Physiological Process of the Symptom Development and Resistance Mechanism in Pine Wilt Disease

Abstract

Pathophysiological changes during the symptom development of pine wilt disease are reconsidered from recent investigations. The symptom development is divided into two stages: the early and the advanced stages. In the early stage, small number of nematodes migrate in cortex, then in xylem of the stem, and induce denaturation and necrosis of parenchyma cells. These changes in parenchyma are regarded as defense reactions of pines which result in terpene synthesis in xylem cells and embolism in tracheids. Such changes in the early stage can be induced in both susceptible and resistant pine species by either virulent or avirulent isolates of pinewood nematode (Bursaphelenchus xylophilus), or by B. mucronatus. No change occur in physiological status of leaves, and nematode reproduction is suppressed during this stage. Pine trees can survive if symptom does not progress from this stage. The symptoms of the advanced stage usually occur only in susceptible pines infected by virulent nematode isolates. At the beginning of the advanced stage, enhanced ethylene production by stem which coincides with cambial destruction occurs, and results in embolism of the outermost xylem in the portion. The embolism causes decrease in leaf water potential and cessation of photosynthesis. After cessation of photosynthesis, symptoms develop drastically with a burst of nematode population. There seems to be some unknown mechanism which suppress nematode reproduction and invasion to the cambial zone. This mechanism is thought to be photosynthesis-dependent, so that in photosynthesis-decreased conditions, even avirulent nematodes can multiply and invade cambium to induce tree death. Water stress in hot and dry summer should accelerates symptom development from the early to the advanced stage through such decrease of photosynthesis-dependent "cambial resistance."

Evidence for the involvement of ACC deaminase from Pseudomonas putida UW4 in the biocontrol of pine wilt disease caused by Bursaphelenchus xylophilus

“…It has been previously demonstrated that ethylene production increases in pine trees during PWN invasion, suggesting that increased ethylene levels are, at least partially, responsible for the development of PWD symptoms (Mori and Inoue 1986;Fukuda et al 1994;Fukuda 1997). The data presented here are consistent with the possibility that, through ACC deaminase production, P. putida UW4 reduces the deleterious ethylene levels in pine seedlings induced by PWN invasion, thereby decreasing the disease severity and progression.…”

“…If the pathogen action is intense, the autocatalytic ethylene synthesis and the consequent high levels of ethylene can be responsible for plant damage and ultimately its death (van Loon 1984). Interestingly, several authors reported an increase of ethylene levels in pine upon PWN invasion, and suggest that ethylene can play a role in PWD development (Mori and Inoue 1986;Fukuda et al 1994;Fukuda 1997).…”

The Developmental Process of Xylem Embolisms in Pine Wilt Disease Monitored by Multipoint Imaging Using Compact Magnetic Resonance Imaging

“…These results confirm the susceptibility of the transition zone to cavitation. Previous studies suggest that the death of phloem and cambium is also an important symptom that occurs at the same time as embolisms in the current-year xylem (Fukuda et al, 1992b;Fukuda, 1997). In our observations, the phloem and cambium did not dry up (die) until runaway embolism occurred (Figs.…”

“…Because the nematode itself rarely enters into the tracheids of living pine (Ichihara et al, 2000), some researchers have attributed the abrupt increase in embolized tracheids to modification of the surface tension of xylem sap (Ikeda and Kiyohara, 1995), cellulase production of PWN (Odani et al, 1985), released oily substance occluding the tracheid lumen and pit membrane (Nobuchi et al, 1984;Hara and Futai, 2001), and abnormal leaks of oleoresin from resin canals (Sasaki et al, 1984). In addition, some researchers have suggested that some compounds, such as terpenoids released from parenchyma cells (Kuroda, 1989(Kuroda, , 1991 and ethylene produced in xylem (Fukuda, 1997), can induce xylem embolism, based on the results of artificial injection of these compounds into the stem. In coniferous species, a significant increase of the cavitation event by water stress is usually synchronized with a drastic decrease of water potential (Brodribb and Cochard, 2009).…”

“…They can then move through the resin canals to reach almost all parts of the stem and branches fairly rapidly (Hashimoto and Kiyohara, 1973;Kuroda and Ito, 1992;Kuroda, 2008). In infected pine trees, both virulent PWN (Sasaki et al, 1984;Tamura et al, 1988;Kuroda, 1991) and avirulent PWN (Fukuda et al, 1992b;Ikeda and Kiyohara, 1995;Fukuda, 1997) cause some localized embolisms in the xylem. The virulent PWN then significantly multiply in the pine stem (Mamiya, 1975;Kiyohara and Suzuki, 1978;Kiyohara and Bolla, 1990), and the leaf-water potential abruptly decreases, inducing death (Hashimoto, 1976;Ikeda et al, 1990;Fukuda et al, 1992a).…”