Roles of the CIC chloride channel CLH-1 in food-associated salt chemotaxis behavior of C. eleagns

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 CIC anion channels/transporters play a pivotal role in cellular ion homeostasis across all phyla. Here, we find a CIC chloride channel is involved in salt concentration chemotaxis of Caenorhabditis elegans. Genetic screening identified two altered-function mutations of clh-1 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 CIC genes appeared to act redundantly in salt chemotaxis. These findings provide insights into the regulatory mechanism of neuronal responsivity by CICs that contribute to modulation of navigation behavior.

Automated summary

Research has found that CIC chloride channels play a crucial role in salt concentration chemotaxis in Caenorhabditis elegans, with mutant CLH-1 reducing the responsiveness of salt-sensing neuron ASER to salt stimuli. This disruption affects the navigation strategy towards preferred salt concentrations.