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Targets of DNA binding, N-terminal, or C-terminal domain swapped mutant forms fo Foxa proteins in induced hepatocyte-like (iHep) cells.

ABSTRACT: Targets of DNA binding, N-terminal, or C-terminal domain swapped mutant forms fo Foxa proteins in induced hepatocyte-like (iHep) cells.

PROVIDER: PRJNA481781 | ENA |

REPOSITORIES: ENA

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Targets of DNA binding, N-terminal, or C-terminal domain swapped mutant forms fo Foxa proteins in induced hepatocyte-like (iHep) cells.

Project description:We have found that three specific combinations of two transcription factors, comprising Hnf4alpha plus Foxa1, Foxa2 or Foxa3, could convert mouse embryonic fibroblasts (MEFs) into cells that closely resemble hepatocytes in vitro, and DNA binding, N-terminal, and C-terminal domains (DBD, NTD, and CTD, respectively) of Foxa proteins are swappable in the direct reprogramming of the iHep cells. Then we used ChIP-seq to explore the targets of the domain swapped mutant forms of Foxa proteins during conversion event to iHep cells.

2020-08-06 | GSE117332 | GEO

Foxa and Hnf4alpha targets during conversion from mouse embryonic fibroblasts (MEFs) to hepatocyte-like (iHep) cells

Project description:We have found three specific combinations of two transcription factors, comprising Hnf4alpha plus Foxa1, Foxa2 or Foxa3, could convert mouse embryonic fibroblasts (MEFs) into cells that closely resemble hepatocytes in vitro. Then we used ChIP-seq to explore the targets of Foxa and Hnf4alpha during conversion event to iHep cells.

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Foxa and Hnf4alpha targets during conversion from mouse embryonic fibroblasts (MEFs) to hepatocyte-like (iHep) cells and hepatocytes (Hep).

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miRNA expression profile of follicular (FO) and marginal zone (MZ) B cells

2011-11-01 | GSE25139 | GEO

miRNA expression profile of follicular (FO) and marginal zone (MZ) B cells

Project description:We have analyzed miRNA expression profile in FO and MZ B cells to identified differentially expressed miRNAs between this two subsets that could be potencially involved in the regulation of terminal B cell differentiation Spleens from CD19-Creki/+Dicerfl/+ and CD19-Creki/+Dicerfl/fl mice were collected and after erythrocyte lysis, splenocytes were stained with anti-B220, anti-CD21 and anti-CD23 antibodies. B220+CD21brightCD23+ (MZ) and B220+CD21+CD23bright (FO) B cell populations were sorted and total RNA of purified populations was extracted with TRIzol. miRNA microarray hybridations were performed on Mouse miRNA Microarray platform (Agilent Technologies).

2011-11-01 | E-GEOD-25139 | biostudies-arrayexpress

Nocardamine-dependent iron uptake in Pseudomonas aeruginosa : exclusive implication of the FoxA outer membrane transporter

Project description:Iron is a key nutrient for almost all living organisms and paradoxically poorly soluble and consequently poorly bioavailable. To get access to this metal, bacteria have developed many different strategies. One of the most common consists of the use of siderophores, small compounds chelating ferric iron with a very high affinity. Many bacteria are able to produce their own siderophores or use those produced by other microorganisms (exosiderophores) in a piracy strategy. Pseudomonas aeruginosa produces two siderophores, pyoverdine and pyochelin and is able to use a large panel of exosiderophores. We investigated the ability of P. aeruginosa to use nocardamine (NOCA) and ferrioxamine B (DFOB) as exosiderophores under iron-limited planktonic growth conditions. Proteomic and RT-qPCR approaches showed an induction of the transcription and expression of the outer membrane transporter FoxA in the presence of NOCA or DFO in the bacterial environment. Expression of the proteins of the heme or pyoverdine and pyochelin dependent iron uptake pathways were not affected in the presence of these two tris-hydroxamate siderophores. 55Fe uptake assays using foxA mutants demonstrated that ferri-NOCA was exclusively transported by FoxA, while ferri-DFO was transported by FoxA and at least one another unidentified transporter. The crystal structure of FoxA in complex with NOCA revealed very similar siderophore binding sites between NOCA and DFO. Iron uptake by hydroxamate exosiderophores in P. aeruginosa cells is discussed in the light of these results.

2021-04-29 | PXD020868 | Pride

Sequence logic at enhancers governs a dual mechanism of endodermal organ fate induction by FOXA pioneer factors

Project description:FOXA pioneer transcription factors (TFs) associate with primed enhancers in endodermal organ precursors. Using a human stem cell model of pancreas differentiation, we here discover that only a subset of pancreatic enhancers is FOXA-primed, whereas the majority is unprimed and engages FOXA upon lineage induction. Primed enhancers are enriched for signal-dependent TF motifs and harbor abundant and strong FOXA motifs. Unprimed enhancers harbor fewer, more degenerate FOXA motifs, and FOXA recruitment to unprimed but not primed enhancers requires pancreatic TFs. Strengthening FOXA motifs at an unprimed enhancer near NKX6.1 renders FOXA recruitment pancreatic TF-independent, induces priming, and broadens the NKX6.1 expression domain. We make analogous observations about FOXA binding during hepatic and lung development. Our findings suggest a dual role for FOXA in endodermal organ development: First, FOXA facilitate signal-dependent lineage initiation via enhancer priming, and second, FOXA enforce organ cell type-specific gene expression via indirect recruitment by lineage-specific TFs.

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Collapse of the hepatic gene regulatory network in the absence of FoxA factors

Project description:FoxA transcription factors are critical for liver development through their pioneering activity, which initiates a highly complex network thought to become resistant to the loss of any individual hepatic transcription factor via mutual redundancy. To investigate the dispensability of FoxA factors for this regulatory network, we ablated all FoxA genes in the adult liver. Remarkably, loss of FoxA caused a rapid and massive reduction in the expression of key liver genes back to the low levels of the fetal prehepatic endoderm stage, leading to necrosis and lethality within days. Mechanistically, we found FoxA proteins to be required for maintaining chromatin activity, nucleosome positioning and binding by other hepatic transcription factors. Thus, the hepatic gene regulatory network is dependent on the FoxA proteins throughout life.

2020-07-10 | GSE140423 | GEO

FoxA-dependent demethylation of DNA initiates epigenetic memory of cellular identity

Project description:Tissue-specific DNA methylation patterns are created by transcription factors that recruit methylation and demethylation enzymes to cis-regulatory elements. To date, it is not known whether transcription factors are needed to continuously maintain methylation profiles in development and mature tissues or whether they only establish these marks during organ development. We queried the role of the pioneer factor FoxA in generating hypomethylated DNA at liver enhancers. We discovered a set of FoxA binding sites that undergo regional, FoxA-dependent demethylation during organ development. Conditional ablation of FoxA genes in the adult liver demonstrated that continued FoxA presence was not required to maintain the hypomethylated state, even when massive cell proliferation was induced. This study provides strong evidence for the stable, epigenetic nature of tissue-specific DNA methylation patterns directed by lineage-determining transcription factors during organ development.

2021-04-20 | GSE124384 | GEO

Gene expression analysis in human colon cancer cells and liver cancer cells with FoxA knockdown.

Project description:FoxA transcription factors are involved in development and tumorigenesis of the gastrointestinal tract. However, the downstream programs controlled by FoxA factors remain poorly understood. The goal of this study is to understand the transcriptional responses regulated by FoxA proteins in liver and colon cancer cells. Human liver cancer cell line HepG2 and colon cancer cell line LS174T infected with lentivirus expressing shRNAs targeting human FoxA1 and FoxA2.

2013-08-01 | E-GEOD-46466 | biostudies-arrayexpress

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