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Homo sapiens

ABSTRACT: Disease Model of GATA4 Mutation Reveals Transcription Factor Cooperativity in Human Cardiogenesis [ATAC-Seq]

PROVIDER: PRJNA339029 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4032265_1.fastq.gz	Fastqsanger.gz
	SRR4032265_2.fastq.gz	Fastqsanger.gz
	SRR4032266_1.fastq.gz	Fastqsanger.gz
	SRR4032266_2.fastq.gz	Fastqsanger.gz
	SRR4032267_1.fastq.gz	Fastqsanger.gz

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Disease Model of GATA4 Mutation Reveals Transcription Factor Cooperativity in Human Cardiogenesis

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Project description:Gata factors are amongst the genes expressed early on in the process of cardiogenesis. We used microarrays to examine the immediate early targets of Gata4 and Gata5 in the Xenopus leavis animal cap cardiogenesis model. We hope to use these data to examine the roles of Gata4 and Gata5 in cardiogenesis and also to begin to dissect out the common and distinct targets of Gata4 and Gata5. Experiment Overall Design: Xenopus leavis embryos were injected at the one cell stage with dexamethasone-inducible Gata4 or Gata5 mRNA constructs (to examine endodermal and mesodermal targets) or with Gata4 in the presence of Dkk1 (to examine mesodermal targets.) Embryos were cultured to stage 9, whereupon animal caps were excised and cultured for 2.5 hours in media containing dexamethasone to induce the constructs and cycloheximide to block de novo protein synthesis and thus give only immediate early targets.

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GATA4 regionalizes intestinal metabolism and commensal bacterial colonization to prevent immunopathology

Project description:Different regions of the gastrointestinal tract have distinct digestive and absorptive functions, which may be locally disrupted by infection or autoimmune disease. Yet, the mechanisms underlying intestinal regionalization and its dysregulation in disease are not well understood. Here, we used mouse models, transcriptomics, and immune profiling to show that regional epithelial expression of the transcription factor GATA4 prevented adherent bacterial colonization and inflammation in the proximal small intestine by regulating retinol metabolism and luminal IgA. Loss of epithelial GATA4 expression increased mortality in mice infected with Citrobacter rodentium which was dependent on commensal microbiota induced immunopathology. In active celiac patients with villous atrophy, low GATA4 expression was associated with metabolic alterations, mucosal Actinobacillus, and increased IL-17 immunity. This study reveals broad impacts of GATA4-regulated intestinal regionalization and highlights an elaborate interdependence of intestinal metabolism, immunity, and microbiota in homeostasis and disease.

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Effect of NKX2-5 or ETS1 on GATA4 pioneer activity [fibroblast]

Project description:GATA4 is a pioneer transcription factor. The mechanisms by which pioneer factors select and occupy specific loci, open chromatin, and activate enhancers is not well understood. To address the influence of partner, non-pioneer factors on pioneer factor activity, we analyzed the effect of NKX2-5 or ETS1 on GATA4 pioneer activity. NIH3T3 cells were transduced with lentivirus to obtain stable cell lines that express GFP (control), GATA4 (G), NKX2-5 (N), ETS1 (E), GATA4+NKX2-5 (GN), and GATA4+ETS1 (GE). We measured chromatin accessibility using ATAC-seq, and enhancer activation using H3K27ac. From these measurements we determined GATA4, GATA4+ETS, and GATA4+NKX2-5 pioneer binding, pioneer opening, and pioneer enhancer activation. Our results show that ETS1 or NKX2-5 alter GATA4 pioneer binding, opening, and enhancer activation.

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