Intracellular Ca2+ signaling and store-operated Ca2+ entry are required in Drosophila neurons for flight
Intracellular Ca2+ signaling and store-operated Ca2+ entry are required in Drosophila neurons for flight
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DOI：
10.1073/pnas.0902982106
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发表时间：
2009-06-23
影响因子：
11.1
通讯作者：
Hasan, Gaiti
中科院分区：
文献类型：
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作者：
Venkiteswaran, Gayatri;Hasan, Gaiti
神经元信号可以影响兴奋性和神经回路的形成。Ca~(2+)信号受细胞内和细胞外环境的Ca~(2+)流量的影响。然而，细胞内钙储存的贡献及其对神经元突起的释放却知之甚少。在这里，我们通过神经元特异性siRNA耗竭表明，最近发现的由Dorai编码的存储操作通道和由dSTIM编码的内质网钙存储传感器的活动对于果蝇飞行运动神经元的正常飞行和相关的节律性放电模式是必需的。此外，在不会飞的果蝇肌醇1，4，5-三磷酸受体(Insp(3)R)突变体中过表达Dorai可以部分补偿它们的飞行损失。Ca~(2+)测量表明，Orai功能增强有助于通过突变的Insp(3)Rs释放Ca~(2+)的量，并增加果蝇神经元中储存操作的Ca~(2+)进入。我们的数据表明，果蝇飞行需要细胞内储存的钙离子的补充。
Neuronal signals can affect excitability and neural circuit formation. Ca2+ signals are modified by Ca2+ flux from intracellular stores as well as the extracellular milieu. However, the contribution of intracellular Ca2+ stores and their release to neuronal processes is poorly understood. Here, we show by neuron-specific siRNA depletion that activity of the recently identified store-operated channel encoded by dOrai and the endoplasmic reticulum Ca2+ store sensor encoded by dSTIM are necessary for normal flight and associated patterns of rhythmic firing of the flight motoneurons of Drosophila melanogaster. Also, dOrai overexpression in flightless mutants for the Drosophila inositol 1,4,5-trisphosphate receptor (InsP(3)R) can partially compensate for their loss of flight. Ca2+ measurements show that Orai gain-of-function contributes to the quanta of Ca2+-release through mutant InsP(3)Rs and elevates store-operated Ca2+ entry in Drosophila neurons. Our data show that replenishment of intracellular store Ca2+ in neurons is required for Drosophila flight.