Plant Pathogenesis and Disease Control

Hachiro Oku

• Editore: CRC Press
• Anno: 2020
• ISBN:
  9781000157901
• Edizione: 1
• Argomento: Biological Sciences
• Categoria: Biology

Environmental pollution resulting from widespread pesticide application has become a serious worldwide problem. Plant Pathogenesis and Disease Control is an important new reference that addresses this problem by exploring the biochemical and molecular mechanisms of plant pathogenesis and emphasizing the use of "pest control agents" rather than "pesticides" for plant disease control. Topics examined include pathogenicity, the resistance of plants against pathogens, the offensive and defensive struggle between hosts and parasites, methods for using natural defense mechanisms to develop environmentally sound disease control agents, and the use of modern biotechnology for plant disease control. The book will be an essential reference for phytopathologists, plant biochemists, pesticide chemists, mycologists, plant cell technologists, and agricultural researchers.

CHAPTER 1

Pathogens and Pathogenicity

I. EVOLUTIONAL ASPECTS OF PLANT PATHOGENS

According to Agrios,¹ about 100,000 species of fungi and 1600 species of bacteria are living on this planet; and among these, about 8000 species of fungi and 200 species of bacteria attack and injure higher plants. Another 100 species of these microorganisms cause diseases in animals. Most of the 100,000, and 1600 species of fungi and bacteria are strictly saprophytic, living on nonliving organic matter and decomposing enormous quantities of animal and plant remains. In other words, saprophytic microorganisms are scavengers of our environment, recycling dead organic matter into simple elements.

Thus, the nutritional procedure of pathogenic microorganisms that derive food materials from plants and animals is the exceptional case in the kingdom of microorganisms. Because most microorganisms are saprophytes, they live in violent competition with each other, seeking food materials and living space. The production of antibiotics is likely to be one of the strategies of microorganisms to defend their living territory.

Ogura² examined the change of microflora on rice straw added in the soil and found that the fungi with fermentation ability came first, and then the fungi were altered by cellulose-decomposing fungi. This alteration seemed to be due to both the production of antibiotics by the latter fungi and the exhaustion of nutrients for the former fungi. These cellulose-decomposing fungi persist for a long time; but when the cellulose is exhausted, these fungi disappear and then lignin-decomposing fungi appear and multiply on it. This model experiment shows the violent competition between soil microorganisms, and the complete decomposition of organic substances by a close cooperation of many microorganisms.

Among these saprophytic microorganisms which compete with each other if one acquires the ability to derive food materials from a plant and multiply on it, the microorganism can escape from the violent competition. The plant pathogenic microorganisms are likely to be developed in such a way from saprophytic ones by parasitic adaptation. This hypothesis might be supported by the evidence that there are varieties of pathogenic fungi of which parasitism is in varying degrees, between obligate parasitic and facultative parasitic. The facultative parasite, which usually lives as a saprophyte but under some conditions can parasitize on a plant, seems to be a pathogen with the lowest parasitic adaptation. On the contrary, the uppermost parasitic adaptation can be seen in the obligate parasite which can derive food materials only from living plant cells but not from dead cells.

Nelson,³ however, hypothesized that fungi had originated from obligate parasitic microorganisms and evolved in the direction of saprophytes. He considered that primitive fungi could not live separately from living plants; however, after acquiring the abilities to produce dormant spores, they became able to live independently from plants as a saprophyte. However, regarding the parasitism of plant pathogenic fungi, he considered that saprophytes regained parasitic ability acquiring beneficial properties from both parasitic and saprophytic life. Obligate parasites, in this sense, completely regained the ancient lifestyle.

The parasitic adaptation for microorganisms to be plant pathogens includes acquisition of the following three abilities:⁴ (1) ability to enter into a plant, (2) ability to overcome the resistance of the host, and (3) ability to evoke disease.

These abilities are essential to plant pathogens, and are not found in saprophytic microorganisms. From these standpoints, many steps of adaptation are found in those three properties in each plant pathogen. In fact, there are varieties of plant pathogens of which parasitic adaptations are different. Relationships between the degree of parasitic adaptation and the three properties of pathogens are indicated in Table 1.

As described, the pathogens of which parasitic adaptations are low usually live as saprophytes on plant and animal remains, but under certain conditions invade plants. These pathogens are called facultative parasites. Many facultative parasites enter into plants through wounds, and have no special way of entering. These pathogens mainly parasitize on organs or tissues in which physiological activity is low, such as fruits and other storage organs, trunks of trees, or vascular bundles. Several fungi which cause damping off of young seedlings belong to facultative parasites and generally have wide host ranges.

On the contrary, obligate parasites such as powdery mildew, downy mildew, rust fungi, and so on seem to have lost the saprophytic ability. For these fungi, death of the host cell results in death of the pathogen itself.

Table 1. Classification of Plant Pathogenic Fungl by Degree of Parasitic Adaptation and Their Properties

Note: NST: nonspecific toxin, HST: host specific toxin.

Obligate parasites have their own procedures for entering into the host plant. The stomatal penetration by rust fungi and downy mildew fungi is likely to be one of the most efficient entrance methods. The tip of the germ tube from the germinated uredospore comes over a stoma, enlarges, and becomes closely appressed to the surface of the guard cells. From the structure thus formed an appressorium, a very fine penetration hypha emerges and enters through the stomatal pore into the substomatal cavity. In downy mildew fungi, the motile zoospore swims in the water film on the leaf surface. When it reaches a stoma, its movement appears subject to some stimulus and the spore comes to rest over the stomatal pore. From the now nonmotile spore, a slender hypha emerges and passes through the pore into the substomatal cavity. The closed stoma can be forced to penetrate through this type of penetration. For fungi which do not form an appressorium and enter through the stomata directly by hyphae like Cladosporium fulvum, the closed stomata seems to contribute a barrier through which this type of growth cannot pass. These facts suggest that the type of stomatal entry shown by rust uredospores and downy mildew cystospores is more likely to be effective.⁵

The other invading procedure for obligate parasite is so-called direct penetration, by which an unbroken plant surface is penetrated. These fungi do not make use of either wound or natural openings.

Obligate parasites seem to have some mechanisms to overcome the defense reaction of the host without killing host cells. Other toxic metabolite or deleterious enzymes for the host cell should not be produced by obligate parasites because this type of pathogen cannot live on dead cells as described previously.

The virulence factors in obligate parasitic diseases may not be due to the direct action of the pathogen, and the mechanism of symptom development seems to be more complex than the other types of diseases. Because obligate parasites cannot live saprophytically, they should overcome adverse conditions by producing dormant organs or by altering the host plant.

Between these two extremes, perthophyte and facultative saprophytes exist. The perthophyte is the pathogen which kills the host cell by toxins or enzymes, and then lives saprophytically on the dead cell. The facultative saprophyte is the pathogen that parasitizes usually on a living host cell, but can live saprophytically under certain conditions.

The pathogen of Helminthosporium leaf blight disease, Cochliobolus miyabeanus; pathogens of many black spot diseases caused by Alternaria spp.; and pathogens of wheat stripe disease, Cephalosporium gramineum, belong to the perthophytes. Many perthophytes produce necrotic symptoms. The perthophytic fungi also have their own way of entering into plants, direct penetration or penetration through natural openings.

The perthophyte produces toxins or deleterious enzymes to overcome the resistance of host plants. These fungi can parasitize on the physiologically active parts of host plants. The host range of the perthophyte is divergent, that is, narrow for some fungi but wider for other fungi. The fungi which have a wide host range generally produce nonspecific toxins or deleterious enzymes to plants; however, some fungi which produce host-specific toxins have a narrow host range, and some parasitize on one species of plants or even on only susceptible cultivars of the species. Further, some perthophytes produce substances that suppress the elicitation of defense reactions of the hosts, which do not give ...

Indice dei contenuti

• Cover
• Title Page
• Copyright Page
• Preface
• The Author
• Table of Contents
• Acknowledgments
• Introduction. Basic Principles for Plant Disease Control
• Chapter 1. Pathogens and Pathogenicity
• Chapter 2. Resistance of Plants Against Pathogens
• Chapter 3. Defense and Offense Between Higher Plants and Microbes and the Mechanism
• Chapter 4. Disease Control Agents Based on Knowledge of Pathogenicity and Disease Resistance
• Chapter 5. Systemic Induced Resistance as a Tool for Disease Control
• Chapter 6. Biotechnology for Plant Disease Control
• Index