Molecular physiology regulating cold tolerance and acclimation of <i>Caenorhabditis elegans</i>

Abstract

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.

Head-tail-head neural wiring underlies gut fat storage in Caenorhabditis elegans temperature acclimation

“…C. elegans possesses cold tolerance, depending on the cultivation temperature ( Fig. 1 A and B ) ( 3 – 7 ). Moreover, temperature acclimation, a phenomenon in which animals acclimate to a new temperature in a few hours, has been observed ( 4 , 5 ).…”

“…1 A and B ) ( 3 – 7 ). Moreover, temperature acclimation, a phenomenon in which animals acclimate to a new temperature in a few hours, has been observed ( 4 , 5 ). Our previous studies reported that ASJ thermosensory neurons respond to thermal stimuli via the cyclic guanosine monophosphate (cGMP)-gated channels TAX-2/TAX-4 ( 3 ).…”

Anticancer drugs affect temperature signaling and epigenetic factors in the cold tolerance of Caenorhabditis elegans

“…In animals cultivated at 15°C, the mutants of the DEG/ENaC-type mechanoreceptor DEG-1 and xanthine dehydrogenase XDH-1 exhibited an abnormal decrease in cold tolerance. In the sensory neuron ASG, DEG-1 receives temperature information and transmits it to the interneurons AVH and AIN, wherein XDH-1 acts as a modulator of the neuronal activity of AVH and AIN 26,27 . Under 15°C cultivation condition, the epistasis analysis indicated that CPT affects cold tolerance downstream of DEG-1 and XDH-1 (Fig.…”

“…To determine the impact of chemical substances on tissues, we examined the drug effect in various mutants defective in genes that regulate cold tolerance or cold acclimation. XDH-1 encoding xanthine dehydrogenase controls cold tolerance by regulating the response to temperature in AIN and AVH 26,27 . Although wild-type animals cultivated at 15°C could survive at 2°C for 48 h, xdh-1 mutant control animals could not survive at 2°C (Fig.…”

“…The DEG/ENaC-type mechanoreceptor DEG-1, also known as a mechanosensory neuron, receives information on not only mechanical stimuli but also temperature from ASG. The information on temperature stimuli received from ASG is transmitted to the downstream interneurons AVH and AIN via XDH-1 encoding xanthine dehydrogenase 26,27 . Thus, multiple novel genes could be identi ed and their molecular mechanisms, neural circuits, and tissue networks could be elucidated by investigating cold tolerance and cold acclimation.…”