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Comparison of histological responses and tissue damage expansion between resistant and susceptible Pinus thunbergii infected with pine wood nematode Bursaphelenchus xylophilus
Authors:Dai Kusumoto  Takashi Yonemichi  Hiroki Inoue  Tomonori Hirao  Atsushi Watanabe  Toshihiro Yamada
Affiliation:1. The University of Tokyo Tanashi Forest, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-8 Midori-cho, Nishi-tokyo, Tokyo, 188-0002, Japan
2. Education and Research Center, The University of Tokyo Forests, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-8657, Japan
6. The University of Tokyo Chiba Forest, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 770 Amatsu, Kamogawa, Chiba, 299-5503, Japan
3. Arboricultural Research Institute, The University of Tokyo Forests, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 457 Kano, Minami-izu-cho, Kamo-gun, Shizuoka, 415-0304, Japan
4. Forest Tree Breeding Center, Forestry and Forest Products Research Institute, 3809-1 Ishi, Juo-cho, Hitachi, Ibaraki, 319-1301, Japan
5. Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka, 812-8581, Japan
Abstract:Pine wilt disease caused by the pine wood nematode (PWN), Bursaphelenchus xylophilus, has been epidemic and has had disastrous impacts on pine forests and forest ecosystems in eastern Asia. Many pine species in this area are susceptible to this disease. Pinus thunbergii is particularly susceptible. In Japan, tree breeders have selected surviving trees from severely damaged forests as resistant candidates, and have finally established several resistant varieties of P. thunbergii. However, this breeding procedure requires much time and effort due to the lack of physiological and phenotypical information about resistance. To investigate the resistance mechanisms of selected P. thunbergii, we compared histochemical responses, tissue damage expansion, and PWN distribution in resistant and susceptible clones of P. thunbergii after PWN inoculation. The results suggested that the mechanisms of resistance are as follows: damage expansion in the cortex, cambium, and xylem axial resin canals are retarded in resistant trees soon after inoculation, probably due to the induction of wall protein-based defenses. Suppression of PWN reproduction was particularly caused by inhibition of damage expansion in the cambium. The slow expansion of damage in each tissue provides time for the host to complete the biosynthesis of lignin in the walls of cells that surround the damaged regions. This lignification of cell walls is assumed to effectively inhibit the migration and reproduction of the PWNs. The mechanism of initial damage retardation is presumed to be a key for resistance.
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