed countries. Predisposition to juvenile NAFLD can be programmed during early life in response to maternal metabolic syndrome (MetS), but the underlying mechanisms are poorly understood. We hypothesized that imprinted genes, defined by expression from a single parental allele, play a key role in maternal MetS-induced NAFLD, due to their susceptibility to environmental stressors and their functions in liver homeostasis. We aimed to test this hypothesis and determine the critical periods of susceptibility to maternal MetS. Approach and Results We established a mouse model to compare the effects of MetS during prenatal and postnatal development on NAFLD. Postnatal but not prenatal MetS exposure is associated with histological, biochemical and molecular signatures of hepatic steatosis and fibrosis in juvenile mice. Using RNA-seq, we show that the Imprinted Gene Network (IGN), including its regulator Zac1, is up-regulated and over-represented among differentially expressed genes, consistent with a role in maternal MetS-induced NAFLD. In support of this, activation of the IGN in cultured hepatoma cells by over-expressing Zac1 is sufficient to induce signatures of profibrogenic transformation. Using chromatin immunoprecipitation, we demonstrate that Zac1 binds the TGF-β1 and COL6A2 promoters, forming a direct pathway between imprinted genes and well-characterized pathophysiological mechanisms of NAFLD. Finally, we show that hepatocyte-specific over-expression of Zac1 is sufficient to drive fibrosis in vivo. Conclusions Our findings identify a novel pathway linking maternal MetS exposure during postnatal development to the programming of juvenile NAFLD, and provide support for the hypothesis that imprinted genes play a central role in metabolic disease programming.

2022-02-14 | GSE183809 | GEO

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