Tomato Wilt Disease Research Articles

Suppression of Bacterial Wilt Disease of Tomato by Root-dipping with Pseudomonas fluorescens PfG32. The Role of Antibiotic Substances and Siderophore Production.

Pseudomonas fluorescens strain PfG32 isolated from the rhizosphere of the onion actively suppressed the occurrence of bacterial wilt disease of tomato (BWT) in vermiculite amended natural soil and produced antibiotic substance(s) and siderophore. To investigate the role of the substances in the biocontrol, several mutants defective in antibiotic substances or Siderophore production were isolated from spontaneous Rifr mutant, PfG32R, by Tn5 insertion. Based on pot experiment, the suppression of BWT by Ant-Sid+ (antibiotics non-producing but siderophore producing) mutants was lower compared to its parental strain and to Ant+Sid- (siderophore non producing but antibiotics producing) mutants. However, Ant-Sid+ mutants still express a significant effect. The suppression of BWT by PfG32R was correlated to the suppression of the population of the pathogen observed on the surface of root and to the delay of appearance of detectable population of the pathogen in root tissues. We consider that the ability of PfG32 to produce antibiotics and siderophore is the important factor on determining its biological control and other factor may act as secondary factor.

SIGNIFICANCE OF THE ROOT SYSTEM IN VERTICILLIUM WILT TOLERANCE IN POTATO AND RESISTANCE IN TOMATO

Reciprocal (susceptible/resistant) grafting experiments were used to determine whether the root is the major site of resistance to Verticillium wilt disease in tomato and tolerance in potato. Increased resistance/tolerance was seen in both species when the resistant cultivar served as rootstock. In potato, however, stem-dipping experiments indicated that tolerance was independent of the root. In experiments designed to determine whether a major gene plays a role in Verticillium wilt tolerance in potato, tomato races 1 and 2 of V. dahliae did not show differential pathogenicity on tolerant potato cultivars inoculated by the root-dip method. The results indicate that the root system plays an important role in the defense mechanisms to Verticillium wilt both in tomato and potato.

Binary Microbe System for Biological Control of Fusarium Wilt of Tomato: Enhanced Root-Colonization of an Antifungal Rhizoplane Bacterium Supported by a Chitin-degrading Bacterium.

An antagonistic rhizoplane bacterium (Serratia Marcescens) and a chitin-degrading microbe (Streptomyces anulatus) were used for establishing a binary microbe system for biological control of Fusarium wilt disease of tomato. For effectively tracing root-colonization, the rhizoplane bacterium was genetically marked with the lux genes and the tetracycline resistance gene through bacterial conjugation. Successful colonization by the bacterium on roots from bacterized seeds was visualized by bioluminescence of the transconjugant into which the lux gene operon had been integrated. Antifungal activity of the transconjugant was stable and effectire even when the bacterium was colonized on tomato roots. Multiplication of the transconjugant in soil was supported by the chitin-degrading microbe which had been previously added in chitin-supplemented soil. The chitin-degrading microbe produced extracellular endochitinases and hydrolyzed chitin which was added to soil. Chitohydrolytic products supported the multiplication and root-colonization of the rhizoplane bacterium in soil. The binary microbe system comprising of chitin-degrading microbe and gene-marked transconjugant was effective in controlling of tomato wilt disease caused by Fusarium oxysporum f. sp. lycopersici.

奈良県におけるトマト黄化えそ病の発生生態とその防除

奈良県におけるトマト黄化えそ病の発生生態とその防除

Verticillium Wilt Disease of Tomato: Influence of Inoculum Density and Root Extension Upon Disease Severity

Verticillium Wilt Disease of Tomato: Influence of Inoculum Density and Root Extension Upon Disease Severity

THE USE OF INTERGENERIC GRAFTS TO DEMONSTRATE TOXINS IN THE FUSARIUM WILT DISEASE OF TOMATO

A NUMBER OF THEORIES have been proposed to explain the mechanism by which the vascular wilt pathogens produce disease symptoms in the host. These include (a) competition for nutrients in the tracheal sap resulting in starvation of the host; (b) necrosis of the root system limiting the water absorbing capacity of the host; (c) occlusion of the vascular elements by the cells of the pathogen; (d) formation of toxins by the host-parasite interaction acting at or beyond the area of infection. Gottlieb (1944a) has reviewed the literature on this subject. The toxin theory has received considerable attention and has gained wide acceptance among investigators of the vascular wilts. Evidence for the toxin theory is based chiefly on the observation that all or part of the disease symptoms may be reproduced by cell-free filtrates from artifical cultures of the pathogen. The inadequacy of this approach has been emphasized by numerous investigators (Rosen, 1926; Brown, 1936; Gottlieb, 1944a; Dimond and Waggoner, 1953). Inasmuch as the products of microbial metabolism -are determined by the growth environment, the metabolites produced in artificial culture may differ from those generated in the host. To overcome the shortcomings of the artificial culture method, Gottlieb (1944a) extracted the tracheal sap from diseased tomato plants infected with Fusarium oxyspo;rum f. lycopersici Snyder and Hanson. He found a toxic component in the tracheal sap of diseased plants which produced vascular discoloration and wilt in healthy tomato seedlings. This component could not be demonstrated in the tracheal sap of healthy plants. However, since the diseased tissue contained the pathogen in the vascular elements, Gottlieb (1944a) was unable to demonstrate that the toxin was present in areas removed from the points of infection. Scheffer and Walker (1953) have recently demonstrated a close association between the location of the pathogen and the appearance of symptoms in the Fusarium wilt disease of tomato. Although adhering to the toxin theory, they conclude, Whereas previous investigations have implied that disease symptoms are brought about by toxic materials being transported in advance of the pathogen, present studies of the distribution of the pathogen does not bear out such a conclusion. Gottlieb's (1944b) observation that newly developed side shoots on severly diseased tomato plants occasionally remain symptomless and free of the pathogen, raises another serious doubt as to

Spotted wilt of the sweet pea

Abstract does not appear. First page follows. Introduction In the coastal counties of California the sweet pea, Lathyrus odoratus L., is frequently afflicted with a streak disease. The cause of the disease is sometimes obscured by viruses of the mosaic type or by resemblance to the description of bacterial streak of sweet pea.(5)4 It has, however, been proved to be a virus identical with that responsible for the spotted wilt disease of tomato. Recently(6) this virus has been reported as the cause of a streak disease of the garden pea, Pisum sativum L. Symptoms A characteristic symptom of the disease on sweet pea is a necrotic streaking of stems and petioles. The streaks are reddish brown to dull purple in color and in the advanced stage are conspicuous. They may run the entire length of the stem, parallel to the long axis, being found on analysis to consist of disconnected short streaks or a continuous long one. They have been seen to develop both above and below the point of virus inception. Leaves and shoots may turn yellow and die. Early symptoms on the foliage appear as spots, usually 5 to 15 mm long, more or less circular or oval in shape, yellowish at first, with diffuse margins. Later the spots become somewhat brownish and form a pattern typical of the virus on other hosts. From these spots are developed yellowish sectors or zones, ordinarily one or only a few on each leaf. The spotting of the foliage is fairly definite in early stages, although not striking; but the general yellowing which may follow becomes a conspicuous symptom. Symptoms of the disease are shown in figure 1, A and D. Blossoms on infected plants have been seen to develop a circular pattern in the pigment and the virus has been recovered from such material. Again, blighting of the whole shoot may occur prior to blossom formation. Variability in the expression of symptoms has been observed. Plants infected early may yellow and die without showing other symptoms.