Electrical silencing of Drosophila pacemaker neurons stops the free-running circadian clock
Electrical silencing of Drosophila pacemaker neurons stops the free-running circadian clock
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DOI：
10.1016/s0092-8674(02)00737-7
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发表时间：
2002-05-17
期刊：
影响因子：
64.5
通讯作者：
Holmes, TC
中科院分区：
文献类型：
--
作者：
Nitabach, MN;Blau, J;Holmes, TC
通过 K+ 通道的靶向表达对果蝇昼夜节律起搏神经元进行电沉默，导致在完全黑暗中自由运行的昼夜节律运动节律严重缺陷。起搏器电沉默还会停止构成细胞自主分子钟核心的 PERIOD (PER) 和 TIMELESS (TIM) 蛋白的自由振荡。相比之下，电沉默无法消除明暗循环中的 PER 和 TIM 振荡，尽管它确实损害了节律行为。基于这些发现，我们提出电活动是起搏神经元自由运行的分子时钟的重要组成部分，以及先前已确定为时钟功能所需的转录因子和调节酶。
Electrical silencing of Drosophila circadian pacemaker neurons through targeted expression of K+ channels causes severe deficits in free-running circadian locomotor rhythmicity in complete darkness. Pacemaker electrical silencing also stops the free-running oscillation of PERIOD (PER) and TIMELESS (TIM) proteins that constitutes the core of the cell-autonomous molecular clock. In contrast, electrical silencing fails to abolish PER and TIM oscillation in light-dark cycles, although it does impair rhythmic behavior. On the basis of these findings, we propose that electrical activity is an essential element of the free-running molecular clock of pacemaker neurons along with the transcription factors and regulatory enzymes that have been previously identified as required for clock function.