Graduate School of Natural Science, Konan University, Kobe 658-8501, Japan.
Center for Integrative Brain Research, Seattle Children's Research Institute, 1900 Ninth Ave., Seattle, WA 98101, USA.
Sci Adv. 2019 Feb 6;5(2):eaav3631. doi: 10.1126/sciadv.aav3631. eCollection 2019 Feb.
Adaptive responses to external temperatures are essential for survival in changing environments. We show here that environmental oxygen concentration affects cold acclimation in and that this response is regulated by a KCNQ-type potassium channel, KQT-2. Depending on culture conditions, mutants showed supranormal cold acclimation, caused by abnormal thermosensation in ADL chemosensory neurons. ADL neurons are responsive to temperature via transient receptor potential channels-OSM-9, OCR-2, and OCR-1-with OCR-1 negatively regulating ADL function. Similarly, KQT-2 and KQT-3 regulate ADL activity, with KQT-2 positively regulating ADL function. Abnormal cold acclimation and acute temperature responses of ADL neurons in mutants were suppressed by an oxygen-receptor mutation in URX coelomic sensory neurons, which are electrically connected to ADL via RMG interneurons. Likewise, low oxygen suppressed supranormal cold acclimation. These data thus demonstrate a simple neuronal circuit integrating two different sensory modalities, temperature and oxygen, that determines cold acclimation.
适应外部温度的变化对于在不断变化的环境中生存至关重要。我们在这里表明，环境氧气浓度会影响 的冷驯化，而这种反应是由一种 KCNQ 型钾通道 KQT-2 调节的。根据培养条件的不同， 突变体表现出超正常的冷驯化，这是由于 ADL 化学感觉神经元的异常热感觉引起的。ADL 神经元通过瞬时受体电位通道-OSM-9、OCR-2 和 OCR-1 对温度做出反应，其中 OCR-1 负调节 ADL 的功能。同样，KQT-2 和 KQT-3 调节 ADL 的活性，其中 KQT-2 正向调节 ADL 的功能。URX 体腔感觉神经元中的氧受体突变抑制了 突变体中 ADL 神经元的异常冷驯化和急性温度反应，URX 体腔感觉神经元通过 RMG 中间神经元与 ADL 电连接。同样，低氧也抑制了超正常的 冷驯化。这些数据表明，一个简单的神经元回路整合了两种不同的感觉模式，温度和氧气，从而决定了冷驯化。
