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Contributors xiii
Preface to Second Edition xvii
Preface to First Edition xix
1 Introduction: Definitions and Some History 1Ray Hammerschmidt
1.1 Induced Resistance: An Established Phenomenon 1
1.2 Terminology and Types of Induced Resistance 2
1.2.1 Local and systemic induction of resistance 2
1.2.2 Systemic acquired resistance (SAR) and induced systemic resistance (ISR) 2
1.2.3 Protection 3
1.2.4 Cross protection 3
1.2.5 Priming 4
1.3 A Little History 4
1.3.1 Early reports 4
1.3.2 Developments leading towards today's state of knowledge 5
1.4 It's All About Interactions 7
1.5 Acknowledgements 8
References 8
2 Agents That Can Elicit Induced Resistance 11Gary D. Lyon
2.1 Introduction 11
2.2 Compounds Inducing Resistance 12
2.2.1 Acibenzolar-S-methyl (ASM) 12
2.2.2 Adipic acid 12
2.2.3 Algal extracts 12
2.2.4 Alkamides 12
2.2.5 Allose 13
2.2.6 Antibiotics 13
2.2.7 Azelaic acid 13
2.2.8 DL-3-Aminobutyric acid (BABA) 13
2.2.9 Benzothiadiazole (BTH) and other synthetic resistance inducers 14
2.2.10 Bestcure® 15
2.2.11 Brassinolide 15
2.2.12 ß-1,4 Cellodextrins 15
2.2.13 Chitin 15
2.2.14 Chitosan 16
2.2.15 Cholic acid 16
2.2.16 Curdlan sulfate 17
2.2.17 Dehydroabietinal 17
2.2.18 3,5-Dichloroanthranilic acid (DCA) 17
2.2.19 Dichloroisonicotinic acid (INA) 17
2.2.20 Dimethyl disulfide 17
2.2.21 Dufulin 17
2.2.22 Ergosterol 17
2.2.23 Ethylene 17
2.2.24 Fatty acids and lipids 18
2.2.25 2-(2-Fluoro-6-nitrobenzylsulfanyl)pyridine-4-carbothioamide 18
2.2.26 Fructooligosaccharide 18
2.2.27 Fungicides 18
2.2.28 Galactinol 19
2.2.29 Grape marc 19
2.2.30 Glucans 19
2.2.31 Harpin 20
2.2.32 Hexanoic acid 20
2.2.33 Imprimatin 20
2.2.34 INF1 elicitin 21
2.2.35 Jasmonates and related compounds 21
2.2.36 Cis-jasmone 21
2.2.37 Laminarin 21
2.2.38 Lipids/fatty acids 21
2.2.39 Lipopolysaccharides (LPS) 22
2.2.40 Nitric oxide 22
2.2.41 Oligo-carrageenans 22
2.2.42 Oligogalacturonides (OGAs) 22
2.2.43 Oligoglucuronans 23
2.2.44 Oxalate 23
2.2.45 Phosphite 23
2.2.46 Phytogard® 23
2.2.47 Pipecolic acid 23
2.2.48 Plant extracts 23
2.2.49 Probenazole (PBZ) 24
2.2.50 Proteins and peptides 24
2.2.51 Psicose 26
2.2.52 Rhamnolipids 26
2.2.53 Saccharin 26
2.2.54 Salicylic acid 26
2.2.55 Silicon 27
2.2.56 Spermine 27
2.2.57 Sphingolipids 27
2.2.58 Sulfated fucan oligosaccharides 27
2.2.59 Tiadinil 27
2.2.60 Vitamins 27
2.2.61 Volatile organic compounds 28
2.3 Redox Regulation 28
2.3.1 Factors affecting efficacy 29
2.4 Elicitor Combinations and Synergism 29
2.5 Assays 30
2.6 Conclusions 30
References 31
3 Transcriptome Analysis of Induced Resistance 41Brendan Kidd, Kemal Kazan and Peer M. Schenk
3.1 Introduction 41
3.2 The Impact of Arabidopsis thaliana on Induced Resistance 42
3.3 Techniques Used for Studying Gene Expression 42
3.3.1 EST sequencing 42
3.3.2 Real-time quantitative RT-PCR (qRT-PCR) 42
3.3.3 cDNA microarrays and DNA chips 43
3.3.4 Novel insights into induced resistance revealed through microarray analysis 45
3.3.5 Systems biology and network approaches using microarrays 48
3.3.6 Next-generation sequencing 48
3.4 How Sequencing Helps Crop Research 50
3.4.1 Converting knowledge from model organisms to crop plants 50
3.5 Conclusion 51
3.6 Acknowledgements 52
References 52
4 Signalling Networks Involved in Induced Resistance 58Corné M.J. Pieterse, Christos Zamioudis, Dieuwertje Van der Does and Saskia C.M. Van Wees
4.1 Introduction 58
4.2 The SA-JA Backbone of the Plant Immune Signalling Network 59
4.2.1 Salicylic acid 60
4.2.2 Jasmonic acid 61
4.3 SA and JA: Important Signals in Systemically Induced Defence 63
4.3.1 Pathogen-induced SAR 63
4.3.2 ISR triggered by beneficial microbes 64
4.3.3 Rhizobacteria-ISR signal transduction 65
4.4 ISR and Priming for Enhanced Defence 66
4.4.1 Molecular mechanisms of priming 67
4.5 Hormonal Crosstalk During Induced Defence 68
4.5.1 Mechanisms of crosstalk between SA and JA signalling 69
4.5.2 Rewiring of the hormone signalling network by plant enemies 70
4.6 Outlook 71
4.7 Acknowledgements 71
References 72
5 Types and Mechanisms of Rapidly Induced Plant Resistance to Herbivorous Arthropods 81Michael J. Stout
5.1 Introduction: Induced Resistance in Context 81
5.2 Comparison of the Threats Posed by Pathogens and Herbivores 83
5.3 Types of Induced Resistance 85
5.3.1 Hypersensitive responses 85
5.3.2 Direct induced resistance 86
5.3.3 Indirect induced resistance 88
5.3.4 Plant stress-induced resistance 90
5.3.5 Tolerance 91
5.3.6 Priming 91
5.3.7 Interplant signalling 92
5.3.8 Concurrent expression of multiple types of induced resistance 92
5.4 Establishing the Causal Basis of Induced Resistance 93
5.4.1 The complex causal basis of induced resistance 93
5.4.2 Approaches to understanding the causal basis of induced resistance 95
5.5 Arthropods as Dynamic Participants in Plant-Arthropod Interactions 98
5.6 Summary and Conclusions 99
References 100
6 Mechanisms of Defence to Pathogens: Biochemistry and Physiology 106Christophe Garcion, Olivier Lamotte, Jean-Luc Cacas and Jean-Pierre Métraux
6.1 Introduction 106
6.2 Structural Barriers 106
6.2.1 Early events: The cytoskeleton and traffic of vesicles 107
6.2.2 The nature of cell wall appositions 108
6.2.3 Lignification 109
6.3 Phytoalexins 109
6.3.1 The concept of phytoalexins 109
6.3.2 Distribution of phytoalexins among taxons and individuals 110
6.3.3 Biosynthetic pathways and their regulation 110
6.3.4 Role of the phytoalexins in the defence response 113
6.4 The Hypersensitive Response (HR) 115
6.4.1 In the death car - en route to plant resistance to pathogens 115
6.4.2 The role of reactive oxygen and nitrogen species (ROS and RNS) 116
6.4.3 On the highway of hypersensitive cell death: Signalling and regulation 118
6.4.4 License to kill: Where do we stand on execution of hypersensitive cell death? 120
6.5 Antimicrobial Proteins or Defence-Related Proteins 122
6.5.1 Introduction 122
6.5.2 Use of PRs for crop protection: Current status 122
6.5.3 Other changes in the transcriptome related to pathogenesis 123
6.6 Conclusions 125
References 125
7 Induced Resistance in Natural Ecosystems and Pathogen Population Biology: Exploiting Interactions 137Adrian C. Newton and Jörn Pons-Kühnemann
7.1 Introduction 137
7.2 Environmental Variability 137
7.3 Ecology of the Plant Environment 139
7.4 Environmental Parameters 140
7.5 Plant and Pathogen Population Genetics 141
7.6 Consequences of Resistance Induction 143
7.7 Conclusions 144
7.8 Acknowledgements 145
References 145
8 Microbial Induction of Resistance to Pathogens 149Dale R. Walters and Alison E. Bennett
8.1 Introduction 149
8.2 Resistance Induced by Plant Growth Promoting Rhizobacteria and Fungi 149
8.2.1 PGPR 150
8.2.1.1 Spectrum of activity 150
8.2.1.2 Interactions between plant roots and PGPR 152
8.2.1.3 PGPR and plant growth 152
8.2.1.4 PGPR in the field 153
8.2.2 PGPF 155
8.3 Induction of Resistance by Biological Control Agents 155
8.4 Resistance Induced by Composts 157
8.5 Disease Control Provided by Endophytes 159
8.6 Arbuscular Mycorrhizal Symbiosis and Induced Resistance 160
8.7 Acknowledgements 162
References 163
9 Trade-offs Associated with Induced Resistance 171Martin Heil
9.1 Introduction 171
9.2 Resistance Inducers 172
9.2.1 Eliciting resistance to biotrophic pathogens 172
9.2.2 Eliciting resistance to necrotrophic pathogens and herbivores 174
9.2.3 Volatile elicitors 176
9.2.4 Priming 177
9.3 Costs of Induced Resistance 178
9.3.1 Allocation costs 179
9.3.2 Priming as cost-reducing mechanism 181
9.3.3 Ecological costs 182
9.3.4 Dependency on cultivars 183
9.3.5 Context dependency 183
9.4 Outlook 184
References 185
10 Topical Application of Inducers for Disease Control 193Christine Tayeh, Ali Siah, Béatrice Randoux, Patrice Halama, Dale R. Walters and Philippe Reignault
10.1 Introduction 193
10.2 Biotic Inducers 193
10.2.1 Chitin and chitosan 196
10.2.2 Fragments and extracts of fungal cell walls 197
10.2.3 Extracts and materials derived from marine macroalgae 198
10.2.4 Lipids 198
10.3 Abiotic Inducers 198
10.3.1 Benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester (BTH)/acibenzolar-S-methyl (ASM) 199
10.3.1.1 Diseases caused by leaf and stem-infecting fungi 199
10.3.1.2 Diseases caused by oomycetes 201
10.3.1.3 Fungal soil-borne diseases 201
10.3.1.4 Fungal postharvest diseases 202
10.3.1.5 Diseases caused by bacteria, viruses and insects 203
10.3.2 Salicylic acid and structurally related compounds 205
10.3.2.1 Salicylic acid 205
10.3.2.2 SA derivatives 207
10.3.3 Proteins, peptides and amino acid-derived inducers 208
10.3.3.1 ß-aminobutyric acid (BABA) 208
10.3.3.2 Harpin 209
10.3.3.3 Other purified proteins 210
10.3.4 Lipids 211
10.3.4.1 Oxylipins 211
10.3.4.2 Fatty acids 214
10.3.5 Active oxygen species 214
10.3.6 Sugars 215
10.3.7 Phytohormones 215
10.3.8 Mineral and ions 216
10.3.8.1 Copper 216
10.3.8.2 Other minerals 216
10.3.8.3 Silicon 216
10.3.8.4 Calcium-based compounds 217
10.3.8.5 Other inducers 217
10.3.9 Vitamins 217
10.3.10 Physical treatments 218
10.4 Conclusions 218
10.5 Acknowledgements 218
References 219
11 How do Beneficial Microbes Induce Systemic Resistance? 232Emily Beardon, Julie Scholes and Jurriaan Ton
11.1 Plant-Beneficial Microbes 232
11.2 The Plant Immune System as a Regulator of Plant-Biotic Interactions 233
11.2.1 The plant innate immune system: Induced defence 234
11.2.2 The plant adaptive immune system: Priming of defence 235
11.3 How do Beneficial Microbes Cope with the Plant Immune System? 236
11.3.1 Evasion and suppression of plant immunity by rhizobia 236
11.3.2 Suppression of plant immunity by mycorrhizal fungi 237
11.3.3 Evasion and suppression of plant immunity by PGPR 238
11.4 The ISR Paradox: Local Suppression of Immunity Leads to Systemic Resistance 239
11.4.1 The hormone hypothesis 239
11.4.2 The autoregulation hypothesis 240
11.4.3 The sRNA hypothesis 241
11.5 Concluding Remarks and Future Directions 241
References 242
12 Implementation of Induced Resistance for Crop Protection 249Tony Reglinski, Elizabeth Dann and Brian Deverall
12.1 Introduction 249
12.2 Induced Resistance for Disease Control 250
12.2.1 Commercially available activators for glasshouse, orchard and field crops 251
12.2.1.1 Acibenzolar-S-methyl 251
12.2.1.2 Tiadinil 253
12.2.1.3 Probenazole 253
12.2.1.4 Isotianil 253
12.2.1.5 Phosphite 254
12.2.1.6 Plant extracts 254
12.2.1.7 Polysaccharides 254
12.2.1.8 Harpin protein 255
12.2.1.9 Silicon 256
12.3 Induced Resistance for Postharvest Disease Control 257
12.4 Compatibility of Activators with Other Control Methods 260
12.4.1 Fungicides 260
12.4.2 Bactericides 262
12.4.3 Insecticides 263
12.4.4 Beneficial microorganisms 264
12.5 Influence of Genotype, Environment and Management Practices on Induced Resistance 266
12.6 Integration of Plant Activators in Crop Management 273
12.7 Challenges and Future Directions 276
12.8 Conclusions 281
References 282
13 Exploitation of Induced Resistance: A Commercial Perspective 300Andy Leadbeater and Theo Staub
13.1 Introduction 300
13.2 Science and Serendipitous Discovery of Resistance-Inducing Compounds 301
13.3 Discovery of INAs and BTHs 302
13.4 Identification of BION® and other SAR Activators 303
13.5 The Role of Basic Studies in the Discovery of BION® and other SAR/ISR Products 304
13.6 Identification of Harpin 305
13.7 Extracts from Reynoutria sachalinensis 305
13.8 The Commercial Development of an Induced Resistance Product 306
13.9 Legislative Framework 308
13.10 Commercial Experiences with Induced Resistance Products 309
13.11 Conclusions 312
References 312
14 Induced Resistance in Crop Protection: The Future, Drivers and Barriers 316Gary D. Lyon, Adrian C. Newton and Dale R. Walters
14.1 Introduction 316
14.2 Strategies to Increase Efficacy and Durability in the Field 317
14.3 What Research is Required to Make Induced Resistance Work in Practice? 318
14.4 Can We Breed Plants with Enhanced Responsiveness to Inducers? 321
14.5 The Potential for GM Plants Containing SAR-related Genes 321
14.6 Political, Economic and Legislation Issues 322
14.7 Conclusion 322
14.8 Acknowledgements 323
References 323
Index 327
Ray Hammerschmidt
Department of Plant, Soil and Microbial Science, Michigan State University, East Lansing, MI, USA
Certain types of pathogen infection, non-pathogen interaction or other treatments are known to induce localized and systemic disease resistance (e.g. Kuć, 1982; Hammerschmidt and Kuć, 1995; Sticher et al., 1997; Hammerschmidt, 2009; Vallad and Goodman, 1994). The induced plant is believed to resist attack by virulent pathogens and other pests because of an enhanced ability to rapidly express defences upon infection and, in some cases, an increase in defences that are expressed in response to the inducing treatment. Although well established and studied, it is important to consider why induced resistance occurs. How can a plant that is known to be susceptible to a pathogen or even multiple pathogens be physiologically or biochemically changed so that it can now resist those infections?
Two basic assumptions must be considered to explain the overall phenomenon of induced resistance. First of all, plants must have all the genes that are necessary to mount an effective defence. Secondly, the inducing treatment should be capable of activating some of the defences directly and, more importantly, that the inducing treatment primes or sensitizes that plant in such a way that allows rapid expression of a broad set of defences upon infection by a pathogen.
The first assumption is easy to support. It is a well known plant pathology concept that plants resist the vast majority of pathogens which exist in nature, and that this phenomenon (non-host resistance) is associated with the expression of defences (Heath, 2000) and is the basis for innate immunity in plants (van Loon, 2009). Most plants, however, are susceptible to some pathogens or specific isolates or races of those pathogens. This does not mean that the plant lacks the defence needed to fend off the pathogen, but rather that the plant does not have the means to rapidly detect the presence of the pathogen (e.g. a major gene for resistance) and induce the expression of genes needed for defence. The second assumption also has significant support: plants that are induced have enhanced capacity to rapidly express defences after a challenge infection (Conrath et al., 2002).
Plant resistance to pathogens and pests can be active and/or passive (Hammerschmidt, and Nicholson, 1999). Passive resistance depends on defences that are constitutively expressed in the plant, while active resistance relies on defences that are induced after infection or attack. Induced resistance is an active process that can describe resistance at two levels. Firstly, active defence to an incompatible race or isolate of a pathogen is a form of induced resistance that is characterized by highly localized expression of defences such as phytoalexins and the hypersensitive response (Hammerschmidt and Nicholson, 1999). Secondly, induced resistance can also describe plants that express resistance to a broad range of compatible pathogens after some initial inducing treatment (Kuć, 1982). It is this latter form of induced resistance that is the focal point of this book. The term induced resistance in itself only describes the general phenomenon and does not imply any specific type of defence expression or regulation.
Induced resistance can be local or systemic. Local induced resistance refers to those cases where the inducing treatment is applied to the same tissue as the subsequent challenge by a pathogen. In some cases, the challenge inoculum is placed directly on the site of the inducing inoculation, while in other cases the phenomenon describes resistance that occurs within a single organ (such as a leaf) after all or part of the leaf was treated with an inducing agent. Systemic induced resistance describes resistance that is induced in a part of the plant that is spatially separated from the point of induction. Although spatially different, both local and systemic resistances are characterized by requiring time to develop after the inducing treatment and the non-specific nature of the resistance. The mechanisms of stopping pathogen development in locally induced resistance may be due to the production of defences such as phytoalexins, PR (pathogenesis-related) proteins and cell wall alterations that are thought to be involved in stopping the development of the inducing inoculum as well as propagules of the challenge pathogen that have the misfortune of landing directly on the site occupied by the inducing inoculum (Hammerschmidt, 1999, 2009). In the case of systemic resistance, the inducing or resistance activating treatments result in a change in cells at a distance from the induction site that allows those cells to rapidly deploy defences upon challenge. This is the part of systemic resistance that is now known as ‘priming’ (Conrath et al., 2002). In addition to being primed, the systemically induced tissues may also have some degree of defence that is established by the induction process that is there prior to any challenge. An obvious example is the systemic expression of PR proteins in certain forms of systemic induced resistance (Van Loon, 1997).
It is very clear that induced resistance to disease is not due to just one phenomenon. At least two forms of induced resistance, known as systemic acquired resistance (SAR) and induced systemic resistance (ISR) have been characterized as distinct phenomena based on the types of inducing agents and host signalling pathways that result in resistance expression (Sticher et al., 1997; Van Loon et al., 1998).
A major characteristic of SAR is of the association of localized necrosis caused by the inducing pathogen. This necrosis can be either a hypersensitive response or a local necrotic lesion caused by a virulent pathogen (Hammerschmidt, 2009). SAR is also dependent on salicylic acid signaling and the systemic expression of pathogenesis related protein genes (Hammerschmidt, 1999, 2009; Sticher et al., 1997). ISR is induced by certain strains of plant growth promoting rhizobacteria (PGPR) (Van Loon et al., 1998; De Vleesschauwer and Höfte, 2009). Unlike SAR, ISR is not associated with local necrotic lesion formation. ISR also differs in that it depends on the perception of ethylene and jasmonic acid and is not associated with expression of the PR genes. Both SAR and ISR do result in broad-spectrum resistance. The differences in mechanisms and signalling leading to SAR and ISR as well as potential trade-offs between these different forms of induced resistance are described in the chapters by Pieterse et al. (Chapter 4) and Heil (Chapter 9), respectively.
It should also be noted that many of the features that have been used to distinguish ISR from SAR are based on studies with Arabidopsis in which specific genetic analyses have been coupled with biochemical and pathological analyses (see Chapter 4). Because the phenotypes of SAR and ISR are similar, if not identical, in terms of reducing the effects of pathogen challenge, distinguishing between ISR and SAR should be approached with caution when dealing with plant–pathogen interactions other than genetically well-defined systems, such as those utilizing Arabidopsis. With the many types of inducing agents that have been identified and the great number of microbes that can also induce resistance (see the chapters by Lyon (Chapter 2), Randoux et al. (Chapter 10), Walters and Bennett (Chapter 8) and Beardon et al. (Chapter 11)), it is likely that other forms of induced resistance may occur. Use of the tools of genomics to understand the molecular basis and regulation of induced resistance, such as those outlined by Kidd et al. (Chapter 3), will be invaluable in sorting out types of induced resistance in model systems as well as those crops in which induced resistance may be applied in the future.
Certain reports from the 1970s used the term ‘protection’ to describe induced resistance (e.g. Hammerschmidt et al., 1976; Kuć et al., 1975; Skipp and Deverall, 1973). These reports on induced resistance in both cucumber and green bean plants described the ability of incompatible fungal pathogens to induce resistance. Although the term ‘protection’ adequately describes what is happening in terms of the end result, this is really too generic to be of use in describing induced resistance.
It has been known for many years that prior infection of plants with milder strains of a virus can result in reduced disease development on subsequent infection by a more severe strain of the same virus (Pennazio et al., 2001; Price, 1940). This phenomenon is known as cross protection, and is really very different from the induced resistance phenomena that are discussed throughout this book. Unlike induced resistance where defences, or the potential to express defences, are activated by the inducing treatment, cross protection is mechanistically very different and relies more on interference of the mild viral stain with the more severe strain than by defensive action (Fulton, 1986). Cross protection also differs from induced resistance in that the protection is only effective against strains of the same virus whereas induced resistance is much broader...
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