Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA290044 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2103780.fastq.gz | Fastqsanger.gz | |||
| SRR2103781.fastq.gz | Fastqsanger.gz | |||
| SRR2103782.fastq.gz | Fastqsanger.gz | |||
| SRR2103783.fastq.gz | Fastqsanger.gz | |||
| SRR2103774.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:Sugar responsive regulatory network that controls organismal carbohydrate, amino acid and lipid homeostasis [set 2]
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Project description:Sugar responsive regulatory network that controls organismal carbohydrate, amino acid and lipid homeostasis
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Project description:Maintaining metabolic homeostasis in response to fluctuating nutrient intake requires intricate coordination between tissues of multicellular animals. The insulin/glucagon axis is well known to hormonally coordinate organism-wide carbohydrate metabolism. The ChREBP/Mondo-Mlx transcription factors regulate glycolytic and lipogenic genes locally in hepatocytes and adipocytes, but its role in systemic metabolic homeostasis has remained poorly understood. We demonstrate that Mondo-Mlx controls gene activity in several peripheral tissues of Drosophila melanogaster, where it regulates nutrient digestion and transport as well as carbohydrate, amino acid and lipid metabolism. In addition to directly regulating metabolic genes Mondo-Mlx controls a regulatory network composed of the Activin ligand Dawdle and GLI similar transcription factor Sugarbabe. Dawdle and Sugarbabe contribute to the regulation of a subset of Mondo-Mlx-dependent processes, including sugar-induced de novo synthesis of serine and fatty acids. In summary, our study establishes Mondo-Mlx sugar sensor as a master regulator of organismal metabolic homeostasis upon sugar feeding.
2015-09-30 | GSE70979 | GEO
Project description:Maintaining metabolic homeostasis in response to fluctuating nutrient intake requires intricate coordination between tissues of multicellular animals. The insulin/glucagon axis is well known to hormonally coordinate organism-wide carbohydrate metabolism. The ChREBP/Mondo-Mlx transcription factors regulate glycolytic and lipogenic genes locally in hepatocytes and adipocytes, but its role in systemic metabolic homeostasis has remained poorly understood. We demonstrate that Mondo-Mlx controls gene activity in several peripheral tissues of Drosophila melanogaster, where it regulates nutrient digestion and transport as well as carbohydrate, amino acid and lipid metabolism. In addition to directly regulating metabolic genes Mondo-Mlx controls a regulatory network composed of the Activin ligand Dawdle and GLI similar transcription factor Sugarbabe. Dawdle and Sugarbabe contribute to the regulation of a subset of Mondo-Mlx-dependent processes, including sugar-induced de novo synthesis of serine and fatty acids. In summary, our study establishes Mondo-Mlx sugar sensor as a master regulator of organismal metabolic homeostasis upon sugar feeding.
2015-09-30 | GSE70978 | GEO
Project description:To cope with food scarcity, animals store energy as lipids, which are produced from carbohydrates via de novo lipogenesis (DNL). The carbohydrate-responsive ChREBP-MLX complex is a master transcriptional regulator for DNL and lipid storage. However, our understanding of molecular mechanisms, particularly signaling pathways, controlling ChREBP-MLX complex remains incomplete. Here, we show that mammalian MLX is phosphorylated on an evolutionarily conserved motif and that MLX phosphorylation is necessary for ChREBP-MLX transcriptional activity. In Drosophila, MLX phosphorylation is essential for lipid storage and sugar tolerance during fly development. Furthermore, we identified CK2 as an MLX kinase. Although glucose phosphorylation is required for ChREBP-MLX activity, accumulation of glucose-6-phosphate (G6P) inhibits CK2-mediated MLX phosphorylation and thereby ChREBP-MLX activity. We propose that the evolutionarily conserved MLX phosphorylation is a rheostat that adjusts ChREBP-MLX activity in response to the carbohydrate availability ultimately controlling energy homeostasis.
2025-03-13 | PXD054667 | Pride
Project description:Transcripts libraries were prepared from three sugarcane genotypes with high-sugar (HS), medium-sugar (MS) or low-sugar (LS) content that were treated with ethylene or H2O. The libraries were sequenced with the Illumina paired-end HiSeq platform.Transcriptomic analyses have identified about 160,000 unigenes of which 86000 annotated genes were classified into functional groups associated with carbohydrate metabolism, signaling, localization, transport, hydrolysis, growth, catalytic activity, membrane and storage, suggesting the structural and functional specification, including sucrose accumulation, occurring in maturing internodes. About 25,000 genes were differentially expressed between all genotypes and treatments combined. Genotype had a dominant effect on differential gene expression than ethylene treatment. Sucrose and starch metabolism genes were more responsive to ethylene treatment in low-sugar genotype. Ethylene caused differential gene expression of many stress-related transcription factors, carbohydrate metabolism, hormone metabolism and epigenetic modification. Ethylene-induced expression of ethylene-responsive transcription factors, cytosolic acid- and cell wall-bound invertases, and ATPase was more pronounced in low- than in high-sugar genotype, suggesting an ethylene-stimulated sink activity and consequent increased sucrose accumulation in low-sugar genotype.
2019-05-07 | GSE130757 | GEO
Project description:Our transcriptome data shows that comparative transcriptomics analysis was performed on L. lactis WH101 and L. lactis NZ9000 to investigated the response mechanisms of microbial cells during acid stress. Carbohydrate metabolism and sugar transporters were strengthened to provide more energy. Amino acids metabolism and transporters were regulated to maintain intracellular pHi homeostasis and generate ATP. Fatty acid metabolism was also regulated to enhance the acid tolerance of cells. Moreover, transcriptional regulators and stress response proteins were also found to be related to acid stress.
2021-07-11 | GSE116952 | GEO
Project description:The number, size, and composition of lipid droplets can be influenced by dietary changes that shift energy substrate availability. This diversification of lipid droplets can promote metabolic flexibility and shape cellular stress responses in unique tissues with distinctive metabolic roles. Using Drosophila, we uncovered a role for myocyte enhancer-factor 2 (MEF2) in modulating diet-dependent lipid droplet diversification within adult striated muscle, impacting mortality rates. Muscle-specific attenuation of MEF2, whose chronic activation maintains glucose and mitochondrial homeostasis, leads to the accumulation of large, cholesterol ester-enriched intramuscular lipid droplets in response to high calorie, carbohydrate sufficient diets. The diet-dependent accumulation of these lipid droplets also correlates with both enhanced stress protection in muscle and increases in organismal lifespan. Furthermore, MEF2 attenuation releases an antagonistic regulation of cell cycle gene expression programs, and up-regulation of Cyclin E is required for diet-and-MEF2 dependent diversification of intramuscular lipid droplets. The integration of MEF2-regulated gene expression networks with dietary responses thus plays a critical role in shaping muscle metabolism and function, further influencing organismal lifespan. Together, these results highlight a potential protective role for intramuscular lipid droplets during dietary adaptation.
2020-08-11 | GSE147676 | GEO
Project description:Carbohydrate Responsive Element-Binding Protein (ChREBP) is a carbohydrate sensing transcription factor that regulates both adaptive and maladaptive genomic responses in coordination of systemic fuel homeostasis. Genetic variants in the ChREBP locus associate with diverse metabolic traits in humans, including circulating lipids. To identify novel ChREBP-regulated hepatokines that contribute to its systemic metabolic effects, we integrated ChREBP ChIP-seq analysis in mouse liver with human genetic and genomic data for lipid traits and identified Hepatocyte Growth Factor Activator (HGFAC) as a promising ChREBP-regulated candidate in mice and humans. HGFAC is a protease that activates the pleiotropic hormone Hepatocyte Growth Factor (HGF). We demonstrate that HGFAC KO mice have phenotypes concordant with putative loss-of-function variants in human HGFAC. Moreover, in gain- and loss-of-function genetic mouse models, we demonstrate that HGFAC enhances lipid and glucose homeostasis, which may be mediated in part through actions to activate hepatic PPARγ activity. Together, our studies show that ChREBP mediates an adaptive response to overnutrition via activation of HGFAC in the liver to preserve glucose and lipid homeostasis.
2022-11-15 | GSE217937 | GEO
Project description:Carbohydrate Responsive Element-Binding Protein (ChREBP) is a carbohydrate sensing transcription factor that regulates both adaptive and maladaptive genomic responses in coordination of systemic fuel homeostasis. Genetic variants in the ChREBP locus associate with diverse metabolic traits in humans, including circulating lipids. To identify novel ChREBP-regulated hepatokines that contribute to its systemic metabolic effects, we integrated ChREBP ChIP-seq analysis in mouse liver with human genetic and genomic data for lipid traits and identified Hepatocyte Growth Factor Activator (HGFAC) as a promising ChREBP-regulated candidate in mice and humans. HGFAC is a protease that activates the pleiotropic hormone Hepatocyte Growth Factor (HGF). We demonstrate that HGFAC KO mice have phenotypes concordant with putative loss-of-function variants in human HGFAC. Moreover, in gain- and loss-of-function genetic mouse models, we demonstrate that HGFAC enhances lipid and glucose homeostasis, which may be mediated in part through actions to activate hepatic PPARγ activity. Together, our studies show that ChREBP mediates an adaptive response to overnutrition via activation of HGFAC in the liver to preserve glucose and lipid homeostasis.
2022-11-15 | GSE217982 | GEO