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Journal Article

Chronic dysfunction of Stromal interaction molecule by pulsed RNAi induction in fat tissue impairs organismal energy homeostasis in Drosophila.

MPS-Authors
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Xu,  Y.
Research Group of Molecular Physiology, MPI for Biophysical Chemistry, Max Planck Society;

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Kühnlein,  R. P.
Research Group of Molecular Physiology, MPI for Biophysical Chemistry, Max Planck Society;

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(Supplementary material), 542KB

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3054147_Suppl_4.xlsx
(Supplementary material), 41KB

Citation

Xu, Y., Borcherding, A. F., Heier, C., Tian, G., Roeder, T., & Kühnlein, R. P. (2019). Chronic dysfunction of Stromal interaction molecule by pulsed RNAi induction in fat tissue impairs organismal energy homeostasis in Drosophila. Scientific Reports, 9: 6989. doi:10.1038/s41598-019-43327-y.


Cite as: http://hdl.handle.net/21.11116/0000-0003-925F-E
Abstract
Obesity is a progressive, chronic disease, which can be caused by long-term miscommunication between organs. It remains challenging to understand how chronic dysfunction in a particular tissue remotely impairs other organs to eventually imbalance organismal energy homeostasis. Here we introduce RNAi Pulse Induction (RiPI) mediated by short hairpin RNA (shRiPI) or double-stranded RNA (dsRiPI) to generate chronic, organ-specific gene knockdown in the adult Drosophila fat tissue. We show that organ-restricted RiPI targeting Stromal interaction molecule (Stim), an essential factor of store-operated calcium entry (SOCE), results in progressive fat accumulation in fly adipose tissue. Chronic SOCE-dependent adipose tissue dysfunction manifests in considerable changes of the fat cell transcriptome profile, and in resistance to the glucagon-like Adipokinetic hormone (Akh) signaling. Remotely, the adipose tissue dysfunction promotes hyperphagia likely via increased secretion of Akh from the neuroendocrine system. Collectively, our study presents a novel in vivo paradigm in the fly, which is widely applicable to model and functionally analyze inter-organ communication processes in chronic diseases.