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Signaling and transcriptional control of metabolic pathways in Drosophila

Fachliche Zuordnung Zellbiologie
Förderung Förderung von 2012 bis 2015
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 216441328
 
Erstellungsjahr 2016

Zusammenfassung der Projektergebnisse

We have analysed two transcription factors in Drosophila that are involved in lipid regulation, a zinc finger protein termed sugarbabe, and a histone acetyltransferase termed enok. Sugarbabe is highly upregulated when animals are fed on a high sugar diet. Based on earlier expression profiling and overexpression analysis, it was proposed that sugarbabe is involved in converting sugar to fat, as well as preventing fat catabolism, in conditions of high sugar. However, a mutant for sugarbabe was not available. We have now generated a null mutant of sugarbabe using the Crispr technology. Our analysis of these mutants demonstrate that sugarbabe is indeed required for normal growth under high sugar conditions, and that the target genes include those involved in lipid catabolism. For enok, we show that enok is involved in regulating fat metabolism and for normal starvation response. When enok is overexpressed in specific tissues, the animals no longer display a starvation response, as seen by its lack of fat breakdown under starvtion condition. In addition to its role in metabolism, enok is also involved in neural stem cell function during development. A potential connection between the metabolic and cell proliferation function of enok is currently being studied.

Projektbezogene Publikationen (Auswahl)

  • (2013). The IGFBP7 homolog Imp-L2 promotes insulin signaling in distinct neurons of the Drosophila brain. J Cell Sci. 126; 2571
    Bader R, Sarraf-Zadeh, Peters M, Moderau N, Stocker H, Köhler K, Pankratz M, Hafen E
  • (2014). Src tyrosine kinase signaling antagonizes nuclear localization of FOXO and inhibits its transcription factor activity. Sci Rep. 4; 4048
    Bülow M, Bülow, T, Hoch M, Pankratz M, Jünger M
    (Siehe online unter https://doi.org/10.1038/srep04048)
 
 

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