Cold acclimation via the KQT-2 potassium channel is modulated by oxygen in <i>Caenorhabditis elegans</i>.

Abstract

Adaptive responses to external temperatures are essential for survival in changing environments. We show here that environmental oxygen concentration affects cold acclimation in <i>Caenorhabditis elegans</i> and that this response is regulated by a KCNQ-type potassium channel, KQT-2. Depending on culture conditions, <i>kqt-2</i> 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 <i>kqt-2</i> 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 <i>kqt-2</i> cold acclimation. These data thus demonstrate a simple neuronal circuit integrating two different sensory modalities, temperature and oxygen, that determines cold acclimation.