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The nematode Caenorhabditis elegans senses temperature primarily via the AFD thermosensory neurons in the head. The response to temperature can be observed as a behavior called thermotaxis on thermal gradients. It has been shown that a cyclic nucleotide-gated ion channel (CNG channel) plays a critical role in thermosensation in AFD. To further identify the thermosensory mechanisms in AFD, we attempted to identity components that function upstream of the CNG channel by a reverse genetic approach. Genetic and behavioral analyses showed that three members of a subfamily of gcy genes (gcy-8, gcy,-18, and gcy-23) encoding guanylyl cyclases were essential for thermotaxis in C. elegans. Promoters of each gene drove reporter gene expression exclusively in the AFD neurons and, moreover tagged proteins were localized to the Sensory endings of AFD. Single mutants of each gcy gene showed almost normal thermotaxis. However animals canting double and triple mutations in these genes showed defective thermotaxis behavior. The abnormal phenotype of the gcy triple mutants was rescued by expression of any one of the three GCY proteins in the AFD neurons. These results suggest that three guanylyl cyclases function redundantly in the AFD neurons to mediate thermosensation by C. elegans.

Animals modify behavioral outputs in response to environmental changes. C elegans exhibits thermotaxis, where well-fed animals show attraction to their cultivation temperature on a thermal gradient without food. We show here that feeding-state-dependent modulation of thermotaxis is a powerful behavioral paradigm for elucidating the mechanism underlying neural plasticity, learning, and memory in higher animals. Starved experience alone could induce aversive response to cultivation temperature. Changing both cultivation temperature and feeding state simultaneously evoked transient attraction to or aversion to the previous cultivation temperature: recultivation of starved animals with food immediately induced attraction to the temperature associated with starvation, although the animals eventually exhibited thermotaxis to the new temperature associated with food. These results suggest that the change in feeding state quickly stimulates the switch between attraction and aversion for the temperature in memory and that the acquisition of new temperature memory establishes more slowly. We isolated aho (abnormal hunger orientation) mutants that are defective in starvation-induced cultivation-temperature avoidance. Some aho mutants responded normally to changes in feeding state with respect to locomotory activity, implying that the primary thermosensation followed by temperature memory formation remains normal and the modulatory aspect of thermotaxis is specifically impaired in these mutants.

HEN-1, a secretory protein with an LDL receptor motif, has been found to regulate sensory integration and learning in Caenorhabditis elegans. It appears that C. elegans can be an ideal model organism for studying informational processing.

An amphid sensory neuron is an important thermosensory neuron and the interneurons AIY and AIZ are responsible for thermophilic and cryophilic movement, respectively, the regulation in opposite direction of which is necessary for thermotaxis. Thermal stimulus is a major factor that influences animal behavior. In Caenorhabditis elegans, the range in the ability to recognize temperature changes is high providing an ideal system to study the cellular and molecular processes in thermosensation and thermal information storage.

Innexins in invertebrates are considered to play roles similar to those of connexins and pannexins in vertebrates. However, it remains poorly understood how innexins function in biological phenomena including their function in the nervous systems. Here, we identified inx‐4, a member of the innexin family in C. elegans, by a forward screening of thermotaxis‐defective mutants. The inx‐4 mutants exhibited abnormal migration to a temperature slightly higher than the cultivation temperature, called mild thermophilic behavior. Rescue experiments revealed that INX‐4 acts in the major thermosensory neuron AFD to regulate thermotaxis behavior. INX‐4::GFP fusion protein localized exclusively along axons in AFD neurons. In addition, over‐expression of INX‐4 in AFD neurons induced a cryophilic behavior, which is opposite to inx-4 mutants. Our findings suggest that INX‐4/Innexin in AFD may fine‐tune the execution of thermotaxis behavior when moving to desired temperatures. [ABSTRACT FROM AUTHOR]