Abstract
Temperature sensing is essential for the survival of living organisms. Some reptile embryos can reposition themselves within the egg to seek optimal temperatures, but the molecular sensors involved in this temperature detection remain unknown. Here, we show that such thermotaxic behavior is directly determined by the activation of two heat-sensitive ion channels of the turtle: the transient receptor potential ankyrin 1 (MrTRPA1) and transient receptor potential vanilloid-1 (MrTRPV1). These two TRP channels were found to exhibit distinctive distributions among turtle dorsal root ganglion (DRG) neurons. Additionally, our laser irradiation assays illustrated that the heat activation thresholds of MrTRPA1 and MrTRPV1 are consistent with the mild (28-33°C) and noxious (>33°C) heat determined by behavioral tests, respectively. Further pharmacological studies have demonstrated that ligand-induced intervention of MrTRPA1 or MrTRPV1 is sufficient to mimic heat stimuli or block temperature signaling, causing changes in embryo movement. These findings indicate that the initiation of thermotaxic response in turtle embryos relies on a delicate functional balance between the heat activation of MrTRPA1 and MrTRPV1. Our study reveals, for the first time, a unique molecular mechanism underlying thermal detection: the two TRP channels act as a physiological tandem to control the thermotaxic behavior of turtle embryos.