Analysis of calcium signaling in C. elegans

线虫体内钙信号的分析 这个项目的目标是分析控制信令的机制 电压激活钙通道(Cav)。在神经元和肌肉中，短暂的细胞质 钙瞬变有效而快速地激活下游效应器，通常是在 毫秒时间尺度。一种提高信号速度和速度的通用机制 效率是CAV通道及其效应器之间的紧密空间耦合，这是 称为钙纳米结构域信号。我们提出了研究纳米域的三个目标 通过CAV通道发送信号。首先，我们确定了促进联结所需的基因 钙激活的BK钾通道和钙激活的BK钾通道 Ryanodine受体(RyR)，内质中的钙释放通道 网状结构。其次，我们测试如何设置活性诱导基因的阈值的模型 转录，如果这个阈值被激活的特定钙的突变所改变 信号成分或内源性神经肽。第三，我们问CaV1和CaV2是如何 通道位于突触前终末，决定神经递质的释放 概率。这些目标涉及控制神经元和 肌肉生理学。

Analysis of calcium signaling in C. elegans The goal of this project is to analyze mechanisms controlling signaling by voltage-activated calcium (CaV) channels. In neurons and muscles, brief cytoplasmic calcium transients efficiently and rapidly activate downstream effectors, often on millisecond time scales. One general mechanism that promotes signal speed and efficiency is tight spatial coupling between CaV channels and their effectors, which is termed calcium nanodomain signaling. We propose three Aims to study nanodomain signaling by CaV channels. First, we identify genes required to promote coupling of CaV1 (L-type) channels to two effectors, calcium activated BK potassium channels and ryanodine receptors (RYR), which are calcium release channels in the endoplasmic reticulum. Second, we test models for how the threshold is set for activity induced gene transcription, and if this threshold is shifted by mutations in specific calcium activated signaling components or by endogenous neuropeptides. Third, we ask how CaV1 and 2 channels are localized at presynaptic terminals, which dictates neurotransmitter release probability. These Aims address fundamental mechanisms controlling neuron and muscle physiology.