The late Emeritus Professor I. Uritani in Nagoya University (1919–2010), one of the professors who contributed to the initial understanding of plant defense physiology, identified ipomeamarone as a phytoalexin produced in sweet potato infected with Ceratocystis fimbriata in 1956. He then primarily investigated phytoalexin biosynthetic pathways in sweet potato plants (Ipomoea batatas). He coined the catch phrase ‘‘From usual to unusual, from unusual to usual’’, defining that ordinary plant physiological phenomena and their targets and mechanisms comprise ‘‘usual’’ plant development to sustain life, while plant defense physiology deals with de novo physiological phenomena generated under ‘‘unusual’’ stress conditions, especially during infection by plant pathogens. He suggested that plant defense physiology focuses on secondary metabolism, which is fully expressed under stress conditions, and a total understanding of both plant physiology and plant defense physiology should enable us to reveal the entire life of the plant. His suggestion that multiple viewpoints are required to elucidate the spatial and temporal changes and the resultant complex phenomena in plant–pathogen interactions is still valuable. The late Emeritus Professor K. Tomiyama in Nagoya University (1917–1998) began detailed studies of hypersensitive cell death at the early stage of resistance reactions in potato tuber slices (Solanum tuberosum) infected with Phytophthora infestans, the potato late blight pathogen. Appressorium formation by the pathogen on a host cell causes cytoplasmic aggregation in the cell, defined as the rapid translocation of cytoplasm and the nucleus to the penetration site of the pathogen. The host cell itself finally dies, causing pathogen to die. The hypersensitive response (HR) that results in hypersensitive cell death is closely related to the production of reactive oxygen species (ROS). In 1983, Emeritus Professor N. Doke in Nagoya University found that superoxide (O2 ), a kind of ROS, was necessary to trigger hypersensitive responses in potato tubers inoculated with an avirulent race of P. infestans. The rapid production of O2 (oxidative burst) can inhibit pathogen infection, by inducing various other defense responses, and is observed in various plant tissues infected with various pathogens. Since then, ROS is considered to be a signal that initiates various other defense responses. However, it is not the only molecule required for inducing defense responses. O2 alone cannot induce hypersensitive cell death in plants; nitric oxide (NO) was thought to be another molecule involved in inducing hypersensitive cell death. In this article, I describe NO function in plant defense responses, the NO-producing system and resistant reactions induced by NO-producing elicitors.
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