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Journal Article

A Drosophila in vivo screen identifies store-operated calcium entry as a key regulator of adiposity.

MPS-Authors
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Hummel,  P.
IT and Electronic Service, MPI for biophysical chemistry, Max Planck Society;

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Bickmeyer,  I.
Department of Molecular Developmental Biology, MPI for biophysical chemistry, Max Planck Society;

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Hildebrandt,  A.
Research Group of Molecular Physiology, MPI for biophysical chemistry, Max Planck Society;

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Riedel,  D.
Facility for Electron Microscopy, MPI for biophysical chemistry, Max Planck Society;

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Jäckle,  H.
Department of Molecular Developmental Biology, 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;

Fulltext (public)

1920419.pdf
(Publisher version), 3MB

Supplementary Material (public)

1920419- Suppl-1.pdf
(Supplementary material), 2MB

1920419-Suppl-2.xlsx
(Supplementary material), 2MB

Citation

Baumbach, J., Hummel, P., Bickmeyer, I., Kowalczyk, K. M., Frank, M., Knorr, K., et al. (2014). A Drosophila in vivo screen identifies store-operated calcium entry as a key regulator of adiposity. Cell Metabolism, 19(2), 331-343. doi:10.1016/j.cmet.2013.12.004.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0015-1D00-4
Abstract
To unravel the evolutionarily conserved genetic network underlying energy homeostasis, we performed a systematic in vivo gene knockdown screen in Drosophila. We used a transgenic RNAi library enriched for fly orthologs of human genes to functionally impair about half of all Drosophila genes specifically in adult fat storage tissue. This approach identified 77 genes, which affect the body fat content of the fly, including 58 previously unknown obesity-associated genes. These genes function in diverse biological processes such as lipid metabolism, vesicle-mediated trafficking, and the universal store-operated calciumentry (SOCE). Impairment of the SOCE core component Stromal interaction molecule (Stim), as well as other components of the pathway, causes adiposity in flies. Acute Stim dysfunction in the fat storage tissue triggers hyperphagia via remote control of the orexigenic short neuropeptide F in the brain, which in turn affects the coordinated lipogenic and lipolytic gene regulation, resulting in adipose tissue hypertrophy.