Environmental oxygen concentration affects cold acclimation via KQT potassium channel in the nematode Caenorhabditis elegans.

Temperature is critical for the survival and proliferation of animals, which must be adapted to cope with environmental temperature changes. In this study, we demonstrated natural variations in the phenotypes of temperature tolerance and temperature acclimation of the nematode Caenorhabditis elegans, and we decoded whole genome sequence of six natural variations, which enabled us to map responsible gene polymorphisms onto specific chromosomal regions. The C. elegans laboratory strain, N2, survives at 2 °C after cultivation at 15 °C but is unable to survive at 2 °C after cultivation at 20 or 25 °C. This cultivation-temperature-dependent cold tolerance occurs within a few hours after the temperature shift and is termed cold acclimation. We measured the cold tolerance and cold acclimation phenotypes of many natural variants isolated from various areas. CB4854 showed weaker cold tolerance associated with gene polymorphisms on the sex chromosome decoded by whole genome sequencing. Variable cold acclimation phenotypes were exhibited in twelve natural isolates and the large difference was seen between CB4856 and AB1 strains. CB4856, isolated from Hawaii, acclimated slowly to a new temperature, whereas AB1, isolated from Australia, acclimated rapidly. By the whole genome sequencing analysis, two different polymorphisms responsible for the accelerated cold acclimation in AB1 were mapped to specific chromosomal regions.Electronic supplementary materialThe online version of this article (doi:10.1007/s00360-016-1011-3) contains supplementary material, which is available to authorized users.

Many organisms can survive and proliferate in changing environmental temperatures. Here, we introduce a molecular physiological mechanism for cold tolerance and acclimation of the nematode Caenorhabditis elegans on the basis of previous reports and a new result. Three types of thermosensory neurons located in the head, ASJ, ASG, and ADL, regulate cold tolerance and acclimation. In ASJ, components of the light-signaling pathway are involved in thermosensation. In ASG, mechanoreceptor DEG-1 acts as thermoreceptor. In ADL, transient receptor potential channels are thermoreceptors; however, the presence of an additional unidentified thermoreceptor is also speculated. ADL thermoresponsivity is modulated by oxygen sensory signaling from URX oxygen sensory neurons via hub interneurons. ASJ releases insulin and steroid hormones that are received by the intestine, which results in lipid composition changing with cold tolerance. Additionally, the intestinal transcriptional alteration affects sperm functions, which in turn affects the thermosensitivity of ASJ; thus, the neuron-intestine-sperm-neuron tissue circuit is essential for cold tolerance.

Temperature is a critical and continuous environmental factor that directly affects biochemical processes within organisms. Animals may habituate to environmental temperature change using a range of mechanisms. To investigate mechanisms of temperature habituation, we exposed Caenorhabditis elegans nematodes to a temperature of 2°C, which is much colder than their normal growing temperature (approximately 10-28°C) and we evaluated their survival rate in recovery from this cold shock. The survival rate after cold shock was different between animals grown at 15°C and 25°C, suggesting that C. elegans exhibits temperature-habituation-linked cold tolerance. Here we show in detail two protocols: a standard cold-tolerance assay after cultivation at constant temperature; and a multistep temperature-shifted cold-tolerance assay.

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Drugs are vital for maintaining the body healthy and treating diseases. As most drugs have side effects, it is important to gain a complete understanding of their action mechanisms. However, significant cost and time are involved in elucidating their mechanisms. We conducted drug screening at a low cost and in a short time using the phenomenon of cold tolerance in the nematode Caenorhabditis elegans. Among ~ 4000 drugs, we screened the anticancer drugs leptomycin B and camptothecin that affect cold tolerance. Leptomycin B and camptothecin inhibited molecular pathway(s) downstream of the thermosensory signaling via the cGMP-dependent channel TAX-4 in ASJ thermosensory neurons and the thermoreceptor DEG-1 in ASG thermosensory neurons. Leptomycin B affected cold tolerance by inhibiting the molecular pathway upstream of the insulin receptor DAF-2 that regulates cold tolerance in the intestine. Camptothecin decreased the expression levels of genes required for epigenetic processes, such as hrde-1 and deps-1 encoding Argonaute and constitutive P granule protein, respectively. Moreover, hrde-1 and deps-1 mutants exhibited abnormal cold tolerance. This study established an experimental model for drug screening using the cold tolerance of C. elegans and proposed that an anticancer drug upregulates cold tolerance via temperature signaling and epigenetic regulation.