2016 Volume 82 Issue 4 Pages 310-317
Ceratocystis ficicola is causing serious wilt disease in many fig orchards in Japan. To elucidate the mechanisms of disease development, we inoculated fig cuttage seedlings with the pathogen and periodically harvested stems for light microscopy to examine the distribution of C. ficicola and responses of host cells before the start of wilt symptoms. As shown by yellow to brown staining of the xylem in fig stems, secondary metabolism was activated in axial and ray parenchyma cells adjacent to hyphae, then the metabolites were secreted into vessels. Above 5 cm from the inoculated holes, few or no hyphae were observed, and accumulation of secondary metabolites was not extensive. When leaf wilting started, hyphae were abundant in the discolored xylem in which secondary metabolites had accumulated. In contrast, the cambium was not necrotic before the wilt symptoms. Symptoms developed as follows: (1) Hyphae of the pathogen elongate in vessels and invade the adjacent parenchyma cells. (2) Secondary metabolism is activated in parenchyma cells. (3) Dark brown discoloration occurs in xylem when the secondary metabolites are produced, and vessels become dysfunctional in the discolored areas. (4) Water supply to leaves decreases, and the wilt symptom starts.
