The balance between cytoplasmic and nuclear CaM kinase-1 signaling controls the operating range of noxious heat avoidance.
The balance between cytoplasmic and nuclear CaM kinase-1 signaling controls the operating range of noxious heat avoidance.
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DOI：
10.1016/j.neuron.2014.10.039
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发表时间：
2014-12-03
期刊：
影响因子：
16.2
通讯作者：
Glauser, Dominique A.
中科院分区：
文献类型：
--
作者：
Schild, Lisa C.;Zbinden, Laurie;Bell, Harold W.;Yu, Yanxun V.;Sengupta, Piali;Goodman, Miriam B.;Glauser, Dominique A.
通过与捕食者，竞争对手和有害刺激的遭遇，动物已经进化出防御反应，以尽量减少伤害，这对生存至关重要。生理适应调节触发这种伤害反应行为的刺激强度，但定义其操作范围的分子网络基本上是未知的。在这里，我们确定了一个新的，获得功能的等位基因cmk-1 CaMKI基因在C。并显示CaMKI酶的调节结构域的损失产生热镇痛，并将伤害性热回避的操作范围转移到更高的温度。这种镇痛依赖于核CMK-1信号传导，而细胞质CMK-1信号传导降低了热回避的阈值。CMK-1在热感受神经元中的热检测下游起作用并控制神经肽释放。我们的研究结果建立了CaMKI作为伤害性行为的操作范围的关键调节器，并建议通过调节CaMKI依赖的信号传导来产生热镇痛的策略。
Through encounters with predators, competitors, and noxious stimuli, animals have evolved defensive responses that minimize injury and are essential for survival. Physiological adaptation modulates the stimulus intensities that trigger such nocifensive behaviors, but the molecular networks that define their operating range are largely unknown. Here, we identify a novel, gain-of-function allele of the cmk-1 CaMKI gene in C. elegans and show that loss of the regulatory domain of the CaMKI enzyme produces thermal analgesia and shifts the operating range for nocifensive heat avoidance to higher temperatures. Such analgesia depends on nuclear CMK-1 signaling, while cytoplasmic CMK-1 signaling lowers the threshold for thermal avoidance. CMK-1 acts downstream of heat detection in thermal receptor neurons and controls neuropeptide release. Our results establish CaMKI as a key regulator of the operating range for nocifensive behaviors, and suggest strategies for producing thermal analgesia through the regulation of CaMKI-dependent signaling.
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