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
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 3550 ;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 PTIA 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 MechanismsType 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 Plants 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 FlowerSignaling Events in the Vegetative to Flowering Transition ;158 11.2.1;A. Flower
ing 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 Sign
aling ;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 Dont 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 ArabidopsisPseudomonas 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 EndophytesRo
le 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 Invol
ves 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 SAJA 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. PlantHerbivore Gene-for-Gene Interactions;623 20.7.2.1;1. Resistance genes;623 20.7.2.2;2. Mi1.2: One genemany 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 PlantPlant Communication;710 22.2.3.1;1. Does plantplant communication exist?;710 22.2.3.2;2. Airborne resistance induction to herbivores and pathogens;710 22.2.3.3;3. Mechanisms of airborne plantplant 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. PlantPlant 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
