Phytotoxins Produced by Plant Parasites

Strobel, G A

doi:10.1146/annurev.pp.25.060174.002545

Cited by 88 publications

(23 citation statements)

References 59 publications

(68 reference statements)

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“…For example, a pathogen might secrete a toxin which kills the plant cells in the region of the pathogen before those cells are capable of synthesizing the enzymes necessary for synthesis of phytoalexins. Pathogens are well known for their ability to secrete phytotoxins (24,47,(55)(56)(57). Another possible mechanism by which a successful pathogen might prevent a plant from accumulating sufficient phytoalexins might be to repress synthesis of one or more enzymes involved in phytoalexin synthesis or else to inhibit the enzymes once they are synthesized.…”

Section: Phytoalexins Are Not Capable By Themselves Of Protecting Pmentioning

confidence: 99%

Host-pathogen interactions in plants. Plants, when exposed to oligosaccharides of fungal origin, defend themselves by accumulating antibiotics.

Albersheim¹,

Valent²

1978

The Journal of Cell Biology

256

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Section: Phytoalexins Are Not Capable By Themselves Of Protecting Pmentioning

confidence: 99%

Host-pathogen interactions in plants. Plants, when exposed to oligosaccharides of fungal origin, defend themselves by accumulating antibiotics.

Albersheim¹,

Valent²

1978

The Journal of Cell Biology

256

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“…Several members of the genus, including H. tyctoriae, H. carbonum, H. maydis, and H. sacchari, produce host-specific toxins. These compounds, which are fungal metabolites toxic only to the susceptible host, produce virtually all of the disease symptoms and are critical for pathogenicity of the fungi (3). Since pathogenicity in these fungi is dependent upon their host-specific toxins, the loss of toxin production and attenuation are synonymous.…”

mentioning

confidence: 99%

Serinol as an activator of toxin production in attenuated cultures of Helminthosporium sacchari

Pinkerton

Strobel

1976

Proc. Natl. Acad. Sci. U.S.A.

140

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Successive transfer in synthetic medium of spores and mycelial fragments from original toxin-producing cultures of Helminthosporium sacchari results in attenuated cultures which do not produce the host-specific toxin helminthosporoside. When attenuated cultures are grown on material obtained from the water wash of sugarcane leaves susceptible to this fungus, the production of heminthosporoside resumes.Cpmpounds that activate toxin production in the fungus are present on the leaf surface and presumably arise via plant metabolism. One activator was identified as a novel free amine, serinol (2-amino-1,3-propanediol). It activates toxin production in attenuated cultures at 1 gM. Several experiments described in this report argue against the selection theory for the attenuation of cultures. The biological significance and some possible mechanisms for the activation of toxin biosynthesis are discussed.Variation within a pathogen population may produce highly efficient biotypes that are extremely successful parasites. Conversely, biotypes may arise in which the ability to persist parasitically is greatly reduced or eliminated. This loss of parasitic capabilities has been labeled attenuation (1).The genus Helminthosporium includes pathogens whose conidial stages are responsible for serious diseases of rice, corn, grasses, and cereals (2). Several members of the genus, including H. tyctoriae, H. carbonum, H. maydis, and H. sacchari, produce host-specific toxins. These compounds, which are fungal metabolites toxic only to the susceptible host, produce virtually all of the disease symptoms and are critical for pathogenicity of the fungi (3). Since pathogenicity in these fungi is dependent upon their host-specific toxins, the loss of toxin production and attenuation are synonymous. Cessation of toxin production has been observed in cultures of H. maydis (4), and H. carbonum and H. vwctoriae (5).Helminthosporium sacchari (Van Breda de Haan) Butler is the causal agent of the eyespot disease of sugarcane. This disease, found in most areas where sugarcane is grown (6), is characterized by the formation of eye-shaped lesions, followed by the development of reddish-brown "runners" which extend from the lesion toward the leaf tip. Runner formation is caused by the host-specific toxin helminthosporoside (7) (2-hydroxycyclopropyl-a-D-galactopyranoside), a fungal metabolite directly involved in the pathogenesis of the eye-spot disease (8).Fortuitously, we observed that when toxin-producing isolates of H. sacchari were grown on a synthetic medium and transferred a number of times through the same medium, they lost their toxin-producing ability: they became attenuated. When an attenuated isolate was transferred to a medium containing an infusion of sugarcane leaves (susceptible clone 51 NG 97), full toxin production was restored. These observations suggested that a compound present in sugarcane is required for toxin biosynthesis.This report describes the isolation, purification, and chemical characterization of one of several "...

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“…40). The toxic polysaccharides can cause many of the symptoms of the pathogen's disease in the absence of the pathogen (40).…”

Section: Discussionmentioning

confidence: 99%

“…Some of the high mol wt polysaccharide toxins have a limited range of plants that they can affect (15,39,40). It is possible that elicitors are similarly specific.…”

Section: Discussionmentioning

confidence: 99%

Host-Pathogen Interactions

Anderson-Prouty

Albersheim²

1975

Plant Physiol.

134

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A polysaccharide from the fungal pathogen Colletotrichum lindemuthianum causes browning and phytoalexin production when applied to the cut surfaces of bean (Phaseolus vulgaris) cotyledons and hypocotyls. The application of an amount of polysaccharide equivalent to less than 100 ng of glucose will elicit this response in the bean tissues. The polysaccharide has been isolated both from culture filtrates and from the mycelial walls of the fungus. Purification of the polysaccharide involved anion and cation exchange chromatography and gel filtration. The polysaccharide has an apparent molecular weight between 1,000,000 and 5,000,000 daltons, and consists predominantly of 3-and 4-linked glucosyl residues.Beans synthesize several phytoalexins in response to attack by pathogens (5-7, 28, 33, 38, 42). Four of these phytoalexins have been isolated and characterized as phaseollin, phaseollidin, phaseollinisoflavan, and kievitone (5,6,30,31,38,42). The synthesis of these phytoalexins has been demonstrated in beans that have responded to attack by C. lindemuthianum (5,7,25). The synthesis of the four phytoalexins occurs much sooner in an incompatible reaction than in a compatible reaction. The incompatible reaction usually involves a hypersensitive response in those cells that are initially invaded by the pathogen (5, 28, 37). It has been suggested (5, 7) that the early synthesis of phytoalexins in an incompatible reaction can account for the restricted growth of the pathogen that is characteristic of the hypersensitive response.Synthesis of phytoalexins in plant tissues can be stimulated by molecules, elicitors (23), that are produced by plant pathogens (12, 23,24,34,43). However, only in one example (12) has the elicitor been purified and partially characterized. This elicitor, a small peptide isolated from the mycelia of Monilinia fructicola, is active on tissues of a nonhost of this pathogen, but the effect of the peptide on tissues of the hosts of M. fructicola has not been reported.

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Phytotoxins Produced by Plant Parasites

Cited by 88 publications

References 59 publications

Host-pathogen interactions in plants. Plants, when exposed to oligosaccharides of fungal origin, defend themselves by accumulating antibiotics.

Host-pathogen interactions in plants. Plants, when exposed to oligosaccharides of fungal origin, defend themselves by accumulating antibiotics.

Serinol as an activator of toxin production in attenuated cultures of Helminthosporium sacchari

Host-Pathogen Interactions

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