IP3R mediated Ca(2+) release regulates protein metabolism in Drosophila neuroendocrine cells: implications for development under nutrient stress.
|Title||IP3R mediated Ca(2+) release regulates protein metabolism in Drosophila neuroendocrine cells: implications for development under nutrient stress.|
|Publication Type||Journal Article|
|Year of Publication||2017|
|Authors||Megha M, Hasan G|
|Date Published||2017 Mar 13|
Successful completion of animal development is fundamentally reliant on nutritional cues. Adaptations for surviving nutritional loss are coordinated in part by neural circuits. As neuropeptides secreted by neuroendocrine (NE) cells critically modulate neural circuits, we investigated NE cell function during development under nutrient stress. Starved Drosophila larvae exhibited reduced pupariation, if either insulin signaling or IP3/Ca(2+) signaling, were down-regulated in NE cells. Moreover, an IP3R (Inositol 1,4,5-trisphosphate receptor) loss-of-function mutant displayed reduced protein synthesis, which was rescued by over-expression of either InR (insulin receptor) or IP3R in NE cells of the mutant, suggesting that the two signaling pathways may be functionally compensatory. Furthermore, cultured IP3R mutant NE cells, but not neurons, exhibited reduced protein translation. Thus cell-specific regulation of protein synthesis by IP3R in NE cells influences protein metabolism. We propose that this regulation helps developing animals survive poor nutritional conditions.