Physiology and Biochemistry of Plant-Pathogen Interactions

by I. J. Misaghi

Overview

There has been a significant surge of interest in the study of the physiology and biochemistry of plant host-parasite interactions in recent years, as evidenced by the number of research papers currently being published on the subject. The increased interest is probably based on the evidence that effective management of many plant diseases is, for the most part, contingent upon a clear understanding of the nature of host-parasite interactions. This intensified research effort calls for a greater number of books, such as this one, designed to compile, synthesize, and evaluate widely scattered pieces of information on this subject. The study of host-parasite interactions concerns the struggle between plants and pathogens, which has been incessant throughout their coevolution. Such in­ teractions are often highly complex. Pathogens have developed sophisticated of­ fensive systems to parasitize plants, while plants have evolved diversified defen­ sive strategies to ward off potential pathogens. In certain cases, the outcome of a specific host-parasite interaction seems to depend upon the presence or efficacy of the plant's defense system. A plant may become diseased when a parasite manages to invade it, unhindered by preexisting defense systems and/or without eliciting the plant's induced resistance response(s). Absence of disease may re­ flect the inability of the invading pathogen to overcome the plant's defense system(s).

Product Details

ISBN-13:	9781468411515
Publisher:	Springer US
Publication date:	02/16/2012
Edition description:	Softcover reprint of the original 1st ed. 1982
Pages:	304
Product dimensions:	5.98(w) x 9.02(h) x 0.03(d)

Table of Contents

1 Definition.- I. Introduction.- II. Definition of a Few Terms.- A. Plant Disease.- B. Symptoms.- C. Pathogenicity and Virulence.- D. Pathogenesis.- E. Tolerance.- F. Compatibility and Incompatibility.- G. Hypersensitive Reaction.- H. Biotrophs.- 2 Attraction to and Penetration of Plants by Pathogens.- I. Introduction.- II. Attraction of Pathogens to Plants.- A. Chemotaxis.- B. Electrotaxis.- C. Motility.- III. Penetration.- A. Passive Penetration.- B. Active Penetration.- IV. Factors Influencing Attraction, Penetration, and Infection Processes.- A. Temperature.- B. Moisture.- C. Gas Composition.- 3 The Role of Pathogen-Produced Cell-Wall-Degrading Enzymes in Pathogenesis.- I. Introduction.- II. Structure and Chemistry of the Cell Wall.- A. Structure of the Cell Wall.- B. Chemistry of Cell Wall Components.- III. Pathogen-Produced Cell-Wall-Degrading Enzymes.- A. Pectolytic Enzymes.- B. Cellulose-Degrading Enzymes.- C. Hemicellulose-Degrading Enzymes.- D. Pattern of Production of Cell-Wall-Degrading Enzymes.- E. Factors Influencing the Activity of Pathogen-Produced Cell-Wall-Degrading Enzymes.- F. Evidence for the Involvement of Pathogen-Produced Enzymes in Pathogenesis.- G. The Role of Cell-Wall-Degrading Enzymes in Tissue Maceration and Cell Death.- 4 The Role of Pathogen-Produced Toxins in Pathogenesis.- I. Introduction.- II. Definition and Classification of Pathogen-Produced Toxins.- III. Toxin Categories.- A. Vivotoxin.- B. Pathotoxin.- C. Host-Selective (-Specific) Toxin.- IV. Evaluation of the Criteria Used to Establish the Role of Toxins in Pathogenesis.- A. Isolation of the Toxin from Diseased Plants.- B. Reproduction of Disease Symptoms by the Toxin.- C. Correlation between Pathogenicity and the Level of Toxin Produced in Vitro.- D. Correlation between Disease Susceptibility and Sensitivity to Toxins.- E. Genetic Analysis of the Host, the Pathogen, or Both.- V. Host-Selective Toxins.- A. Victorin.- B. T Toxin.- C. HC Toxin.- D. HS Toxin.- E. PC Toxin.- F. PM Toxin.- G. AK Toxin.- H. AM Toxin.- I. AA Toxin.- VI. Nonselective Toxins.- A. Amylovorin.- B. Tentoxin.- C. Phaseolotoxin.- D. Tabtoxin and Tabtoxinine-?-lactam.- E. Syringomycin and Syringotoxin.- F. Coronatine.- G. Fusicoccin.- H. Fumaric Acid.- I. Oxalic Acid.- J. Fusaric Acid.- K. Ethyl and Methyl Acetate.- L. Ammonia.- VII. Mode of Action of Toxins.- A. Effect on Mihondria.- B. Effect on Membrane Permeability.- C. Effect on Photosynthesis.- D. Effect on Enzymes.- E. Growth Regulator Effect.- VIII. Toxin Binding Sites.- IX. Mechanism of Plant Resistance to Toxin-Producing Pathogens.- 5 Alterations in Permeability Caused by Disease.- I. Introduction.- II. Composition and Structure of Membranes.- III. Cell Permeability Theories.- A. Membrane Theory.- B. Sorption Theory.- C. Cytotic Theory.- IV. Changes in Cell Permeability Caused by Disease.- V. Mechanisms of Permeability Changes in Diseased Plants.- A. Activation of the Plasmalemma ATPase.- B. Effects of Pathogen-Produced Toxins on Specific Components of the Transport System.- C. Disruption of Energy Supply for the Maintenance and Repair of Membranes.- D. Degradation of Lipid and Protein Components of Membranes by Pathogen-Produced Enzymes.- 6 Alterations in Water Relations Caused by Disease.- I. Introduction.- II. Definition of a Few Terms.- A. Water Potential.- B. Osmotic, Pressure, and Matric Potentials.- C. Relative Water Content.- III. Water Movement in Plants.- A. Water Movement in Healthy Plants.- B. Water Movement in Diseased Plants.- IV. Transpiration.- A. Transpiration in Healthy Plants.- B. Transpiration in Diseased Plants.- V. Disruption of Membrane Permeability in Leaf Cells by Pathogen-Produced Substances.- VI. Water Potential and Disease Severity.- VII. Assessment of the Nature of Water Relations Changes in Diseased Plants.- 7 Disease-Induced Alterations in Carbohydrate Metabolism.- I. Introduction.- II. Disease-Induced Alterations in Photosynthesis.- A. Changes in Photosynthesis in Plants Infected with Viruses and Biotrophic Fungi.- B. Changes in Photosynthesis in Plants Infected with Nonbiotrophs.- III. Mechanism of Disease-Induced Alterations in Photosynthesis.- A. Decline in the Capture of Light Energy.- B. Changes in the Rate of CO2 Uptake.- C. Effect of Pathogen-Produced Toxins.- IV. Disease-Induced Alterations in Transport of Photoassimilates.- V. Mechanism of Disease-Induced Alterations in Photoassimilate Transport.- VI. Disease-Induced Increases in Respiration.- VII. Mechanism of Disease-Induced Increases in Respiration.- A. Uncoupling of Phosphorylation from Electron Transport.- B. Increased Activity of Pentose Phosphate Pathway.- C. Increased Activity of Noncyhrome Oxidases.- VIII. Regulation of Carbohydrate Metabolism.- IX. Significance of Disease-Induced Alterations in Respiration.- X. Future Studies.- 8 Pathological Alterations in Transcription and Translation.- I. Introduction.- II. Disease-Induced Alterations in Transcription.- A. Changes in Chromatin.- B. Changes in the Activity of RNA Polymerases.- C. Changes in the Activity of Ribonucleases.- D. Changes in the Level of RNA.- E. Changes in Plant Nuclei.- III. Disease-Induced Alterations in Translation.- A. Changes in Enzymes.- B. Changes in Proteins.- IV. Conclusions.- 9 Alterations in Phenol Metabolism Caused by Disease.- I. Introduction.- II. Biosynthetic Pathways of Phenolic Compounds.- III. Disease-Induced Alterations in Phenol Metabolism.- A. Changes in the Level of Phenolic Compounds.- B. Changes in the Activities of Enzymes Involved in Phenol Metabolism.- 10 Growth Regulator Imbalance in Plant Disease.- I. Introduction.- II. Known Growth Regulators.- A. Indoleacetic Acid.- B. Ethylene.- C. Cytokinins.- D. Gibberellins.- E. Abscisic Acid.- III. Pathogen-Produced Toxins with Growth Regulator Activity.- IV. Involvement of Growth Regulators in Certain Disease-Induced Abnormalities.- A. Gall and Overgrowth.- B. Fasciation of Peas.- C. Excessive Elongation.- D. Stunting.- E. Water Stress and Wilting.- F. Leaf Abscission.- G. Green-Island Formation.- H. Altered Translocation.- V. Mechanisms of Change in Indoleacetic Acid Content of Diseased Tissue.- A. Changes in the Level of Indoleacetic Acid Precursors.- B. Indoleacetic Acid Oxidation.- C. Conjugation of Indoleacetic Acid with Inactivator and Protector Molecules.- D. Interference with Indoleacetic Acid Transport.- VI. Influence of Growth Regulators on the Outcome of Disease Reaction.- A. Indoleacetic Acid.- B. Cytokinins.- C. Ethylene.- VII. Limitations of Growth Regulator Studies.- VIII. Discussion.- 11 Crown Gall Tumor Formation.- I. Introduction.- II. The Bacterium.- III. Physiology of Crown Gall Tumor.- A. Phytohormone Independence.- B. Synthesis of Opines.- IV. Tumor Development.- A. Attachment of the Bacterium to Plant Cell—Wound Requirement.- B. The Nature of the Tumor-Inducing Principle.- V. Relations among Bacterial Plasmids.- VI. Mechanism of Transformation.- A. Acquisition of Bacterial Plasmid DNA.- B. Incorporation of T-DNA into Plant DNA.- C. Transcription of Incorporated T-DNA in Tumors.- VII. Identification of Plasmid and Chromosomal Genes Involved in Oncogenicity.- VIII. Tumor Reversal.- 12 Mechanism of Disease Resistance.- I. Introduction.- II. Preformed Resistance Factors—Structural Features.- A. Cuticles.- B. Stomates.- C. Plant Hairs.- III. Preformed Resistance Factors—Preformed Antimicrobial Substances.- A. Cathechol and Proatechuic Acid.- B.—-Tomatine.- C. Unsaturated Lactones.- D. Sulfur Compounds (Leek Oils and Mustard Oils).- E. Extruded Materials.- F. Plant Glucanases and Chitinases.- IV. Infection-Induced Resistance Factors—Physical Features.- A. Periderm and Callose.- B. Gels and Tyloses.- C. Cell Wall Modifications.- V. Infection-Induced Resistance Factors—Chemical Features.- A. Hypersensitive Reaction.- B. Peroxidases.- C. Phenolic Compounds.- D. Catalase.- E. Glycosides.- F. Ethylene.- G. Histones.- H. Phytoalexins.- VI. The Dynamic and Coordinated Nature of Resistance.- 13 Induced Resistance.- I. Introduction.- II. Induced Resistance to Fungi.- III. Induced Resistance to Bacteria.- IV. Induced Resistance to Viruses.- V. Induced Resistance to Viroids.- VI. Some Features of Induced Resistance.- 14 Specificity in Plant-Pathogen Interactions.- I. Introduction.- II. Mechanisms of Specificity.- A. Hypersensitive Response.- B. Phytoalexins.- C. Selective Plant Toxins.- D. Common Antigens.- E. Recognition Phenomenon.- Some Useful Books.- References.