Ontology highlight
ABSTRACT:
PROVIDER: PRJNA547759 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9214502.fastq.gz | Fastqsanger.gz | |||
| SRR9214503.fastq.gz | Fastqsanger.gz | |||
| SRR9214504.fastq.gz | Fastqsanger.gz | |||
| SRR9214505.fastq.gz | Fastqsanger.gz | |||
| SRR9214506.fastq.gz | Fastqsanger.gz |
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Project description:Foxa2 is required for endoderm differentiation into hepatic lineage. The mechanism of activation for Foxa2 during this developmental process has not been elucidated yet. We established an in vitro system to guide ES cells differentiating into definitive endoderm (DE) cells and the following DE cells to early hepatic cells. ChIP-seq assays have been successfully performed to assess Foxa2 binding profile. Over 50% of Foxa2 target genes in DE cells were found being activated in hepatic cells which were at a stage later than DE stage. Therefore, our finding at genome-wide level proved Foxa2 serving as a pioneer factor at DE stage. Furthermore, Foxa2 could specifically induce H3K4me2 modifications to the promoter/enhancer regions of many hepatic genes to pre-mark the chromatin, and determine the hepatic lineage differentiation competence. Our study illustrated the wide existence of Foxa2M-bM-^@M-^Ys pioneer factor function and uncovered the correlation between pioneer factor and chromatin pre-mark. These findings will be helpful for understanding the developmental process of hepatogenesis and efficiently controlling Foxa2 during hepatic induction for generating functional hepatocytes. Examination of Foxa2 binding sites in mESC-derived DE cells
2012-08-29 | E-GEOD-40423 | biostudies-arrayexpress
Project description:Foxa2 is required for endoderm differentiation into hepatic lineage. The mechanism of activation for Foxa2 during this developmental process has not been elucidated yet. We established an in vitro system to guide ES cells differentiating into definitive endoderm (DE) cells and the following DE cells to early hepatic cells. ChIP-seq assays have been successfully performed to assess Foxa2 binding profile. Over 50% of Foxa2 target genes in DE cells were found being activated in hepatic cells which were at a stage later than DE stage. Therefore, our finding at genome-wide level proved Foxa2 serving as a pioneer factor at DE stage. Furthermore, Foxa2 could specifically induce H3K4me2 modifications to the promoter/enhancer regions of many hepatic genes to pre-mark the chromatin, and determine the hepatic lineage differentiation competence. Our study illustrated the wide existence of Foxa2’s pioneer factor function and uncovered the correlation between pioneer factor and chromatin pre-mark. These findings will be helpful for understanding the developmental process of hepatogenesis and efficiently controlling Foxa2 during hepatic induction for generating functional hepatocytes.
2012-08-29 | GSE40423 | GEO
Project description:Foxa2 is required for endoderm differentiation into the hepatic lineage. The mechanism of activation for Foxa2 during this developmental process has not been elucidated yet. We established an in vitro system to guide ES cells differentiating into definitive endoderm (DE) cells and the following DE cells to early hepatic cells. ChIP-seq assays have been successfully performed to assess the Foxa2 binding profile. Over 50% of Foxa2 target genes in DE cells were found to be activated in hepatic cells which were at a stage later than the DE stage. Therefore, our finding at the genome-wide level proved Foxa2 serves as a pioneer factor at the DE stage. Furthermore, Foxa2 could specifically induce H3K4me2 modifications to the promoter/enhancer regions of many hepatic genes to pre-mark the chromatin, and determine the hepatic lineage differentiation competence. Our study illustrated the wide existence of Foxa2's pioneer factor function and uncovered the correlation between pioneer factor and chromatin pre-mark. These findings will be helpful for understanding the developmental process of hepatogenesis and efficiently controlling Foxa2 during hepatic induction for generating functional hepatocytes. To further gain a genome-wide view of Foxa2's effects on its target gene expression, 3 representative time points from the ES cell differentiation process to hepatic cells were selected for cDNA microarray analysis: 1) Day 0, representing ES cells, where there was no Foxa2 expression; 2) Day 5, representing DE cells; and 3) Day 7, representing early hepatic cells.
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2014-03-28 | E-GEOD-56332 | biostudies-arrayexpress
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
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Project description:Long noncoding RNAs (lncRNAs) have emerged as important components of gene regulatory network in embryonic stem cells (ESCs). However, the function and molecular mechanism of lncRNAs are still largely unknown. Here we identified Trincr1 (TRIM71 interacting long noncoding RNA 1) lncRNA that regulates the FGF/ERK signaling and self-renewal of ESCs. Trincr1 is exported by THOC complex to cytoplasm where it binds and represses TRIM71, leading to the downregulation of SHCBP1 protein. Knocking out Trincr1 leads to the upregulation of phosphorylated ERK and ERK pathway target genes and the decrease of ESC self-renewal, while knocking down Trim71 completely rescues the defects of Trincr1 knockout. Furthermore, ectopic expression of Trincr1 represses FGF/ERK signaling and the self-renewal of neural progenitor cells. Together, this study reveals more regulators in FGF/ERK signaling pathway and highlights lncRNA as an important player in cell signaling network to coordinate cell fate specification.
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