Temperature Acclimation and Cold Tolerance in are Regulated by Multiorgan Coordination.

To ensure survival and reproduction, organisms must continually adapt to environmental fluctuations, such as temperature, humidity, oxygen level, and salinity. Particularly, temperature profoundly influences biochemical reactions crucial for survival. Here, we present the mechanisms employed by the nematode to anticipate and respond to cold temperatures.

Molecular, neural, and tissue circuits underlying physiological temperature responses in Caenorhabditis elegans.

Temperature is a constant environmental factor on Earth, acting as a continuous stimulus that organisms must constantly perceive to survive. Organisms possess neural systems that receive various types of environmental information, including temperature, and mechanisms for adapting to their surroundings. This paper provides insights into the neural circuits and intertissue networks involved in physiological temperature responses, specifically the mechanisms of "cold tolerance" and "temperature acclimation," based on an analysis of the nematode Caenorhabditis elegans as an experimental system for neural and intertissue information processing.

Cold Tolerance in the Nematode Caenorhabditis elegans.

Organisms receive environmental information and respond accordingly in order to survive and proliferate. Temperature is the environmental factor of most immediate importance, as exceeding its life-supporting range renders essential biochemical reactions impossible. In this chapter, we introduce the mechanisms underlying cold tolerance and temperature acclimation in a model organism-the nematode Caenorhabditis elegans, at molecular and physiological levels.

The intron binding protein EMB-4 is an opposite regulator of cold and high temperature tolerance in .

Adaptation and tolerance to changes in heat and cold temperature are essential for survival and proliferation in plants and animals. However, there is no clear information regarding the common molecules between animals and plants. In this study, we found that heat, and cold tolerance of the nematode is oppositely regulated by the RNA-binding protein EMB-4, whose plant homolog contains polymorphism causing heat tolerance diversity.

G protein-coupled receptor-based thermosensation determines temperature acclimatization of Caenorhabditis elegans.

Animals must sense and acclimatize to environmental temperatures for survival, yet their thermosensing mechanisms other than transient receptor potential (TRP) channels remain poorly understood. We identify a trimeric G protein-coupled receptor (GPCR), SRH-40, which confers thermosensitivity in sensory neurons regulating temperature acclimatization in Caenorhabditis elegans. Systematic knockdown of 1000 GPCRs by RNAi reveals GPCRs involved in temperature acclimatization, among which srh-40 is highly expressed in the ADL sensory neuron, a temperature-responsive chemosensory neuron, where TRP channels act as accessorial thermoreceptors.

Temperature acclimation: Temperature shift induces system conversion to cold tolerance in C. elegans.

Acclimation to temperature is one of the survival strategies used by organisms to adapt to changing environmental temperatures. Caenorhabditis elegans' cold tolerance is altered by previous cultivation temperature, and similarly, past low-temperature induces a longer lifespan. Temperature is thought to cause a large shift in homeostasis, lipid metabolism, and reproduction in the organism because it is a direct physiological factor during chemical events.

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

Animals maintain the ability to survive and reproduce by acclimating to environmental temperatures. We showed here that exhibited temperature acclimation plasticity, which was regulated by a head-tail-head neural circuitry coupled with gut fat storage. After experiencing cold, individuals memorized the experience and were prepared against subsequent cold stimuli.

Molecular physiology regulating cold tolerance and acclimation of Caenorhabditis elegans.

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.

OSM-9 and OCR-2 TRPV channels are accessorial warm receptors in Caenorhabditis elegans temperature acclimatisation.

Caenorhabditis elegans (C. elegans) exhibits cold tolerance and temperature acclimatisation regulated by a small number of head sensory neurons, such as the ADL temperature-sensing neurons that express three transient receptor potential vanilloid (TRPV) channel subunits, OSM-9, OCR-2, and OCR-1. Here, we show that an OSM-9/OCR-2 regulates temperature acclimatisation and acts as an accessorial warmth-sensing receptor in ADL neurons.

The mechanoreceptor DEG-1 regulates cold tolerance in Caenorhabditis elegans.

Caenorhabditis elegans mechanoreceptors located in ASG sensory neurons have been found to sense ambient temperature, which is a key trait for animal survival. Here, we show that experimental loss of xanthine dehydrogenase (XDH-1) function in AIN and AVJ interneurons results in reduced cold tolerance and atypical neuronal response to changes in temperature. These interneurons connect with upstream neurons such as the mechanoreceptor-expressing ASG.

Cold acclimation via the KQT-2 potassium channel is modulated by oxygen in .

Adaptive responses to external temperatures are essential for survival in changing environments. We show here that environmental oxygen concentration affects cold acclimation in and that this response is regulated by a KCNQ-type potassium channel, KQT-2. Depending on culture conditions, mutants showed supranormal cold acclimation, caused by abnormal thermosensation in ADL chemosensory neurons.

Endoribonuclease ENDU-2 regulates multiple traits including cold tolerance via cell autonomous and nonautonomous controls in .

Environmental temperature acclimation is essential to animal survival, yet thermoregulation mechanisms remain poorly understood. We demonstrate cold tolerance in as regulated by paired ADL chemosensory neurons via Ca-dependent endoribonuclease (EndoU) ENDU-2. Loss of ENDU-2 function results in life span, brood size, and synaptic remodeling abnormalities in addition to enhanced cold tolerance.

Natural variations of cold tolerance and temperature acclimation in 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.

Diverse Regulation of Temperature Sensation by Trimeric G-Protein Signaling in Caenorhabditis elegans.

Temperature sensation by the nervous system is essential for life and proliferation of animals. The molecular-physiological mechanisms underlying temperature signaling have not been fully elucidated. We show here that diverse regulatory machinery underlies temperature sensation through trimeric G-protein signaling in the nematode Caenorhabditis elegans.

Caenorhabditis elegans homologue of Prox1/Prospero is expressed in the glia and is required for sensory behavior and cold tolerance.

The Caenorhabditis elegans (C. elegans) amphid sensory organ contains only 4 glia-like cells and 24 sensory neurons, providing a simple model for analyzing glia or neuron-glia interactions. To better characterize glial development and function, we carried out RNA interference screening for transcription factors that regulate the expression of an amphid sheath glial cell marker and identified pros-1, which encodes a homeodomain transcription factor homologous to Drosophila prospero/mammalian Prox1, as a positive regulator.

Sperm Affects Head Sensory Neuron in Temperature Tolerance of Caenorhabditis elegans.

Tolerance to environmental temperature change is essential for the survival and proliferation of animals. The process is controlled by various body tissues, but the orchestration of activity within the tissue network has not been elucidated in detail. Here, we show that sperm affects the activity of temperature-sensing neurons (ASJ) that control cold tolerance in Caenorhabditis elegans.

Light and pheromone-sensing neurons regulates cold habituation through insulin signalling in Caenorhabditis elegans.

Temperature is a critical environmental stimulus that has a strong impact on an organism's biochemistry. Animals can respond to changes in ambient temperature through behaviour or altered physiology. However, how animals habituate to temperature is poorly understood.

Molecular mechanism for trimetric G protein-coupled thermosensation and synaptic regulation in the temperature response circuit of Caenorhabditis elegans.

How the nervous system controls the sensation and memory of information from the environment is an essential question. The nematode Caenorhabditis elegans is a useful model for elucidating neural information processing that mediates sensation and memory. The entire nervous system of C.

Development of a human herpesvirus 6 species-specific immunoblotting assay.

In order to assess the full spectrum of human herpesvirus 6A (HHV-6A)- and HHV-6B-associated diseases, we sought to develop an HHV-6 species-specific serological assay based on immunoblot analysis. The immunodominant proteins encoded by open reading frame U11, p100 for HHV-6A (strain U1102) and 101K for HHV-6B (strain Z29), were selected to generate virus species-specific antigens. Recombinant p100 and 101K were produced in a prokaryotic expression system.

Herpes simplex virus type 1 UL14 tegument protein regulates intracellular compartmentalization of major tegument protein VP16.

Background: Herpes simplex virus type 1 (HSV-1) has a complicated life-cycle, and its genome encodes many components that can modify the cellular environment to facilitate efficient viral replication. The protein UL14 is likely involved in viral maturation and egress (Cunningham C. et al), and it facilitates the nuclear translocation of viral capsids and the tegument protein VP16 during the immediate-early phase of infection (Yamauchi Y.

Novel and conserved protein macoilin is required for diverse neuronal functions in Caenorhabditis elegans.

Neural signals are processed in nervous systems of animals responding to variable environmental stimuli. This study shows that a novel and highly conserved protein, macoilin (MACO-1), plays an essential role in diverse neural functions in Caenorhabditis elegans. maco-1 mutants showed abnormal behaviors, including defective locomotion, thermotaxis, and chemotaxis.

Mitochondria and viruses.

Mitochondria are involved in a variety of cellular metabolic processes, and their functions are regulated by extrinsic and intrinsic stimuli including viruses. Recent studies have shown that mitochondria play a central role in the primary host defense mechanisms against viral infections, and a number of novel viral and mitochondrial proteins are involved in these processes. Some viral proteins localize in mitochondria and interact with mitochondrial proteins to regulate cellular responses.

Recombinant human monoclonal antibodies to human cytomegalovirus glycoprotein B neutralize virus in a complement-dependent manner.

Human antibodies specific for HCMV are currently considered as potential anti-HCMV therapeutic agents. In this study, we used a combinatorial human antibody library to isolate and characterize complete human monoclonal antibodies that effectively neutralize HCMV in a complement-dependent manner. One hundred and six clones were isolated in two independent screens using HCMV virions and recombinant glycoprotein B, gB654, as antigens.