3.8.3S
EVIDENCE FOR INDUCED SYSTEMIC RESISTANCE AS A MECHANISM FOR DISEASE SUPPRESSION IN HYDROPONIC SYSTEMS

TC PAULITZ and C CHEN

Dept. of Plant Science, Macdonald Campus of McGill University, Ste. Anne de Bellevue, Que, H9X 3V9 CANADA

Background and objectives
Some of the most important diseases in open or closed hydroponic systems are root and crown rots caused by Pythium spp., especially P. aphanidermatum. Although these systems may start out as pathogen free, inoculum can be introduced from contaminated water, transplants, soil, or insects. Pythium zoospores can readily be dispersed around entire system in a short time, resulting in crop loss. Plant growth-promoting rhizobacteria (PGPR) and other bacteria have been tested as biocontrol agents in hydroponic systems. Many of these bacteria act by producing antibiotics, siderophores, or through nutrient competition. In the early 1990s, evidence mounted that PGPR could also induce systemic resistance (ISR) against wilt and foliar pathogens. Since no work had been done on root-rotting pathogens such as Pythium, we initiated a program in 1991 to investigate the hypothesis that PGPR could also induce resistance in the root. Previous research had selected a number of Pseudomonas spp., including P. corrugata strain 13 and P. fluorescens strain 15, that reduced root rot of cucumber caused by P. aphanidermatum in rockwool production [1, 2].

Results and conclusions
To investigate the possibility of ISR, we used cucumber (Cucumis sativus cv. Corona) growing in rockwool as a model system. Roots were split into two separate pots, one side was treated with bacterial suspensions of strain 13, strain 15, or water. The other side was treated zoospores of P. aphaniderinatum or water, either simultaneous with bacterial inoculation or 1 week later. Disease incidence and severity were decreased and root volume was increased in treatments where the pathogen was spatially separated from the biocontrol agent [3]. To provide further proof of ISR, the activities of defense enzymes such as phenylalanine ammonia lyase (PAL), peroxidase (PO), and polyphenoloxidase (PPO) were examined in roots induced with different strains of PGPR. Strain 13 and P. aureofaciens strain 63-28 induced higher levels of these enzymes 2-5 days after bacterization before challenge with the pathogen. Challenge with the pathogen induced even higher levels of enzymes, but after challenge there were no differences between bacterized and non bacterized treatments [4]. This same increase in defense enzyme activity was also detected on the opposite side of split root systems, when one side was bacterized and the other side (induced) was treated with buffer, indicating a translocated effect [5]. The rate at which P. aphanidermatum moved up the root system to the crown from a root tip inoculation was significantly reduced when the opposite side was bacterized with PGPR. Root bacterization with these same strains also reduced the lesion size of Colletotrichum orbiculare on challenged leaves. In an ultrastructural study, bacterization of pea roots with strain 63-28 induced physical barriers and other plant defense reactions to Fusarium oxysporum f. sp. pisi, but had direct antagonistic toxic effects on Pythium ultimum [6]. This research provides evidence that PGPR induce systemic resistance to P. aphanidermatum in cucumber, in addition to other foliar and wilt pathogens. ISR offers a number of advantages for control of diseases in hydroponic systems. The inducer can be economically introduced into the entire crop of a hydroponic system, unlike with field crops. Since inoculum for hydroponic diseases is usually introduced later in the cropping period, plants can be induced at the start and protected during the most susceptible period. One induction treatment may protect against multiple pathogens. Since the effect is translocated, the biocontrol agent does not need to be at the infection site.

References
1. Rankin L, Paulitz TC, 1994. Plant Disease 78, 447-451.
2. Paulitz TC, Zhou T, Rankin L, 1992. Biological Control 2, 226-237.
3. Zhou T, Paulitz TC, 1994 Journal of Phytopathology 142, 51-63.
4. Chen C, Paulitz T, Benhamou N, Belanger R, 1996. Phytopathology 86, S52
5. Chen C, Paulitz T, Belanger R, Benhamou N, 1997. Phytopathology 87: S18
6. Benhamou N, Belanger R, Paulitz T, 1996. Phytopathology 86, 1174 - 1185.