CRYPTOCHROME-mediated phototransduction by modulation of the potassium ion channel β-subunit redox sensor
CRYPTOCHROME-mediated phototransduction by modulation of the potassium ion channel β-subunit redox sensor
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DOI：
10.1073/pnas.1416586112
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发表时间：
2015-02-17
影响因子：
11.1
通讯作者：
Holmes, Todd C.
中科院分区：
文献类型：
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作者：
Fogle, Keri J.;Baik, Lisa S.;Holmes, Todd C.
蓝光激活光感受器CRY（cryopreceptor）可引起果蝇昼夜节律和觉醒神经元的快速去极化和动作电位放电增加。在这里，我们表明，急性唤醒行为反应蓝光显着不同的突变体缺乏CRY，以及突变体与中断视蛋白为基础的光转导。光激活的CRY通过电压门控钾（K+）通道β亚基（Kv β）高动力（Hk）的一个非常保守的氧化还原传感器与膜去极化偶联。神经元光响应在hk（-/-）突变体中几乎完全不存在，但通过WT Hk的遗传靶向神经元表达而不是通过使Hk氧化还原传感器功能失效的Hk点突变而在功能上被拯救。与Hk共组装的多个K+通道α亚基（包括Shaker、Ether-a-go-go和Ether-a-go-go相关基因）是CRY/Hk耦合光响应的离子传导通道。CRY的光激活被Kv β亚基氧化还原传感器转导为膜去极化、增加的放电率和急性行为反应。
Blue light activation of the photoreceptor CRYPTOCHROME (CRY) evokes rapid depolarization and increased action potential firing in a subset of circadian and arousal neurons in Drosophila melanogaster. Here we show that acute arousal behavioral responses to blue light significantly differ in mutants lacking CRY, as well as mutants with disrupted opsin-based phototransduction. Light-activated CRY couples to membrane depolarization via a well conserved redox sensor of the voltage-gated potassium (K+) channel beta-subunit (Kv beta) Hyperkinetic (Hk). The neuronal light response is almost completely absent in hk(-/-) mutants, but is functionally rescued by genetically targeted neuronal expression of WT Hk, but not by Hk point mutations that disable Hk redox sensor function. Multiple K+ channel alpha-subunits that coassemble with Hk, including Shaker, Ether-a-go-go, and Ether-a-go-go-related gene, are ion conducting channels for CRY/Hk-coupled light response. Light activation of CRY is transduced to membrane depolarization, increased firing rate, and acute behavioral responses by the Kv beta subunit redox sensor.