Cold acclimation via the KQT-2 potassium channel is modulated by oxygen in Caenorhabditis elegans
Cold acclimation via the KQT-2 potassium channel is modulated by oxygen in Caenorhabditis elegans
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DOI：
10.1126/sciadv.aav3631
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发表时间：
2019-02-01
期刊：
影响因子：
13.6
通讯作者：
Kuhara, Atsushi
中科院分区：
文献类型：
--
作者：
Okahata, Misaki;Wei, Aguan D.;Kuhara, Atsushi
对外界温度的适应性反应对于在不断变化的环境中生存至关重要。我们在这里表明，环境氧浓度影响秀丽隐杆线虫的冷驯化，这种反应是由kcnq型钾通道KQT-2调节的。根据培养条件的不同，kqt-2突变体表现出异常的冷适应，这是由ADL化学感觉神经元异常的热感觉引起的。ADL神经元通过瞬时受体电位通道osm -9、OCR-2和OCR-1对温度产生响应，其中OCR-1负向调节ADL功能。同样，KQT-2和KQT-3调节ADL活性，其中KQT-2正向调节ADL功能。通过RMG中间神经元与ADL电连接的URX体腔感觉神经元的氧受体突变抑制了kqt-2突变体ADL神经元异常的冷驯化和急性温度反应。同样，低氧抑制了超常的kqt-2冷驯化。因此，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，决定了冷适应。
Adaptive responses to external temperatures are essential for survival in changing environments. We show here that environmental oxygen concentration affects cold acclimation in Caenorhabditis elegans and that this response is regulated by a KCNQ-type potassium channel, KQT-2. Depending on culture conditions, kqt-2 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 kqt-2 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 kqt-2 cold acclimation. These data thus demonstrate a simple neuronal circuit integrating two different sensory modalities, temperature and oxygen, that determines cold acclimation.