Zac1 target genes during mouse tongue and cartilage development
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE93418 | GEO | 2022/11/02
REPOSITORIES: GEO
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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
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.
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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
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
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
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.
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Project description:Background and Aims: Cadmium (Cd) exposure in adulthood is associated with non-alcoholic fatty liver disease (NAFLD), characterized by steatosis, inflammation, and fibrosis. NAFLD is the leading type of chronic liver disease, resulting in $103 billion per year in medical costs and affecting 30 % of the adult US population. Diagnosis of NAFLD is occurring at increasingly younger ages, with up to 20 % of adolescents and young adults currently affected, suggesting that susceptibility to NAFLD may be programmed by the environment during early life. However, the role of developmental Cd exposure in programming NAFLD and the underlying mechanisms remain unclear. We have proposed that imprinted genes are strong candidates for connecting the early life environment and later disease. Approach and Results: We established a hybrid mouse model of developmental Cd exposure in which dams were exposed to 0 or 50 ppm CdCl2 five weeks prior to mating until their offspring reached postnatal day (PND) 10. CdCl2 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 developmental Cd-induced NAFLD. In support of this, we show that hepatocyte-specific over-expression of Zac1 is sufficient to drive lipid accumulation in vitro. Conclusions: Our findings demonstrate that developmental CdCl2 exposure is sufficient to program NAFLD in later life, and with our previous work, establish Zac1 and the IGN as key regulators of prosteatotic and profibrotic pathways, two of the major pathological hallmarks of NAFLD
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2014-07-01 | E-GEOD-54246 | biostudies-arrayexpress
Project description:To examine the unbiased global gene expression of over-expression of Prg4 in superficial zone articular chondrocytes in mice. This approach allows us to define novel signaling changes caused by the over-expression of Prg4 in superficial zone articular chondrocytes Total RNA was isolated from superficial zone chondrocytes in P1 articular cartilage in hind limbs (n=3) by laser capture microdissection. Same tissue from wild type mice served as control
2013-06-24 | E-GEOD-43663 | biostudies-arrayexpress