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Annual Plant Reviews, Plant-Pathogen Interactions

De
264 pages
Annual Plant Reviews, Volume 11

Plant diseases are destructive and threaten virtually any crop grown on a commercial scale. They are kept in check by plant breeding strategies that have introgressed disease resistance genes into many important crops, and by the deployment of costly control measures, such as antibiotics and fungicides. However, the capacity for the agents of plant disease – viruses, bacteria, fungi and oomycetes – to adapt to new conditions, overcoming disease resistance and becoming resistant to pesticides, is very great. For these reasons, understanding the biology of plant diseases is essential for the development of durable control strategies.


This volume provides an overview of our current knowledge of plant-pathogen interactions and the establishment of plant disease, drawing together fundamental new information on plant infection mechanisms and host responses. The role of molecular signals, gene regulation and the physiology of pathogenic organisms are emphasised, but the role of the prevailing environment in the conditioning of disease is also discussed.


This is a book for researchers and professionals in plant pathology, cell biology, molecular biology and genetics.

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Contents
List of Contributors Preface
1
2
Emerging themes in plant–pathogen interactions NICHOLAS J. TALBOT
1.1 Introduction 1.2 Breaching the host cuticle 1.2.1 MAP kinase signalling during infectionrelated development by fungi 1.3 Invading host tissue 1.4 Subverting host metabolism and defence 1.4.1 Effector proteins deployed by pathogenic bacteria 1.4.2 Host mimicry 1.5 Perception of pathogens 1.5.1 Recognition in geneforgene interactions and the guard hypothesis 1.6 Genomelevel analysis of pathogens 1.6.1 Fungal and oomycete phytopathogen genomics 1.7 The future References
Tobacco mosaic virus JOHN PETER CARR
2.1 2.2
2.3
2.4
Introduction Tobacco mosaic virus: virion and genome structure 2.2.1 Genome structure and the taxonomy of TMV and related viruses 2.2.2 The TMV virion 2.2.3 Virion assembly 2.2.4 Proteins encoded by the TMV genome 2.2.5 Untranslated and regulatory RNA sequences within the TMV genome 2.2.6 The establishment of TMV infection TMV replication and the synthesis of subgenomic mRNAs 2.3.1 The process of replication and subgenomic RNA synthesis 2.3.2 The composition of the TMV replicase complex and its location in the infected cell Movement of TMV within the host 2.4.1 Celltocell movement of tobamoviruses 2.4.1.1 Plasmodesmata and the viral movement protein 2.4.1.2 Interactions of the TMV MP with host cell ultrastructure 2.4.1.3 Interactions of the TMV MP with host proteins 2.4.1.4 Are other virusencoded proteins involved in celltocell movement?
x xii
1
1 1 2 4 4 7 8 9 14 15 17 18 19
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27 28 28 29 29 30
32 32 34 34
35 38 38 38 40 41
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vi
3
4
CONTENTS
2.4.2 Systemic movement of tobamoviruses 2.4.2.1 Virus movement and the phloem 2.4.2.2 The movement protein 2.4.2.3 The coat protein and systemic movement 2.4.2.4 The replicase proteins, virus replication, and systemic movement 2.4.2.5 The role of the host in the systemic movement of tobamoviruses 2.5 Host reactions to TMV 2.5.1 The ‘susceptible’ host 2.5.1.1 Chlorosis and vein clearing in systemically infected plants 2.5.1.2 Mosaic symptoms in systemically infected plants: an effect of localized RNA silencing? 2.5.2 Resistance to tobamoviruses 2.5.2.1 TheNresistance gene 2.5.2.2 Resistance genes that are elicited by the tobamoviral CP 2.5.2.3 Genes for resistance to tobamoviruses in tomato 2.5.2.4 Genetically engineered resistance to tobamoviruses 2.6 Future directions for TMV research: making an old foe into a new friend? Acknowledgments References
Infection with potyviruses MINNALIISA RAJAMÄKI, TUULA MÄKIVALKAMA, KRISTIINA MÄKINEN and JARI P.T. VALKONEN
3.1 Infection cycle (general summary) 3.2 Architecture of virions 3.3 Entry of virions into the cell, disassembly and assembly 3.4 Translation and polyprotein processing 3.4.1 Translation initiation 3.4.2 Polyprotein processing 3.5 RNA synthesis and viral genome replication 3.6 Virus movement 3.6.1 Intracellular movement 3.6.2 Celltocell movement 3.6.3 Vascular movement 3.7 Induction of symptoms 3.8 Transmission 3.8.1 Transmission by aphids 3.8.2 Seed transmission 3.8.3 Mechanical transmission 3.9 Variability and evolution Acknowledgments References
TheRalstonia solanacearum–plant interaction CHRISTIAN BOUCHER and STÉPHANE GENIN
4.1
The pathogen 4.1.1 A major plant pathogen with an unusually wide host range 4.1.2 Taxonomical status of the species and infraspecific classification
43 43 43 45
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47 47 47 49
49 51 51 52 52 53 54 55 55
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68 70 72 72 72 73 74 76 76 77 78 79 81 81 81 82 82 84 85
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92 92 92
5
6
CONTENTS
4.1.3R. solanacearum, a vascular pathogen that promotes xylem vessel occlusion 4.1.4 Epidemiology and environmental survival 4.2 Molecular studies of pathogenicity determinants 4.2.1 Exopolysaccharide I 4.2.2 Protein secretion systems 4.2.2.1 Plant cell wall degrading enzymes and proteins secreted through the General Secretory Pathway 4.2.2.2 The Type III secretion system (TTSS) 4.2.3 Motility and attachment to host cell surfaces 4.2.3.1 Swimming motility 4.2.3.2 Type IV pili 4.2.4 Regulation of pathogenicity 4.2.4.1 PhcA, a global regulator controlling phenotypic conversion 4.2.4.2 An atypical cellsensing system 4.2.4.3 A multicomponent network regulating virulence functions 4.2.4.4hrpgene activation in response to plant cell contact 4.2.5 Genomewide identification of candidate genes potentially involved in pathogenicity Acknowledgment References
ThePseudomonas syringae–bean system SUSAN S. HIRANO and CHRISTEN D. UPPER
5.1 Introduction 5.2 The system 5.3 Population sizes of Pss on populations of leaf habitats 5.4 Population processes: searching for causes of variability in pathogen population sizes 5.4.1 Immigration and multiplication 5.4.2 Emigration and death 5.4.3 The four processes working together 5.4.4 Enter the environment 5.4.5 Enter the host 5.5 Pss population sizes and the likelihood of disease development 5.6 How does Pss cause brown spot lesions? 5.6.1 Growth chamber assays 5.6.2 Field experiments 5.6.2.1 Germinating bean seeds 5.6.2.2 Leaves 5.6.2.3 Brown spot disease 5.6.3 Growth chamber assays revisited 5.6.4 Reconciliation 5.7 Summary References
Fungal pathogenesis in the rice blast fungusMagnaporthe griseaCHAOYANG XUE, LEI LI, KYEYONG SEONG and JINRONG XU
6.1 6.2
Introduction Life cycle ofMagnaporthe grisea
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94 95 97 97 98
98 100 102 102 102 103 104 104 104 105
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113 114 114
117 118 120 120 121 123 124 125 127 129 129 129 130 131 131 132 134
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7
6.3 6.4 6.5 6.6 6.7 6.8 6.9
CONTENTS
Conidium attachment and germination 6.3.1 Attachment 6.3.2 Germination Appressorium morphogenesis 6.4.1 Surface recognition and appressorium initiation 6.4.2 Appressorium maturation 6.4.3 The role of cAMP signaling in surface recognition and appressorium initiation 6.4.4PMK1regulates appressorium formation and maturation 6.4.5 HydrophobinMPG1and surface recognition 6.4.6 Other factors affecting appressorium formation 6.4.7 Other mutants defective in appressorium morphogenesis Penetration 6.5.1 Penetration peg 6.5.2 Forces of penetration 6.5.3 Turgor generation 6.5.4 Other genes involved in appressorial penetration Infectious growth and lesion formation 6.6.1 Infectious hyphae 6.6.2 Phytotoxins produced byM. grisea6.6.3 Avirulence genes 6.6.4 Nutritional requirements and metabolic activities during infectious growth 6.6.5 Other mutants defective in infectious growth and lesion formation 6.6.6 Genes specifically or highly expressed during infectious growth Conidiation Genomics studies Future perspectives References
TheUstilago maydis–maize interaction MARIA D. GARCIAPEDRAJAS, STEVEN J. KLOSTERMAN, DAVID L. ANDREWS and SCOTT E. GOLD
7.1 7.2 7.3 7.4
7.5
7.6
Introduction Teliospore germination and meiosis Mating and dikaryon formation Penetration 7.4.1 Infection structures inU. maydis7.4.2 Can haploid strains penetrate plant cells? 7.4.3 Regulation of appressorium formation and plant penetration 7.4.4 Potential role of lytic enzymes in penetration Colonization of maize tissue 7.5.1 Proliferation of hyphae 7.5.2 Interspecies signaling and colonizationspecific fungal gene expression 7.5.3 The biotrophic interface Gall formation and teliosporogenesis 7.6.1 Developmental stages during gall formation and teliosporogenesis 7.6.2 Genetic regulation of gall formation and teliosporogenesis 7.6.3 Completion of sexual cyclein vitro7.6.4 Role of phytohormones in gall formation
141 141 142 142 142 143
144 145 147 147 148 149 149 149 150 151 152 152 153 153
154 155 156 157 158 159 159
166
166 168 169 178 178 180 181 181 182 182
184 185 186 186 187 190 191
8
9
7.7 Survival 7.8 Genetic diversity inU. maydis7.9 Host resistance 7.10 Conclusions Acknowledgements References
CONTENTS
Blumeria graminisf. sp.hordei, an obligate pathogen of barley MAIKE BOTH and PIETRO D. SPANU
8.1 Introduction 8.2 Life cycle – an overview 8.3 Conidia and germination 8.4 Surface perception and early events following contact with the surface 8.5 Signal transduction during early development ofB. graminisf. sp.hordei8.5.1 cAMP and PKA 8.5.2 MAP kinases 8.5.3 PKC 8.5.4 Gproteins 8.6 Penetration 8.7 The haustorium 8.8 Vegetative growth and sporulation 8.9 Outlook References
ThePhytophthora infestans–potato interaction PIETER VAN WEST and VIVIANNE G.A.A. VLEESHOUWERS
9.1 Introduction 9.2 History of late blight 9.3 Economic and social impact ofPhytophthoraplant pathogens 9.4Phytophthora infestansand its taxonomic position 9.5 The disease cycle ofPhytophthora infestans9.5.1 Molecular and cellular events during the disease cycle ofP. infestans 9.5.1.1 Release of zoospores from sporangia 9.5.1.2 Encystment, germination, and appressoria formation 9.5.1.3 Mating 9.5.1.4In plantagene expression 9.6 The plant response 9.6.1 Compatible interactions 9.6.2 Incompatible interactions 9.6.2.1 Racespecific resistance and the hypersensitive response 9.6.2.2 Avirulence genes 9.6.2.3 Resistance genes 9.6.2.4 Nonhost resistance 9.6.2.5 Partial resistance 9.6.3 Durable resistance 9.7 Future perspectives Acknowledgements References
Index
ix
191 192 193 194 195 195
202
202 203 205 206 209 209 210 211 212 212 213 215 216 217
219
219 219 220 221 221 223 223 225 227 228 231 231 231 231 231 232 233 234 234 235 236 236
243