RT Journal Article SR Electronic T1 Cold acclimation via the KQT-2 potassium channel is modulated by oxygen in Caenorhabditis elegans JF Science Advances JO Sci Adv FD American Association for the Advancement of Science SP eaav3631 DO 10.1126/sciadv.aav3631 VO 5 IS 2 A1 Okahata, Misaki A1 Wei, Aguan D. A1 Ohta, Akane A1 Kuhara, Atsushi YR 2019 UL http://advances.sciencemag.org/content/5/2/eaav3631.abstract AB 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.