Plants are continuously exposed to deleterious biotic and abiotic stresses. In rice, WRKY45 is a crucial transcription factor in the salicylic acid defense signaling pathway, on which several chemical-defense inducers act. We have developed transgenic rice lines using WRKY45 that are resistant to multiple diseases, and during that work, found that the extremely strong disease resistance that results from the overexpression of WRKY45 renders rice hypersensitive to low temperature and high salinity due to antagonistic crosstalk of defense signaling against abiotic stress signaling. Here, we introduce molecular mechanisms underlying the trade-off between disease resistance and abiotic stress responses, highlighting strategies involving crosstalk between signaling pathways.

Rice blast, caused by the fungal pathogen Magnaporthe oryzae, is one of the most economically devastating diseases of food crops worldwide. Approaches to controlling blast disease have mainly been via the deployment of nucleotide-binding leucine-rich repeat receptors (NLRs). M. oryzae secretes a battery of small effector proteins to manipulate host functions for its successful infection, and some of them are recognized by host NLR proteins as avirulence effectors (AVRs), which turns on strong immunity. Therefore, the analysis of interactions between AVRs and their cognate NLR proteins provide crucial insights into the molecular basis of plant–fungal interactions.

Ceratocystis ficicola causes serious wilt disease in many fig orchards in Japan. To elucidate the process of symptom development in the disease, we macroscopically examined external symptoms and assessed xylem sap flow in fig plants inoculated with C. ficicola. External symptoms were classified as follows: (1) no external symptoms (NS), (2) leaf wilt (LW), and (3) dead (D). Perithecial development of C. ficicola on stem segments was observed within a relatively narrow range, 5 cm above and below the inoculation site of each NS plants. In plants with LW, perithecial development was observed on segments from a wider range, 10 cm above and below the inoculation sites. In D plants, perithecial development was observed on segments from a narrower range than that of the LW plants. Xylem discoloration was observed near the inoculation site, in the range of 5 cm above and 10 cm below the inoculation site, in NS plants. The maximum percentage of xylem discoloration (discolored area/cross-section area) in each NS plants ranged from 1.3 to 16.4%. The range of discoloration extended 15 cm above and 10 cm below the inoculation site, and the maximum value of the xylem discoloration in each LW plants ranged from 16.5 to 52.4%. Discoloration similar to that in LW was observed in each D plants. Water conductivity was evaluated as the percentage of stem dyed pink with acid fuchsin solution absorbed by the roots. Water conductivity by NS plants was similar to that in the controls. Water conductivity was lower in each LW plant than in the NS, and the minimum dyed pink area on cut stem segments was less than 4.6%. The dyed area was barely recognizable in D plants. Leaves of LW or D plants did not have any dyed areas. Symptom development after inoculation of fig trees with C. ficicola can be explained as follows: (1) Xylem discoloration expands from the inoculation site corresponding to the expanding distribution of C. ficicola. (2) Xylem discoloration is correlated with xylem dysfunction. (3) When conductivity of the xylem falls to a certain threshold value in a cross section near the inoculation site, the water supply to leaves decreases, causing leaf wilting. (4) Extensive xylem dysfunction results in tree death.

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.

A new disease of bird’s-nest fern (Asplenium nidus, cv. Emerald) with dark-green, water-soaked lesions on the leaves has been found in Fukuoka Prefecture, Japan since approximately 1996. The lesions gradually extended from the lower part of the leaves near the soil to the tip of the leaves under high humidity. Affected leaves and petioles softened, turned dark-brown and dry. When severely infected, plants had rotted petioles and withered. A causal fungus was isolated from the infected tissues, and these isolates caused the same symptoms on cvs. Abis and Emerald of bird’s-nest fern in inoculation tests. The pathogen was identified as Rhizoctonia solani based on the morphological and cultural characteristics, and the hyphal anastomosis group and the cultural type were determined as AG-1 IB, confirmed with PCR analysis using specific DNA primer sets for the anastomosis groups. The name leaf blight was proposed for this disease on bird’s-nest fern.