Department of Biological Sciences, School of Science, The University of Tokyo, Tokyo, Japan.
Laboratory of Physiology, Atmosphere and Ocean Research Institute, The University of Tokyo, Chiba, Japan.
Elife. 2021 Jan 25;10:e55701. doi: 10.7554/eLife.55701.
The ability of animals to process dynamic sensory information facilitates foraging in an ever-changing environment. However, molecular and neural mechanisms underlying such ability remain elusive. The ClC anion channels/transporters play a pivotal role in cellular ion homeostasis across all phyla. Here, we find a ClC chloride channel is involved in salt concentration chemotaxis of . Genetic screening identified two altered-function mutations of that disrupt experience-dependent salt chemotaxis. Using genetically encoded fluorescent sensors, we demonstrate that CLH-1 contributes to regulation of intracellular anion and calcium dynamics of salt-sensing neuron, ASER. The mutant CLH-1 reduced responsiveness of ASER to salt stimuli in terms of both temporal resolution and intensity, which disrupted navigation strategies for approaching preferred salt concentrations. Furthermore, other ClC genes appeared to act redundantly in salt chemotaxis. These findings provide insights into the regulatory mechanism of neuronal responsivity by ClCs that contribute to modulation of navigation behavior.
动物处理动态感觉信息的能力促进了在不断变化的环境中的觅食。然而,这种能力的分子和神经机制仍然难以捉摸。ClC 阴离子通道/转运体在所有门中都对细胞离子动态平衡起着关键作用。在这里,我们发现 ClC 氯离子通道参与了 的盐浓度趋化性。遗传筛选确定了两种改变功能的 突变,这些突变破坏了经验依赖性盐趋化性。使用遗传编码荧光传感器,我们证明 CLH-1 有助于调节盐敏感神经元 ASER 的细胞内阴离子和钙动态。突变的 CLH-1 降低了 ASER 对盐刺激的反应性,无论是在时间分辨率还是强度方面,这破坏了接近首选盐浓度的导航策略。此外,其他 ClC 基因似乎在盐趋化性中具有冗余作用。这些发现为 ClC 调节神经元反应性的机制提供了深入了解,有助于调节导航行为。