Metabolic gene regulation by Drosophila GATA transcription factor Grain
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA701606 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13697049.fastq.gz | Fastqsanger.gz | |||
| SRR13697050.fastq.gz | Fastqsanger.gz | |||
| SRR13697051.fastq.gz | Fastqsanger.gz | |||
| SRR13697052.fastq.gz | Fastqsanger.gz | |||
| SRR13697053.fastq.gz | Fastqsanger.gz |
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Project description:Nutrient-dependent gene regulation critically contributes to homeostatic control of animal physiology in changing nutrient landscape. In Drosophila, dietary sugars activate transcription factors (TFs), such as Mondo-Mlx, Sugarbabe and Cabut, which control metabolic gene expression to mediate physiological adaptation to high sugar diet. TFs that correspondingly control sugar responsive metabolic genes under conditions of low dietary sugar remain, however, poorly understood. We have used de novo motif prediction to uncover a significant over-representation of GATA-like motifs on the promoters of sugar-responsive genes in Drosophila larvae. GATA TF Grain was found to contribute to the regulation of sugar-responsive genes, and consequently to central carbon and lipid metabolism, primarily on low sugar diet. Grain targets include known sugar responsive TFs, cabut and smad on X (smox). Moreover, Grain promotes the expression of genes involved in de novo lipogenesis. Grain chromatin binding sites significantly converge with those of Sugarbabe. Grain and Sugarbabe both activate lipogenic genes, but display functional predominance on low and high sugar conditions, respectively. Collectively, our data provides evidence for a metazoan GATA transcription factor in nutrient-responsive metabolic regulation in vivo.
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Project description:Vascular endothelial dysfunction underlies the genesis and progression of numerous diseases. Whereas the GATA transcription factor GATA-2 is expressed in endothelial cells and is implicated in coronary heart disease, it has been studied predominantly as a master regulator of hematopoiesis. As many questions remain unanswered regarding GATA-2 function in the vascular biology realm, we used ChIP-seq and loss-of-function strategies to define the GATA-2-instigated genetic network in human endothelial cells. By contrast to erythroid cells, GATA-2 occupied a unique target gene ensemble, consisting of genes encoding key determinants of endothelial cell identity and inflammation. GATA-2-occupied sites characteristically contained motifs that bind Activator Protein-1 (AP-1), a pivotal regulator of inflammatory genes. GATA-2 frequently occupied the same chromatin sites as c-JUN and c-FOS, heterodimeric components of AP-1. Though all three components were required for maximal AP-1 target gene expression, GATA-2 was not required for AP-1 chromatin occupancy. GATA-2 conferred maximal phosphorylation of chromatin-bound c-JUN at Ser 73, which stimulates AP-1-dependent transactivation, in a chromosomal context-dependent manner. This work establishes a link between a GATA factor and inflammation, mechanistic insights underlying GATA-2-AP-1 cooperativity, and a rigorous genetic framework for understanding GATA-2 function in normal and pathophysiological vascular states. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
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Project description:GATA factors interact with simple DNA motifs (WGATAR) to regulate critical processes, including hematopoiesis, but very few WGATAR motifs are occupied in genomes. Given the rudimentary knowledge of mechanisms underlying this restriction, and how GATA factors establish genetic networks, we used ChIP-seq to define GATA-1 and GATA-2 occupancy genome-wide in erythroid cells. Coupled with genetic complementation analysis and transcriptional profiling, these studies revealed a rich collection of targets containing a characteristic binding motif of greater complexity than WGATAR. GATA factors occupied loci encoding multiple components of the Scl/TAL1 complex, a master regulator of hematopoiesis and leukemogenic target. Mechanistic analyses provided evidence for cross-regulatory and autoregulatory interactions among components of this complex, including GATA-2 induction of the hematopoietic corepressor ETO-2 and an ETO-2 negative autoregulatory loop. These results establish fundamental principles underlying GATA factor mechanisms in chromatin and illustrate a complex network of considerable importance for the control of hematopoiesis. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Examination of GATA1 and GATA2 occpancy in K562 cells
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