• Title/Summary/Keyword: Flightless-1

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Potential involvement of Drosophila flightless-1 in carbohydrate metabolism

  • Park, Jung-Eun;Jang, Jinho;Lee, Eun Ji;Kim, Su Jung;Yoo, Hyun Ju;Lee, Semin;Kang, Min-Ji
    • BMB Reports
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    • v.51 no.9
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    • pp.462-467
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    • 2018
  • A previous study of ours indicated that Drosophila flightless-1 controls lipid metabolism, and that there is an accumulation of triglycerides in flightless-1 (fliI)-mutant flies, where this mutation triggers metabolic stress and an obesity phenotype. Here, with the aim of characterizing the function of FliI in metabolism, we analyzed the levels of gene expression and metabolites in fliI-mutant flies. The levels of enzymes related to glycolysis, lipogenesis, and the pentose phosphate pathway increased in fliI mutants; this result is consistent with the levels of metabolites corresponding to a metabolic pathway. Moreover, high-throughput RNA sequencing revealed that Drosophila FliI regulates the expression of genes related to biological processes such as chromosome organization, carbohydrate metabolism, and immune reactions. These results showed that Drosophila FliI regulates the expression of metabolic genes, and that dysregulation of the transcription controlled by FliI gives rise to metabolic stress and problems in the development and physiology of Drosophila.

Flightless-I Controls Fat Storage in Drosophila

  • Park, Jung-Eun;Lee, Eun Ji;Kim, Jung Kwan;Song, Youngsup;Choi, Jang Hyun;Kang, Min-Ji
    • Molecules and Cells
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    • v.41 no.6
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    • pp.603-611
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    • 2018
  • Triglyceride homeostasis is a key process of normal development and is essential for the maintenance of energy metabolism. Dysregulation of this process leads to metabolic disorders such as obesity and hyperlipidemia. Here, we report a novel function of the Drosophila flightless-I (fliI) gene in lipid metabolism. Drosophila fliI mutants were resistant to starvation and showed increased levels of triglycerides in the fat body and intestine, whereas fliI overexpression decreased triglyceride levels. These flies suffered from metabolic stress indicated by increased levels of trehalose in hemolymph and enhanced phosphorylation of eukaryotic initiation factor 2 alpha ($eIF2{\alpha}$). Moreover, upregulation of triglycerides via a knockdown of fliI was reversed by a knockdown of desat1 in the fat body of flies. These results indicate that fliI suppresses the expression of desat1, thereby inhibiting the development of obesity; fliI may, thus, serve as a novel therapeutic target in obesity and metabolic diseases.