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Transforming growth factor β/activin signaling functions as a sugar-sensing feedback loop to regulate digestive enzyme expression.

ABSTRACT: Organisms need to assess their nutritional state and adapt their digestive capacity to the demands for various nutrients. Modulation of digestive enzyme production represents a rational step to regulate nutriment uptake. However, the role of digestion in nutrient homeostasis has been largely neglected. In this study, we analyzed the mechanism underlying glucose repression of digestive enzymes in the adult Drosophila midgut. We demonstrate that glucose represses the expression of many carbohydrases and lipases. Our data reveal that the consumption of nutritious sugars stimulates the secretion of the transforming growth factor β (TGF-β) ligand, Dawdle, from the fat body. Dawdle then acts via circulation to activate TGF-β/Activin signaling in the midgut, culminating in the repression of digestive enzymes that are highly expressed during starvation. Thus, our study not only identifies a mechanism that couples sugar sensing with digestive enzyme expression but points to an important role of TGF-β/Activin signaling in sugar metabolism.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE54755 | GEO | 2014/09/10

SECONDARY ACCESSION(S): PRJNA237553

REPOSITORIES: GEO

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TGF β signaling functions as a sugar sensing feedback loop to regulate digestive enzyme expression.

Project description:Organisms need to assess their nutritional state and adapt their digestive capacity to the demands for various nutrients. Modulation of digestive enzyme production represents a potential step to regulate nutriment intake. However, the role of digestion in nutrient homeostasis has been largely neglected. In this study, we analyzed the mechanism underlying glucose repression of amylase in the adult Drosophila midgut. We demonstrated that glucose represses many carbohydrases and lipases. Our data shows that the consumption of nutritious sugars stimulates the secretion of the TGFβ ligand, Dawdle. Dawdle then acts via the circulation to activate TGFβ/Activin signaling in the midgut, culminating in the repression of digestive enzyme expression. Thus, our study not only identifies a mechanism coupling sugar sensing to digestive enzyme expression but points to an important role of TGFβ/Activin signaling in sugar metabolism. RNA-sequencing of whole guts from Drosophila melannogaster OregonR adult females was performed under three feeding conditions: Standard medium, glucose, and agar. Three biological repeats were performed for each condition.

2014-09-10 | E-GEOD-54755 | biostudies-arrayexpress

Drosophila melanogaster

Project description:Transforming growth factor β/activin signaling functions as a sugar-sensing feedback loop to regulate digestive enzyme expression.

| PRJNA237553 | ENA

Sugar responsive regulatory network that controls organismal carbohydrate, amino acid and lipid homeostasis [set 2]

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

Sugar responsive regulatory network that controls organismal carbohydrate, amino acid and lipid homeostasis [set 1]

2015-09-30 | GSE70978 | GEO

RNA-seq analysis to profile TGF-beta/Activin signaling-dependent gene expression in Drosophila larval skeletal muscle

Project description:We performed RNA-seq analysis to identify genes whose expression is regulted or influenced by TGF-beta/Activin signaling in Drosophila larval skeletal muscle. We used two sample sets. One is composed of wild-type and smox (the sole R-smad of TGF-beta/Activin signaling in Drosophila). The other is composed of control and larvae of muscle-specific expression of activated Baboo (Type I receptor). By comparing differential expressions from these two sets, we were able to identify genes whose expression is regulated by TGF-beta/Activin pathway in the skeletal muscle of Drosophila larvae.

2020-12-08 | GSE162810 | GEO

mRNA profiling of mouse embryonic cells with activin or SB431542 treatment

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The TGF-β superfamily cytokine Activin-A is induced during autoimmune neuroinflammation and drives pathogenic Th17 cell differentiation

Project description:Th17 cells are known to exert pathogenic and non-pathogenic functions. Although the cytokine transforming growth factor β1 (TGF-β1) is instrumental for Th17 cell differentiation, it is dispensable for generation of pathogenic Th17 cells. Here, we examined the T cell-intrinsic role of Activin-A, a TGF-β superfamily member closely related to TGF-β1, in pathogenic Th17 cell differentiation. Activin-A expression was increased in individuals with relapsing-remitting multiple sclerosis and in mice with experimental autoimmune encephalomyelitis. Stimulation with interleukin-6 and Activin-A induced a molecular program that mirrored that of pathogenic Th17 cells and was inhibited by blocking Activin-A signaling. Genetic disruption of Activin-A and its receptor ALK4 in T cells impaired pathogenic Th17 cell differentiation in vitro and in vivo. Mechanistically, extracellular-signal-regulated kinase (ERK) phosphorylation, which was essential for pathogenic Th17 cell differentiation, was suppressed by TGF-β1-ALK5 but not Activin-A-ALK4 signaling. Thus, Activin-A drives pathogenic Th17 cell differentiation, implicating the Activin-A-ALK4-ERK axis as a therapeutic target for Th17 cell-related diseases.

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2024-06-28 | GSE270911 | GEO

Activin A in Combination with ERK1/2 MAPK Pathway Inhibition Sustains Propagation of Mouse Embryonic Stem Cells

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