Plant Innate Immunity

1. Auflage 2009
ISBN: 978-0-08-088879-8
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 795 Seiten

Plant innate immunity is a collective term to describe a complex of interconnected mechanisms that plants use to withstand potential pathogens and herbivores. The last decade has seen a rapid advance in our understanding of the induction, signal transduction and expression of resistance responses to oomycetes, fungi, bacteria, viruses, nematodes and insects. This volume aims at providing an overview of these processes and mechanisms. Edited by Jean-Claude Kader and Michel Delseny and supported by an international Editorial Board, Advances in Botanical Research publishes in-depth and up-to-date reviews on a wide range of topics in plant sciences. * Multidisciplinary reviews written from a broad range of scientific perspectives

* For over 40 years, series has enjoyed a reputation for excellence

* Contributors internationally recognized authorities in their respective fields

Autoren/Hrsg.

Inhaltsverzeichnis

1;Front Cover;1
2;Advances in Botanical Research;4
3;Copyright Page;5
4;Contents;6
5;Contributors to Volume 51;12
6;Preface: Plant Innate Immunity;16
7;Contents of Volumes 35–50;20
8;Chapter 1: PAMP-Triggered Basal Immunity in Plants;34
8.1;I. The Concept of Plant Immunity;35
8.2;II. Signals Mediating the Activation of Plant Defense Responses;37
8.2.1;A. Pathogen-Associated Molecular Patterns;37
8.2.2;B. Damage-Associated Molecular Patterns;44
8.2.3;C. Pathogen-Derived Toxins as Triggers of Plant Immunity;45
8.3;III. Receptors Mediating Pattern Recognition in Plant Immunity;48
8.4;IV. Signal Transduction in PTI;54
8.5;V. Suppression of PTI—A Major Virulence Strategy of Phytopathogenic Bacteria;58
8.6;VI. Concluding Remarks;60
8.7;Acknowledgments;61
8.8;References;61
9;Chapter 2: Plant Pathogens as Suppressors of Host Defense;72
9.1;I. Introduction;73
9.2;II. Suppressors Produced by Fungal and Oomycete Pathogens;75
9.2.1;A. Suppressors Comprise a Wide Group of Metabolites;75
9.2.2;B. Race-Specific Elicitors Turn Out to Suppress Defenses;77
9.2.3;C. Concluding Remarks;81
9.3;III. Suppressors Produced by Bacterial Pathogens;81
9.3.1;A. Bacterial Evolution to Overcome Plant Resistance;81
9.3.2;B. Bacterial Suppression of PTI;83
9.3.2.1;1. Calcium signaling suppression by extracellular polysaccharides (EPS);84
9.3.2.2;2. Coronatine toxin suppression of stomatal closure;85
9.3.3;C. Type III Protein Secreted Effectors are Used to Suppress PTI;85
9.3.4;D. Multifunctional Effectors;86
9.3.4.1;1. avrPto;86
9.3.4.2;2. avrPtoB (hopAB2);87
9.3.4.3;3. avrRpt2;88
9.3.4.4;4. xopD;89
9.3.5;E. RNA and RNA-Binding Protein Targeting;89
9.3.5.1;1. hopU1 (hopPtoS2);89
9.3.5.2;2. hopT1-1;90
9.3.6;F. Attack of Negative Regulators of PTI;90
9.3.6.1;1. avrB;90
9.3.6.2;2. avrRpm1;91
9.3.7;G. Targeting Hormone Signaling?;91
9.3.7.1;1. hopAN (avrE1/wtsE/dspA/dspE);91
9.3.7.2;2. hopAM1 (avrPpiB);92
9.3.8;H. Disruption of Vesicle Trafficking;92
9.3.8.1;1. hopM1 (hopPtoM);92
9.3.9;I. Targeting MAP Kinase Signaling;94
9.3.9.1;1. HopAI1;94
9.3.10;J. Other Effectors Involved in PTI Suppression for Which Targets are Unknown;94
9.3.10.1;1. avrRps4;94
9.3.10.2;2. hopAO1 (hopPtoD2);95
9.3.11;K. Other Effectors Involved in PTI Suppression, but Lacking Functional Information;95
9.3.12;L. Other Potential Mechanisms—Type VI Secretion;96
9.3.13;M. Complexity and Evolution of PTI Suppression by Bacterial Pathogens;96
9.4;IV. RNA Silencing, the Plant's Innate Immune System Against Viruses;98
9.4.1;A. The Discovery of RNA Silencing as the Plant’s Innate Immune System Against Viruses;98
9.4.2;B. Current Views of RNA Silencing as Antiviral Mechanism in;99
9.4.2.1;1. The siRNA pathway;100
9.4.2.2;2. The miRNA pathway;102
9.4.3;C. Viral Suppressors of RNA Silencing;102
9.4.4;D. Possible Interactions Between Plant Viruses and the miRNA Pathway;105
9.4.5;E. Is Antiviral RNAi Restricted to Plants and Insects?;106
9.5;Acknowledgments;107
9.6;References;107
10;Chapter 3: From Nonhost Resistance to Lesion-Mimic Mutants: Useful for Studies of Defense Signaling;124
10.1;I. Introduction;125
10.2;II. Defense Induction Mediated by PAMPs and Effectors;126
10.3;III. Signaling Downstream of Pathogen Detection;129
10.3.1;A. The SA-Signaling Pathway;130
10.4;IV. Commonalities in the Defense Response of Host and Nonhost Resistance;132
10.4.1;A. Penetration Resistance of Arabidopsis;133
10.4.2;B. Nonhost Resistance to Bacteria;136
10.5;V. What is the Explanation for Nonhost Resistance?;137
10.6;VI. Lesion-Mimic Mutants;140
10.7;VII. Mutant Screens Without Pathogens for Finding Genes in Defense Signaling;141
10.7.1;A. SSD Mutants;141
10.7.2;B. SFD Mutants;143
10.7.3;C. MOS Mutants;144
10.8;VIII. Conclusion;145
10.9;Acknowledgments;145
10.10;References;145
11;Chapter 4: Action at a Distance: Long-Distance Signals in Induced Resistance;156
11.1;I. Introduction;157
11.2;II. Time to Flower—Signaling Events in the Vegetative to Flowering Transition;158
11.2.1;A. Flowering Time as a Model for Long-Distance Signaling;158
11.2.2;B. Control of Flowering Occurs in Distinct Stages;158
11.2.3;C. The Long-Distance Flowering Signal is Phloem Mobile and Highly Conserved;159
11.2.4;D. Candidates for the Floral Long-Distance SignalmdashThe Identity of "Florigen";160
11.2.4.1;1. Sucrose, cytokinins, and gibberellins;160
11.2.4.2;2. Characterization of genes involved in the regulation of flowering time;161
11.2.4.3;3. FT protein is phloem-mobile;162
11.2.4.4;4. FT, a near universal flowering signal: ‘‘florigen’’ revealed;163
11.2.5;E. Salicylic Acid and FloweringmdashConvergence of Signaling Mechanisms?;164
11.3;III. Mechanisms of Signaling During the Wound Response;165
11.3.1;A. Role of Systemin in Systemic Wound Signaling;166
11.3.2;B. Wound-Response Mutants are Deficient in the Biosynthesis or Perception of JA, or in Systemin Functioning;167
11.3.3;C. Systemin and JA Production in Wounded Leaves and JA Perception in Distant Tissue;168
11.3.4;D. JA Biosynthesis Occurs in the Sieve Element/Companion Cell Complex;169
11.3.5;E. JA-Mediated Wound Response is Modulated by Other Signals;170
11.3.6;F. Mechanism of JA Action on Effector Genes;171
11.4;IV. Long-Distance Signaling in SAR;171
11.4.1;A. SAR Develops in Distinct Stages;172
11.4.1.1;1. Induction;172
11.4.1.2;2. Movement of a long-distance signal(s);173
11.4.1.3;3. Establishment of the ‘‘primed’’ plant;173
11.4.1.4;4. Manifestation;174
11.4.2;B. Role of SA and NPR1 in SAR;174
11.4.3;C. SAR Signal Transport;175
11.4.4;D. Candidates for the SAR Long-Distance Signal;176
11.4.5;E. Other Genes Involved in SAR Long-Distance Signaling;179
11.4.6;F. Role of ET in SAR Long-Distance Signaling;182
11.4.7;G. SAR Long-Distance Signaling Across Species;182
11.5;V. Systemic Induced Susceptibility (SIS);183
11.6;VI. Signaling During ISR;184
11.6.1;A. Induction of ISR;184
11.6.2;B. Signal Perception and Priming During the Development of ISR;185
11.7;VII. Techniques to Further Elucidate Long-Distance Signaling;186
11.8;VIII. Concluding Remarks;188
11.9;References;189
12;Chapter 5: Systemic Acquired Resistance;206
12.1;I. Introduction;207
12.1.1;A. Systemic Acquired Resistance;208
12.1.2;B. Other Forms of Induced Resistance;209
12.2;II. The Biological Spectrum of SAR;210
12.3;III. The Induction of SAR;210
12.3.1;A. Necrotizing Pathogens;210
12.3.2;B. The Hypersensitive Response;211
12.3.3;C. Is Pathogen-Induced Necrosis Needed for SAR Induction?;212
12.3.4;D. Pathogen-Produced Inducers of SAR;214
12.3.5;E. Chemical Induction of SAR;214
12.3.5.1;1. Salicylic acid;215
12.3.5.2;2. 2,6-Dichloroisonicotinic acid;215
12.3.5.3;3. Acibenzolar-S-methyl;216
12.3.5.4;4. Tiadinil;217
12.3.5.5;5. Other chemical inducers;217
12.4;IV. Systemic Biochemical Changes;218
12.4.1;A. Pathogenesis-Related Proteins;218
12.4.2;B. Other Proteins;219
12.4.3;C. SA Accumulation;220
12.5;V. How SAR Protects Plants Against Pathogens;221
12.5.1;A. Priming;221
12.5.2;B. Protection Against Fungi and Oomycetes;221
12.5.2.1;1. Cucurbits;221
12.5.2.2;2. Legumes;225
12.5.2.3;3. Solanaceous species;227
12.5.2.4;4. Arabidopsis;229
12.5.2.5;5. Japanese pear;230
12.5.2.6;6. Cereals;230
12.5.3;C. Protection Against Bacteria;231
12.5.3.1;1. Examples of induced resistance to bacterial pathogens;231
12.5.3.2;2. How SAR protects against bacterial pathogens;232
12.5.4;D. Protection Against Viruses;234
12.5.4.1;1. Decrease in lesion size and number;234
12.5.4.2;2. Inhibition of virus replication;235
12.5.4.3;3. Inhibition of cell-to-cell movement;235
12.5.4.4;4. Inhibition of systemic movement;235
12.5.4.5;5. Does SA induce a different form of resistance to viruses?;236
12.5.5;E. Mechanisms of Defense in Summary;237
12.5.5.1;1. Enhancing basal defense;237
12.5.6;B. What Don’t We Know?;240
12.6;VI. Concluding Comments;242
12.7;Acknowledgment;242
12.8;References;242
13;Chapter 6: Rhizobacteria-Induced Systemic Resistance;256
13.1;I. Introduction;257
13.1.1;A. PAMP- And Effector-Triggered Immunity;257
13.1.2;B. Systemic Acquired Resistance or Salicylic Acid-Induced Systemic Resistance;258
13.1.3;C. Rhizobacteria-Induced Systemic Resistance;259
13.1.4;D. Rhizobacteria Known to Trigger ISR;260
13.1.5;E. Scope of this Review;266
13.2;II. Recognition;266
13.2.1;A. Flagella;267
13.2.2;B. Lipopolysaccharides;273
13.2.3;C. Biosurfactants;276
13.2.4;D. N-acyl-L-homoserine lactone;278
13.2.5;E. N-alkylated benzylamine;279
13.2.6;F. Siderophores;279
13.2.6.1;1. Pseudobactins;280
13.2.6.2;2. SA and SA-containing siderophores;284
13.2.7;G. Antibiotics;286
13.2.7.1;1. 2,4-Diacetylphloroglucinol;286
13.2.7.2;2. Pyocyanin;287
13.2.8;H. Volatiles;288
13.2.9;I. Exopolysaccharides;290
13.2.10;J. Other Bacterial Determinants;291
13.3;III. Signalling in Rhizobacteria-Induced Systemic Resistance;291
13.3.1;A. The Arabidopsis–Pseudomonas fluorescens WCS417r System: A Paradigm for SA-Independent ISR Signalling;291
13.3.2;B. SA-Dependent ISR Signalling;296
13.3.3;C. SA-Dependent and SA-Independent Signalling;297
13.4;IV. Final Remarks;298
13.5;References;299
14;Chapter 7: Plant Growth-Promoting Actions of Rhizobacteria;316
14.1;I. Introduction;317
14.2;II. Modes of Action;318
14.2.1;A. Plant Growth-Promoting Substances;318
14.2.1.1;1. Auxins;319
14.2.1.2;2. Cytokinins;324
14.2.1.3;3. Gibberellins;325
14.2.1.4;4. Ethylene;326
14.2.1.5;5. Abscisic acid;328
14.2.2;B. Nitrogen Transformations;329
14.2.2.1;1. Biological nitrogen fixation;329
14.2.2.2;2. Nitrate uptake by roots as affected by bacteria;329
14.2.2.3;3. Denitrification;330
14.2.3;C. Phosphate and Micronutrient Availability;331
14.2.3.1;1. Phosphate;331
14.2.3.2;2. Vitamins;331
14.2.3.3;3. Iron and other microelements;331
14.2.4;D. Emerging Signals;332
14.2.4.1;1. Signals related to QS;332
14.2.4.2;2. Volatile compounds;333
14.2.4.3;3. Nitric oxide;333
14.2.5;E. Biocontrol in the Rhizosphere;334
14.2.5.1;1. Competition;334
14.2.5.2;2. Antibiosis;335
14.3;III. Agricultural Aspects and Relevance;337
14.3.1;A. PGPR and Endophytes—Role of Bacterial Numbers;337
14.3.2;B. PGPR and Other Symbiotic Systems such as Rhizobium-Legumes;338
14.3.3;C. Vegetative Growth and Grain Filling;339
14.3.4;D. Inoculant Technology;339
14.3.5;E. Probiotics in Agriculture;341
14.4;IV. Perspectives;341
14.5;Acknowledgments;342
14.6;References;343
15;Chapter 8: Interactions Between Nonpathogenic Fungi and Plants;354
15.1;I. Introduction;355
15.2;II. Interactions Between Plants and Endophytic Fungi;356
15.2.1;A. Plants and AM Fungi;356
15.2.1.1;1. Plant root colonization;357
15.2.1.2;2. Improvement of plant nutrition;357
15.2.1.3;3. Induction of plant resistance;359
15.2.2;B. Plants and Other Endophytic Fungi;362
15.2.2.1;1. Piriformospora indica;362
15.2.2.2;2. Binucleate Rhizoctonia;364
15.3;III. Interactions Between Plants and Free-Living Opportunistic Symbiotic Fungi;365
15.3.1;A. Plants and Trichoderma spp. BCAs;365
15.3.1.1;1. Plant root colonization;366
15.3.1.2;2. Improvement of plant nutrition;368
15.3.1.3;3. Induction of plant resistance;369
15.3.2;B. Plants and Nonpathogenic F. oxysporum;375
15.3.3;C. Plants and Nonpathogenic Penicillium spp., Phoma spp., and Pythium oligandrum;377
15.4;IV. Overview of Plant Defense Mechanisms Induced by Nonpathogenic Fungi;380
15.5;References;383
16;Chapter 9: Priming of Induced Plant Defense Responses;394
16.1;I. Introduction;395
16.2;II. Types of IR;395
16.2.1;A. Systemic Acquired Resistance (SAR);395
16.2.2;B. Resistance Induced by Beneficial Microorganisms;396
16.2.2.1;1. Induced systemic resistance (ISR);396
16.2.2.2;2. Resistance induced by symbiotic fungi;397
16.2.3;C. Resistance Induced by Chemicals;397
16.2.3.1;1. Synthetic SA analogs;397
16.2.3.2;2. beta-Aminobutyric acid;398
16.2.4;D. Resistance Induced by Wounding;398
16.2.5;E. Resistance Induced by Modifications of Primary Metabolism;399
16.3;III. Priming is a Mechanism of IR;400
16.3.1;A. History;400
16.3.2;B. Elucidation of Priming in Parsley Cell Cultures;400
16.3.3;C. Priming in SAR;402
16.3.3.1;1. Tobacco;402
16.3.3.2;2. Arabidopsis;402
16.3.3.3;3. Other species;404
16.3.4;D. Priming Induced by Beneficial Microorganisms;405
16.3.4.1;1. Priming in ISR;405
16.3.4.2;2. Priming in beneficial interactions other than ISR;406
16.3.4.3;3. Priming by bacterial lipopolysaccharides;407
16.3.5;E. Priming in BABA-IR;407
16.3.5.1;1. Biotic stress;407
16.3.5.2;2. Abiotic stress;409
16.3.6;F. Priming in Wound-Induced Resistance;409
16.3.6.1;1. Priming in IR to herbivores;409
16.3.6.2;2. Priming between plant species;411
16.3.7;G. Priming by Modifications in Primary Metabolism;411
16.4;IV. Relevance of Priming in Plant Production;412
16.4.1;A. Costs and Benefits of Priming;412
16.4.2;B. Exploiting Priming in Greenhouse and Field;413
16.5;V. Conclusions;417
16.6;Acknowledgments;417
16.7;References;417
17;Chapter 10: Transcriptional Regulation of Plant Defense Responses;430
17.1;I. Plant Immune Signaling Pathways;431
17.2;II. Defense Signaling Regulatory Compounds;433
17.2.1;A. Jasmonate Signal Transduction;433
17.2.2;B. Ethylene Signal Transduction;435
17.2.3;C. SA Signal Transduction;437
17.3;III. Transcription Factors Regulating Plant Defense Gene Expression;440
17.3.1;A. AP2/ERF Transcription Factors;441
17.3.2;B. MYB Transcription Factors;443
17.3.3;C. MYC Transcription Factors;445
17.3.4;D. bZIP Transcription Factors;446
17.3.5;E. WRKY Transcription Factors;448
17.4;IV. Regulation of Plant Defenses at the Chromosomal Level;453
17.4.1;A. Chromatin Modifications and Gene Expression;453
17.4.2;B. Chromatin Modifications in Plants;454
17.4.3;C. Chromatin Modifications at Promoters Involved in Innate Immunity;455
17.4.3.1;1. The SA pathway;455
17.4.3.2;2. The JA pathway;457
17.5;Acknowledgment;459
17.6;References;459
18;Chapter 11: Unexpected Turns and Twists in Structure/Function of PR-Proteins that Connect Energy Metabolism and Immunity;472
18.1;I. Historical Perspective Leading to the Recognition of Innate Immunity in Plants;473
18.1.1;A. Plant Immunity Involves Pathogenesis-Related (PR) Proteins;474
18.1.2;B. Definition and Classification of PR-proteins;475
18.2;II. Roles of PR-proteins Revealed by Studies of PR gene Expression;477
18.2.1;A. Cross-talk Between Overlapping Biotic and Abiotic Stress Response Pathways and Hormone Signaling Precludes Identification of Clear Roles for PR-proteins;477
18.2.2;B. Nutrient Acquisition Strategies of Pathogens Are Associated with Distinct PR gene Sets;479
18.2.3;C. The Connection Between Energy Balance and Immunity;482
18.3;III. PR-5 Protein Structure Reveals the Primitive Relationship Between Pathogen Defense and Energy Balance;483
18.3.1;A. Structural Features of PR-5 Proteins;483
18.3.2;B. Function of PR-5 Proteins in Plants;483
18.3.3;C. Information on Plant PR-5 Proteins in Genomic Databases;487
18.3.4;D. Comparison of THN Domain with C1q-TNF Domains;496
18.3.5;E. THN Domain Proteins and C1q-TNF Domains Across Phyla;502
18.4;IV. Directions in Which Current Classification or Definition of PR-proteins May Change in the Coming Years as Advanced Functional Studies Progress;505
18.5;References;507
19;Chapter 12: Role of Iron in Plant-Microbe Interactions;524
19.1;I. Introduction;525
19.2;II. Strategies of Iron Acquisition and Homeostasis by Plants and Microorganisms;527
19.2.1;A. Plants;527
19.2.1.1;1. Iron uptake by plant roots;527
19.2.1.1.1;a. Iron uptake in grasses (Strategy II;527
19.2.1.1.2;b. Iron uptake in the non?grass model plant;529
19.2.1.2;2. Organic compound exudates from roots and iron uptake;530
19.2.1.3;3. Regulation of high-affinity iron-transport systems;530
19.2.1.3.1;a. Transcriptional and translational regulation;530
19.2.1.3.2;b. Hormonal regulation;532
19.2.2;B. Microorganisms;532
19.2.2.1;1. Siderophore-mediated iron uptake;532
19.2.2.1.1;a. Iron uptake by fluorescent pseudomonads;533
19.2.2.1.2;b. Iron uptake in Erwinia;535
19.2.2.2;2. Regulation of the high-affinity iron-transport systems;536
19.3;III. Reciprocal Interactions Between Plants and Microorganisms During Their Saprophytic Life;538
19.3.1;A. Impact of Plant Iron Acquisition on Associated Microbes;538
19.3.1.1;1. Diversity;538
19.3.1.2;2. Activity;542
19.3.2;B. Impact of Microbial Iron Acquisition on the Host Plant;543
19.3.2.1;1. Plant health;543
19.3.2.1.1;a. Microbial antagonism;544
19.3.2.1.2;b. Induced systemic resistance;547
19.3.2.2;2. Plant growth and nutrition;549
19.4;IV. Reciprocal Interactions Between Plants and Microorganisms During Pathogenesis;551
19.4.1;A. Iron And Microbial Virulence: Role of High-Affinity Iron Assimilation Systems;552
19.4.1.1;1. Siderophore-controlled iron acquisition and Er. chrysanthemi pathogenicity;554
19.4.1.2;2. Siderophore-controlled iron acquisition and Er. amylovora pathogenicity;556
19.4.1.3;3. Siderophore-mediated iron acquisition and pathogenicity of ascomycete fungi;558
19.4.1.4;4. High-affinity iron acquisition and Ustilago maydis pathogenicity;559
19.4.2;B. Iron and Plant Defense;560
19.4.2.1;1. Iron homeostasis in wheat upon infection by Blumeria graminis;560
19.4.2.2;2. Involvement of ferritin in the response of potato to Phytophthora infestans;561
19.4.2.3;3. Iron homeostasis and resistance of Arabidopsis to Er. chrysanthemi;562
19.5;V. Conclusions;563
19.6;References;565
20;Chapter 13: Adaptive Defense Responses to Pathogens and Insects;584
20.1;I. Introduction;585
20.2;II. Co‐evolution of Defense Strategies;587
20.3;III. Portals of Entry and Activation of Defenses;589
20.3.1;A. Microbial Invasion Strategies: From Accessing the Apoplast to Haustoria Formation;590
20.3.2;B. Defense Pathway Activation by Microbes;591
20.3.3;C. Herbivore-Feeding Guilds: Mechanisms to Violate the Integrity of Plant Cells;592
20.3.3.1;1. Tissue-damaging herbivores: Modes of feeding;593
20.3.3.2;2. Tissue-damaging herbivores: Defense signaling and discerning the role of injury;594
20.3.3.3;3. Phloem-feeding hemipterans;596
20.4;IV. Perceiving Pathogen and Pest Visitations: The Role of Microbial and Herbivore Elicitors and Molecular Patterns;597
20.4.1;A. PAMPs, Pattern-Recognition Receptors, and BAK1;597
20.4.2;B. Elicitors of Plant Origin;598
20.4.3;C. Herbivore Elicitors;600
20.4.3.1;1. Lipid signals without receptors: Volicitin and caeliferin;601
20.4.3.2;2. Peptide elicitors of volatile emissions: Inceptin and beta-glucosidase;604
20.4.3.3;3. Oviduct secretions: Elicitors of defense gene expression and volatile emissions;605
20.4.3.4;4. Chitin;607
20.4.3.5;5. Salivary proteins as elicitors;607
20.4.3.5.1;a. Lysozyme;607
20.4.3.5.2;b. Hemipteran saliva;608
20.5;V. Integrating Signals and Activating Defenses;609
20.5.1;A. Mitogen-Activated Protein Kinase Signaling Cascades;610
20.5.2;B. Linking PAMPs to SA-, JA-, and ET-Regulated Defense Responses;613
20.6;VI. Adaptations to Unfriendly Hosts: Effectors and Evasion Tactics;614
20.6.1;A. Microbial Effectors;614
20.6.2;B. Herbivore Effectors;615
20.6.2.1;1. Effectors in regurgitant;615
20.6.2.2;2. Effectors in saliva;616
20.6.2.2.1;a. Glucose oxidase: A salivary effector that suppresses wound signaling;616
20.6.2.2.2;b. Decoy defenses: Suppressing effective defenses using SA–JA cross-talk;617
20.6.2.2.3;c. Antagonizing wound healing with calcium-binding proteins;619
20.6.2.2.4;d. Salivary oxidases and the Redox Hypothesis;620
20.6.2.2.5;e. Specialist insects: Tolerating toxic phytochemicals;621
20.7;VII. Effector-Triggered Immunity: Resistance to Pathogens and Pests;622
20.7.1;A. The Guard and Decoy Models;622
20.7.2;B. Plant–Herbivore Gene-for-Gene Interactions;623
20.7.2.1;1. Resistance genes;623
20.7.2.2;2. Mi1.2: One gene—many herbivores;624
20.7.2.3;3. Medicago resistance to aphids: A JA-dependent event;625
20.8;VIII. Summary and Future Prospects;626
20.9;Acknowledgments;628
20.10;References;628
21;Chapter 14: Plant Volatiles in Defence;646
21.1;I. Introduction to Volatile Organic Compounds (VOCs) From Plants;647
21.2;II. Herbivore-Produced Elicitors and Suppressors of Plant VOC Emission;649
21.3;III. Biosynthesis of Plant VOCs;652
21.3.1;A. Linoleic Acid/Octadecanoid Pathway-Related Compounds;652
21.3.2;B. Phenylalanine-Derived Volatiles;654
21.3.3;C. Terpenoids;655
21.3.4;D. Methanol;656
21.3.5;E. Ethylene;657
21.4;IV. Volatile Metabolism in Plant Trichomes;657
21.4.1;A. Trichome Function and Occurrence;657
21.4.2;B. Trichome Metabolomics and Transcriptomics;658
21.5;V. Volatile Defence Hormones MeJA, MeSA and Ethylene;660
21.6;VI. VOC Signals Are Influenced by Abiotic Factors and Plant Developmental Stage;665
21.7;VII. Natural Variation in VOC Production;668
21.8;VIII. VOC-Mediated Specificity of Indirect Defences;672
21.9;IX. VOCs as Alarm Signals for Neighbouring Plants;676
21.9.1;A. Transcriptional Responses to VOC Exposure;676
21.9.2;B. Priming of Plant Defences by Volatiles;679
21.10;References;684
22;Chapter 15: Ecological Consequences of Plant Defence Signalling;700
22.1;I. Introduction;701
22.2;II. Signalling at Three Different Levels;702
22.2.1;A. Local Signalling;702
22.2.1.1;1. Pathogen recognition;702
22.2.1.2;2. Resistance hormones;703
22.2.1.3;3. Further plant hormones;704
22.2.1.4;4. Cross-talk between growth and defence;706
22.2.2;B. Systemic Within-Plant Signalling;706
22.2.2.1;1. Systemic signals triggering herbivore resistance;707
22.2.2.2;2. Systemic signals triggering pathogen resistance;708
22.2.2.3;3. Small RNA signalling;709
22.2.2.4;4. Airborne systemic signals;709
22.2.3;C. Airborne Plant–Plant Communication;710
22.2.3.1;1. Does ‘plant–plant communication’ exist?;710
22.2.3.2;2. Airborne resistance induction to herbivores and pathogens;710
22.2.3.3;3. Mechanisms of airborne plant–plant communication;712
22.2.3.4;4. Priming by VOCs;713
22.3;III. Costs of Induced Resistance;713
22.3.1;A. Allocation Costs;714
22.3.2;B. Ecological Costs;716
22.3.2.1;1. Trade-offs with resistance to insects;716
22.3.2.2;2. Trade-offs with mutualistic symbioses;718
22.3.2.3;3. Does induced resistance alter phytobacterial communities?;719
22.3.2.4;4. Ecological costs of resistance to biotrophic versus necrotrophic pathogens;719
22.4;IV. Resistance Induced by Mutualistic Micro-organisms;720
22.4.1;A. Resistance Mediated by Plant Growth-Promoting Rhizobacteria (PGPR);720
22.4.2;B. Resistance Induction by Mycorrhiza;722
22.5;V. Defence Signalling at the Level of Plant Individual, Community and Evolution;723
22.5.1;A. Variable Resistance at the Genetic Level;723
22.5.2;B. Variable Resistance at the Phenotypic Level;724
22.5.3;C. Plant–Plant Communication at the Community Level?;724
22.5.4;D. Evolutionary Considerations;726
22.5.5;E. Predicting Patterns of Induced Resistance Responses;726
22.5.5.1;1. Growth-differentiation balance hypothesis (GDBH) and optimal defencehypothesis (ODH);727
22.5.5.2;2. Carbon/nutrient balance hypothesis (CNBH) and resource availabilityhypothesis (RAH);728
22.6;VI. Conclusions and Outlook;731
22.7;Acknowledgments;732
22.8;References;732
23;Author Index;750
24;Subject Index;772
25;Color Plates;788