Journal
JOURNAL OF GENETICS AND GENOMICS
Volume 41, Issue 5, Pages 283-292Publisher
SCIENCE PRESS
DOI: 10.1016/j.jgg.2014.03.005
Keywords
Plc21C; G alpha q; G gamma 1; Calcium; Fat storage; Adipokinetic hormone
Funding
- Max Planck Society
- German research foundation [DFG KU 2866/1-1]
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Adaptive mobilization of body fat is essential for energy homeostasis in animals. In insects, the adipokinetic hormone (Akh) systemically controls body fat mobilization. Biochemical evidence supports that Akh signals via a G protein-coupled receptor (GPCR) called Akh receptor (AkhR) using cyclic-AMP (cAMP) and Ca2+ second messengers to induce storage lipid release from fat body cells. Recently, we provided genetic evidence that the intracellular calcium (iCa(2+)) level in fat storage cells controls adiposity in the fruit fly Drosophila melanogaster. However, little is known about the genes, which mediate Akh signalling downstream of the AkhR to regulate changes in iCa(2+). Here, we used thermogenetics to provide in vivo evidence that the GPCR signal transducers G protein alpha q subunit (G alpha q), G protein gamma 1 (G gamma 1) and Phospholipase C at 21C (Plc21C) control cellular and organismal fat storage in Drosophila. Transgenic modulation of G alpha q, G gamma 1 and Plc21C affected the iCa(2+) of fat body cells and the expression profile of the lipid metabolism effector genes midway and brummer, which results in severely obese or lean flies. Moreover, functional impairment of G alpha q, G gamma 1 and Plc21C antagonised Akh-induced fat depletion. This study characterizes G alpha q, G gamma 1 and Plc21C as anti-obesity genes and supports the model that Akh employs the G alpha q/G gamma 1/Plc21C module of iCa(2+) control to regulate lipid mobilization in adult Drosophila.
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