Lepidopteran species utilize chemical signal called sex pheromone for intraspecific sexual communication. Here we summarize how male moths, receivers of pheromone, process the chemical signal. We first describe the structure of the olfactory neural circuits in the brain. We then focus about processing for multicomponent pheromones and neuronal signal which command walking behavior for odor-source localization behavior. We discuss about several hypotheses about the neuronal mechanisms by exemplifying the knowledge in insects and other model organisms. These facilitate to understand the diversity and evolution of pheromone communication system.

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The c-Jun N-terminal kinase(JNK), which belongs to the mitogen-activated protein kinase family, plays important roles in a broad range of physiological processes. JNK is controlled by two upstream regulators, mitogen-activated protein kinase kinase(MKK)4 and MKK7, which are activated by various MAPKKKs. These two MAPKKs directly phosphorylate specific Tyr and Thr residues located in the activation loop of the JNK protein and activate this kinase in response to environmental stress, pro-inflammatory cytokines or developmental cues. Recent studies, including the analysis with MKK4 and MKK7 knockout mice, have increased our understanding of the physiological roles of JNK signaling in the brain and liver formation, but the precise functions of JNK signaling during early embryogenesis have remained a mystery until relatively recently. Studies employing a range of animal models have now revealed the essential roles of MAPKKs in diverse developmental contexts, including in dorsoventral patterning, convergent extension and somitogenesis. Focusing primarily on extensive work done in zebrafish models, this paper summarizes the functional properties of MKK4 and MKK7 during vertebrate and invertebrate development, and the mechanisms by which these two MAPKKs regulate multiple steps in the formation of the body plan of an organism.

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Once a hornet is captured within a bee ball, the temperature, CO₂ concentration, and humidity in the bee ball are increased rapidly by honeybees’ respiration. Within 5 min after capture, the temperature reaches 46℃ and CO₂ concentration 4％, and the relative humidity rises gradually as high as 90％ or above in 3-4 min. Normally, the hornet dies within about 10 min in the bee ball. To investigate conditional changes within the bee ball, i.e., the main causes of hornet mortality, we determined the lethal temperature on the 10-minute exposure of hornets in various conditions of the temperature, humidity, and CO₂/O₂ concentration. In expiratory air (3.7％ CO₂), the lethal temperature was 2℃ or more lower than that of the normal atmosphere. All four hornet species used in the experiment were killed at 44-46℃. Death was not caused by oxygen deficiency because the lethal temperature shows no change even if oxygen is supplied to compensate for the reduced oxygen due to increased CO₂. Honeybees adapt to a high CO₂ and high humidity environment because they normally cluster. Thus, the lethal temperature of honeybees is 50-51℃ in such an environment, almost the same as that in the normal atmosphere. Japanese honeybees generate heat by intense respiration. They simultaneously produce a high CO₂ and high humidity environment to lower the lethal temperature of hornets. European honeybees are usually victims of genocide without our protection in the habitat of hornets, but Japanese honeybees kill the predator without sacrificing themselves using heat and all by-products of respiration.

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