Fungal pathogenesis in plants and crops: molecular biology and host defense mechanisms
Gespeichert in:
| 1. Verfasser: | |
|---|---|
| Format: | Buch |
| Sprache: | English |
| Veröffentlicht: |
Boca Raton, Fla. [u.a.]
CRC Press
2008
|
| Ausgabe: | 2. ed. |
| Schriftenreihe: | Books in soils, plants, and the environment
|
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XXIII, 509 S. graph. Darst. |
| ISBN: | 9780849398674 0849398673 |
Internformat
MARC
| LEADER | 00000nam a2200000 c 4500 | ||
|---|---|---|---|
| 001 | BV021626311 | ||
| 003 | DE-604 | ||
| 005 | 20070917 | ||
| 007 | t | ||
| 008 | 060622s2008 d||| |||| 00||| eng d | ||
| 020 | |a 9780849398674 |9 978-0-8493-9867-4 | ||
| 020 | |a 0849398673 |9 0-8493-9867-3 | ||
| 035 | |a (OCoLC)255959352 | ||
| 035 | |a (DE-599)BVBBV021626311 | ||
| 040 | |a DE-604 |b ger |e rakwb | ||
| 041 | 0 | |a eng | |
| 049 | |a DE-M49 |a DE-1029 | ||
| 050 | 0 | |a SB733 | |
| 082 | 0 | |a 632.4 | |
| 084 | |a WN 9350 |0 (DE-625)151120: |2 rvk | ||
| 084 | |a 23 |2 ssgn | ||
| 084 | |a LAN 244f |2 stub | ||
| 100 | 1 | |a Vidhyasekaran, P. |e Verfasser |4 aut | |
| 245 | 1 | 0 | |a Fungal pathogenesis in plants and crops |b molecular biology and host defense mechanisms |c P. Vidhyasekaran |
| 250 | |a 2. ed. | ||
| 264 | 1 | |a Boca Raton, Fla. [u.a.] |b CRC Press |c 2008 | |
| 300 | |a XXIII, 509 S. |b graph. Darst. | ||
| 336 | |b txt |2 rdacontent | ||
| 337 | |b n |2 rdamedia | ||
| 338 | |b nc |2 rdacarrier | ||
| 490 | 0 | |a Books in soils, plants, and the environment | |
| 650 | 4 | |a Fungal diseases of plants | |
| 650 | 4 | |a Plant molecular biology | |
| 650 | 4 | |a Plant-pathogen relationships | |
| 650 | 4 | |a Plants |x Disease and pest resistance |x Molecular aspects | |
| 650 | 0 | 7 | |a Wirtspflanzen |0 (DE-588)4444525-8 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Phytopathogene Pilze |0 (DE-588)4045992-5 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Pathogenese |0 (DE-588)4115512-9 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Abwehrreaktion |0 (DE-588)4416206-6 |2 gnd |9 rswk-swf |
| 689 | 0 | 0 | |a Phytopathogene Pilze |0 (DE-588)4045992-5 |D s |
| 689 | 0 | 1 | |a Pathogenese |0 (DE-588)4115512-9 |D s |
| 689 | 0 | |5 DE-604 | |
| 689 | 1 | 0 | |a Phytopathogene Pilze |0 (DE-588)4045992-5 |D s |
| 689 | 1 | 1 | |a Wirtspflanzen |0 (DE-588)4444525-8 |D s |
| 689 | 1 | 2 | |a Abwehrreaktion |0 (DE-588)4416206-6 |D s |
| 689 | 1 | |5 DE-604 | |
| 856 | 4 | 2 | |m OEBV Datenaustausch |q application/pdf |u http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=014841284&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |3 Inhaltsverzeichnis |
| 999 | |a oai:aleph.bib-bvb.de:BVB01-014841284 | ||
Datensatz im Suchindex
| _version_ | 1804135421249060864 |
|---|---|
| adam_text | CONTENTS PREFACE XXI AUTHOR XXIII CHAPTER 1 PERCEPTION AND TRANSDUCTION
OF PLANT SIGNALS IN PATHOGENS.. 1 1.1 INTRODUCTION ,. 1 1.2 SIGNALING
AND TRANSDUCTION SYSTEMS IN FIRST TOUCH AND ADHESION OF FUNGAL
SPORES..........................................................................................................
1 1.2.1 FIRST TOUCH OR INITIAL CONTACT TRIGGERS THE INFECTION PROEESS 1
1.2.2 ADHESION OR CLOSE CONTACT TRIGGERS FUNGAL INFECTION PROCESS 3
1.2.3 ADHESION OF SPORES DUE TO HYDROPHOBIE INTERAETION 3 1.2.4 ADHESION
OF SPORES IS ACEOMPANIED BY RELEASE OF EXTRAEELLULAR MATERIAL... 4 1.2.5
INVOLVEMENT OF CUTINASES IN SPORE ADHESION 5 1.2.6 SOME PLANT SIGNALS
MAY BE NEEDED FOR ADHESION OF SPORES 5 1.3 SIGNALING IN FUNGAL SPORE
GERMINATION...................................................................
... 6 1.3.1 PLANT SIGNALS TRIGGER STRUCTURAL CHANGES IN SPORES BEFORE
GERMINATION 6 1.3.2 PLANT-SURFAEE SIGNALS TRIGGER SPORE GERMINATION 7
1.3.3 FLAVONOIDS SIGNALING SPORE GERMINATION 8 1.4 SIGNALING IN
DIFFERENTIATION OF GERM TUBES INTO INFECTION STRUCTURES 8 1.4.1 ADHESION
OF GERMLINGS AND INFECTION
STRUCTURES.............................................. 8 1.4.2
EXTRAEELLULAR MATRIX IN GERMLING ADHESION 9 1.4.3 EXTRAEELLULAR MATRIX
IN APPRESSORIAL ADHESION 11 1.4.4 TOPOGRAPHIE SIGNALS IN APPRESSORIUM
FORMATION.. 11 1.4.5 PLANT-SURFACE WAX SIGNALS APPRESSORIUM FORMATION 13
1.4.6 CUTIN MONOMERS AS SIGNAL MOLECULES 14 1.4.7 ETHYLENE SIGNALS
APPRESSORIUM FORMATION 14 1.4.8 FUNGAL SIGNALS IN INDUCTION OF
APPRESSORIUM FORMATION 15 1.5 SIGNAL TRANSDUETION IN FUNGAL PATHOGENESIS
16 1.5.1 TRANSMEMBRANE REEEPTOR FOR EXTRACELLULAR SIGNALS 16 1.5.2
G-PROTEINS 17 1.5.3 CALCIUM/CALMODULIN-DEPENDENT SIGNALING 20 1.5.4
CAMPJPROTEIN KINASE SIGNALING PATHWAY 21 1.5.5 MITOGEN-ACTIVATED PROTEIN
KINASE SIGNALING CASCADES 24 1.5.6 LIPID-INDUEED PROTEIN KINASE
SIGNALING 28 1.5.7 PAKSIGNALING 28 1.5.8 PHOSPHORYLATION AND
DEPHOSPHORYLATION CASCADES 29 1.5.9 P-TYPE ADENOSINE TRIPHOSPHATASE
SIGNALING 29 1.6 GENES INVOLVED IN FORMATION OF INFECTION STRUETURES 30
1.7 SIGNALS IN FUNGAL INFECTION PROCESS 32 1.7.1 MAGNAPORTHE GRISEA 32
1.7.2 BLUMERIA GRAMINIS 34 IX X 1.7.3 COLLETOTRICHUM
GLOEOSPORIOIDES......... 35 1.7.4 USTILAGO MAYDIS 36 1.7.5 FUSARIUM
OXYSPORUM 37 1.8 CONCLUSION 37 REFERENCES 38 CHAPTER 2 PERCEPTION AND
TRANSDUCTION OF PATHOGEN SIGNALS IN PLANTS 55 2.1 INTRODUCTION 55 2.2
WHAT ARE ELICITORS? 56 2.3 OLIGOSACCHARIDE ELICITORS 57 2.3.1
CHITOOLIGOSACCHARIDE ELICITORS 57 2.3.2 CHITOSAN ELICITORS 58 2.3.3
OLIGOGLUCAN ELICITORS 58 2.3.4 OTHER CARBOHYDRATE ELICITORS 60 2.4
PROTEIN/PEPTIDE ELICITORS 60 2.4.1 ELICITINS..... 60 2.4.2 XYLANASE
ELICITOR 64 2.4.3 PANIE213 ELICITOR...... 64 2.4.4 NEPL ELICITOR 64
2.4.5 NIP1 ELICITOR 64 2.4.6 PB90 ELICITOR 65 2.5 GLYCOPROTEIN ELICITORS
65 2.5.1 CARBOHYDRATE MOIETY IN THE GLYCOPROTEIN ELICITOR MAY CONFER
ELICITOR ACTIVITY 65 2.5.2 PROTEIN MOIETY IN GLYCOPROTEIN ELICITORS MAY
CONFER ELICITOR ACTIVITY 66 2.5.3 FUNCTIONS OF GLYCOPROTEIN ELICITORS 67
2.6 LIPID ELICITORS 67 2.6.1 SPHINGOLIPIDS 67 2.6.2 ARACHIDONIC AND
EICOSAPENTAENOIC ACIDS 68 2.6.3 ERGOSTEROLS 68 2.7 TOXINS AS ELICITOR
MOLEEULES 69 2.8 PLANT CELL WALL-DEGRADING ENZYMES AS ELICITORS 69 2.9
RACE-SPECIFIC AND CULTIVAR-SPECIFIC ELICITORS 70 2.10 SPECIFICITY OF
GENERAL ELICITORS 72 2.11 ENDOGENOUS OLIGOGALACTURONIDE ELICITORS 73
2.12 MULTIPLE ELICITORS MAY BE NEEDED TO ACTIVATE DEFENSE RESPONSES 74
2.12.1 ELICITOR COMPLEX 74 2.12.2 NETWORK OF ELICITOR MOLECU1ES 74 2.13
AVAILABILITY OF FUNGAL ELICITORS AT THE SITE OF FUNGAL INVASION IN
PLANTS 75 2.14 RECEPTORS FOR ELICITOR SIGNALS IN PLANT CELL MEMBRANE 76
2.14.1 RECEPTOR SITES FOR BINDING OLIGOSACCHARIDE ELICITORS 76 2.14.2
RECEPTOR SITES FOR BINDING PROTEINACEOUS ELICITORS 77 2.14.3 PROTEIN
KINASES AS RECEPTOR SITES 78 2.14.4 LRR-TYPE RECEPTORS 78 2.14.5 LEETINS
AS RECEPTORS 79 2.14.6 RESISTANCE GENE PRODUCTS AS RECEPTORS 79 2.15
CALCIUM ION MAY ACT AS SECOND MESSENGER 79 2.15.1 FUNCTION OF CALCIUM
ION AS SECOND MESSENGER 79 2.15.2 UPSTREAM EVENTS OF CA 2 + SIGNALING 81
2.15.3 DOWNSTREAM EVENTS OF CA 2 + SIGNALING 82 XI 2.16 PHOSPHORYLATION
OF PROTEINS AS A COMPONENT IN SIGNAL TRANSDUCTION SYSTEM 83 2.16.1
PHOSPHORY1ATIONJDEPHOSPHORYLATION EVENTS.......... 83 2.16.2 CALCIUM ION
IN PHOSPHORYLATION 83 2.17 MITOGEN-ACTIVATED PROTEIN KINASE CASCADES IN
SIGNAL TRANSDUCTION 84 2.18 PHOSPHOLIPID-SIGNALING SYSTEM 85 2.18.1
PLANT CELL MEMBRANE PHOSPHOLIPIDS AS SIGNAL
MOLECULES......................... 85 2.18.2 ROLE OFPHOSPHOLIPASE A IN
PHOSPHOLIPID-SIGNALING SYSTEM 86 2.18.3 PHOSPHOLIPASE C IN
PHOSPHOLIPID-SIGNALING SYSTEM 87 2.18.4 PHOSPHOLIPASE D IN
PHOSPHOLIPID-SIGNALING SYSTEM 89 2.19 ANION CHANNELS IN SIGNAL
TRANSDUCTION 90 2.19.1 ANION CHANNELS IN THE SIGNALING SYSTEM 90 2.19.2
UPSTREAM EVENTS OF ANION CHANNEL-SIGNALING SYSTEM 91 2.19.3 DOWNSTREAM
OF ANION CHANNEL-SIGNALING SYSTEM 91 2.20 EXTRACELLULAR ALKALINIZATION
AND CYTOPLASMIC ACIDIFICATION IN SIGNALING SYSTEM 91 2.21 REACTIVE
OXYGEN SPECIES IN SIGNAL TRANSDUCTION 92 2.21.1 OXIDATIVE
BURST..........................................................................................
92 2.21.2 MECHANISMS OF PRODUCTION OF REACTIVE OXYGEN SPECIES 93
2.21.2.1 PRODUCTION OF 02 93 2.21.2.2 PRODUCTION OF H2 0 2 94 2.21.2.3
PRODUCTION OF OH RADICAL... 95 2.21.2.4 PRODUCTION OF SINGLET OXYGEN
E02) 95 2.21.3 UPSTREAM OF ROS SIGNALING 96 2.21.4 DOWNSTREAM OF ROS
SIGNALING 96 2.22 NITRIC OXIDE IN SIGNAL TRANSDUCTION 97 2.22.1
INCREASES IN NITRIC OXIDE................ 97 2.22.2 BIOSYNTHESIS OF
NITRIC OXIDE 97 2.22.3 UPSTREAM EVENTS OF NITRIC OXIDE SIGNALING 98
2.22.4 DOWNSTREAM EVENTS OF NITRIC OXIDE SIGNALING..... 99 2.23
SALICYLICACID-SIGNALING SYSTEM.................. 100 2.23.1 SALICYLIC
ACID IN SIGNALING DEFENSE RESPONSE IN PLANTS 100 2.23.2 BIOSYNTHESIS OF
SALICYLIC ACID 101 2.23.3 SIGNAL PERCEPTION 102 2.23.4 UPSTREAM SIGNALS
FOR INDUCTION OF SYNTHESIS OF SALICYLIC ACID 102 2.23.5 DOWNSTREAM OF
SALICYLIC ACID SIGNALING 103 2.23.6 METHYL SALICYLATE 104 2.23.7
SALICYLATE-INDEPENDENT SIGNALING SYSTEMS 105 2.24 JASMONATE-SIGNALING
PATHWAY 105 2.24.1 JASMONATE SIGNALING IN INDUCTION OF DEFENSE
RESPONSES........................ 105 2.24.2 BIOSYNTHESIS OF
JASMONATES......................................................................
106 2.24.3 PERCEPTION OF JASMONATE SIGNALS 108 2.24.4
JASMONATE-SIGNALING SYSTEM MAY BEHAVE DIFFERENTLY IN PROTECTING PLANTS
AGAINST VARIOUS PATHOGENS 108 2.24.5 INDUCTION OF INTERCELLULAR AND
INTERPLANT SYSTEMIC TRANSDUCTION OF JASMONATE
SIGNALS.......................................................................
........ 109 2.24.6 UPSTREAM OF JASMONATE SIGNALING 109 2.24.7
DOWNSTREAM OF JASMONATE SIGNALING 109 2.24.8 TRANSCRIPTIONAL REGULATION
OF JA-RESPONSIVE GENES 109 2.24.9 JASMONIC ACID, METHYL JASMONATE, AND
CYCLIC PRECURSORS AND DERIVATIVES OF JASMONIC ACID AS SIGNAL MO1ECU1ES
110 2.25 ROLE OF SYSTEMIN IN SIGNAL TRANSDUCTION SYSTEM 111 2.26
ETHYLENE-DEPENDENT SIGNALING PATHWAY 112 XII 2.26.1 ETHY1ENE-SIGNALING
SYSTEM INDUCING DISEASE RESISTANCE OR SUSCEPTIBILITY 112 2.26.2
BIOSYNTHESIS OF ETHY1ENE..... 112 2.26.3 UPSTREAM SIGNALS IN INDUCTION
OF SYNTHESIS OF ETHYLENE 113 2.26.4 ETHY1ENE SIGNAL PERCEPTION 114
2.26.5 DOWNSTREAM EVENTS IN ETHYLENE SIGNALING 114 2.27 ABSCISICACID
SIGNALING...........................................................................................
115 2.28 FATTY ACIDS AS SYSTEMIC SIGNAL MOLECULES 116 2.29 OTHER
SIGNALING SYSTEMS........... 116 2.30 NETWORK AND INTERPLAY OF SIGNALING
PATHWAYS 116 2.30.1 REGULATORY INTERACTION AND COORDINATION AMONG
SALICYLATE-, JASMONATE-, AND ETHYLENE-SIGNALING PATHWAYS 116 2.30.2
CCORDINATED REGULATION OF ETHYLENE- AND JASMONATE-SIGNALING PATHWAYS...,
117 2.30.3 INTERPLAY BETWEEN SALICYLATE- AND JASMONATE-SIGNALING
PATHWAYS 118 2.30.4 INTERPLAY BETWEEN SALICYLATE AND ETHYLENE PATHWAYS
118 2.30.5 CROSS TALK BETWEEN SALICYLATE AND JASMONATE/ETHYLENE PATHWAYS
119 2.30.6 CROSS TALK BETWEEN ABSCISIC ACID-, JASMONATE-, AND ETHYLENE-
DEPENDENT SIGNALING PATHWAYS 120 2.30.7 REGULATORY SWITCHES TO FINE-TUNE
SIGNALING PATHWAYS 121 2.31 INDUCTION OF DEFENSE GENES MAY REQUIRE
DIFFERENT SIGNAL TRANSDUCTION SYSTEMS 121 2.32 PERCEPTION AND
TRANSDUCTION OF PATHOGEN SIGNALS IN PLANTS LEADING TO
SUSCEPTIBILITY.......................................................................................................
123 2.32.1 DIFFERENTIAL EXPRESSION OF SIGNALING SYSTEM LEADING TO
SUSCEPTIBILITY OR RESISTANCE 123 2.32.2 SLOWER ACCUMULATION OF
ELICITOR-RELEASING ENZYMES IN SUSCEPTIBLE INTERACTIONS 124 2.32.3
SUSCEPTIBLE VARIETIES MAY RELEASE LESS AMOUNT OF ELICITORS FROM FUNGAL
PATHOGEN CELL WALLS 124 2.32.4 DE1AYED RELEASE OF ELICITORS IN
SUSCEPTIBLE INTERACTIONS 127 2.32.5 ELICITOR OF COMPATIBLE PATHOGENS
INDUCES LESS DEFENSE-RE1ATED ACTIONS THAN THAT OFINCOMPATIBLE PATHOGENS
127 2.32.6 DEGRADATION OF FUNGAL ELICITORS BY PLANT ENZYMES IN PLANT
TISSUES MAY LEAD TO SUSCEPTIBILITY....................... 128 2.32.7
FUNGAL PATHOGENS MAY DEGRADE HOST E1ICITORS DURING SUSCEPTIB1E
INTERACTIONS 129 2.32.8 ELICITORS MAY BE RELEASED DURING PATHOGENESIS
BUT MAY NOT BE ACTIVE OR LESS ACTIVE IN SUSCEPTIBLE PLANTS 130 2.32.9
SOMEELICITORS DO NOT ACT OR SHOW LITTLE ACTIVITY ON SUSCEPTIBLE
CUITIVARS 132 2.32.10 SPEED OF EXPRESSION OF SIGNAL TRANSDUCTION SYSTEM
MAY DETERMINE SUSCEPTIBILITY OR RESISTANCE 134 2.32.11 REDUCED
ACCUMULATION OF SIGNALS MAY LEAD TO SUSCEPTIBILITY 134 2.32.12 ELICITORS
MAY INDUCE GENES INVO1VED IN SUPPRESSION OF DEFENSE-RELATED GENES IN
SUSCEPTIBLE INTERACTIONS..... 135 2.32.13 SUPPRESSORS NEGATING
ELICITOR-INDUCED DEFENSE RESPONSES IN SUSCEPTIBLE INTERACTIONS .. 137
2.32.14 SUSCEPTIBLE P1ANTS MAY HAVE SUPPRESSORS TO SUPPRESS ACTION OF
FUNGAL ELICITORS ;........................... 140 2.32.15 DOWNREGULATION
OF FUNCTIONS OF ELICITORS IN SUSCEPTIBLE INTERACTIONS .... 140 XIII
2.32.16 ACTIVATION OF AN UNSUITAB1E SIGNA1ING SYSTEM FOR INDUCTION OF
DEFENSE RESPONSES MAY LEAD TO SUSCEPTIBILITY 141 2.33 SIGNA1ING SYSTEMS
IN SUSCEPTIBLE INTERACTIONS 143 2.33.1 ABSCISIC ACID-SIGNALING SYSTEM
143 2.33.2 ETHY1ENE-SIGNALING SYSTEM....... 144 2.33.3 SIGNAL
TRANSDUCTION SYSTEMS MAY INDUCE SUSCEPTIBILITY-RELATED RESPONSES 144
2.34 CONCLUSION 144 REFERENCES 147 CHAPTER 3 DISEASE RESISTANCE AND
SUSCEPTIBILITY GENES IN SIGNAL PERCEPTION AND EMISSION............. 193
3.1 INTRODUCTION 193 3.2 MO1ECU1AR STRUCTURE OF RESISTANCE GENES 195
3.2.1 LRR DOMAINS 195 3.2.2 NBS DOMAINS 195 3.3 C1ASSIFICATION OF
RESISTANCE GENES BASED ON MO1ECU1AR STRUCTURE OF R GENE-ENCODED PROTEINS
196 3.3.1 RESISTANCE GENES ENCODING TIR-NBS-LRR PROTEINS 196 3.3.2
RESISTANCE GENES ENCODING NON-TIR-NBS-LRR PRO TEINS 197 3.3.3 RESISTANCE
GENES ENCODING LRR PROTEINS LACKING NBS DOMAIN 199 3.3.4 RESISTANCE
GENES ENCODING PROTEINS LACKING LRR DOMAIN 200 3.3.4.1 LRD PROTEINS 200
3.3.4.2 INTRACELLU1AR PROTEIN KINASES 200 3.3.4.3 TRANSMEMBRANE PROTEINS
201 3.3.4.4 LEETIN-TYPE PROTEINS 202 3.3.4.5 BEAT SHOCK PROTEIN-LIKE
PROTEINS 202 3.3.4.6 NADPB-DEPENDENT REDUCTASE-TYPE PROTEIN 202 3.3.4.7
PLANT ER GENES ENCODING PHOTORESPIRATORY PEROXISOMAL ENZYME PROTEINS 202
3.4 MO1ECU1AR STRUCTURE OF RECESSIVE GENES 202 3.4.1 BARLEY MLO
GENE..........................................................................
.............. 202 3.4.2 ARABIDOPSIS PMR6 GENE 203 3.4.3 ARABIDOPSIS
RRS1-R GENE 203 3.4.4 ARABIDOPSIS SSI4 GENE 203 3.5 PERCEPTION OF
PATHOGEN SIGNALS BY RESISTANCE GENES 204 3.5.1 FUNCTIONS OF DIFFERENT
DOMAINS OF R PROTEINS IN PATHOGEN RECOGNITION 204 3.5.1.1 LRR DOMAIN 204
3.5.1.2 NBS DOMAIN 204 3.5.1.3 TIR DOMAIN 205 3.5.1.4 CC DOMAIN 205
3.5.1.5 C-TERMINA1 NON-LRR REGION 206 3.5.1.6 C-TERMINUS TRANSCRIPTIONA1
ACTIVATION DOMAIN 206 3.5.1.7 PROTEIN KINASE DOMAIN 206 3.5.1.8
TRANSMEMBRANE DOMAIN 206 3.5.1.9 CALMODULIN-BINDING PROTEIN 207 3.5.1.10
LEETIN-TYPE PROTEIN 207 3.5.1.11 BEAT SHOCK PROTEIN (BSP)-LIKE PROTEIN
207 3.5.2 R GENE PRODUCT MAY ACT AS A RECEPTOR THAT RECOGNIZES AN A VR
GENE
PRODUCL............................................................................................
207 3.7.2 3.7.3 3.7.4 XIV 3.5.3 R PROTEIN MAY DETECT BINDING OF AN AVR
PROTEIN TO A DIFFERENT PROTEIN IN THE PLANT 208 3.6 ACTIVATION OF R
PROTEIN AND EMISSION OF SIGNALS TO OTHER COMPONENTS IN THE CELLO 209 3.7
DOWNSTREAM COMPONENTS OF R GENE-SIGNALING SYSTEMS 211 3.7.1 REGULATORY
GENES (OR COMPLEMENTARY GENES OR R GENE-SIGNALING COMPONENTS) 211
EDSI-PAD4 PROTEINS 212 NDRI PROTEINS 213 RAR1-SGTL-HSP90 PROTEINS 214
3.7.4.1 RARI 214 3.7.4.2 SGTI 215 3.7.4.3 RAR1/SGTI COMPLEX 217 3.7.4.4
INTERACTION OF RAR1/SGTL WITH HSP90 217 3.7.5 NPR1 218 3.7.6 PRF-PTO-PTI
SIGNALING SYSTEM 219 3.7.7 OTHERREGUIATORY GENES * 219 3.8 DOWNSTREAM
SIGNALINGEVENTS IN R GENE-MEDIATED RESISTANCE 221 3.9
SUSCEPTIBILITYGENES IN SIGNAL TRANSDUCTION 222 3.9.1 SUSCEPTIBILITY
ALLELES OFRESISTANCE GENES 222 3.9.2 SUSCEPTIBILITY GENES 222 3.9.3
RESISTANCE GENE MAY ACT AS SUSCEPTIBILITY GENE AGAINST SOME PATHOGENS
223 3.9.4 LOW EXPRESSION OF RESISTANCE GENES MAY LEAD TO SUSCEPTIBILITY
224 3.9.5 SUSCEPTIBILITY ALLELES OF RESISTANCE GENES MAY NEGATE THE
FUNCTION OF RESISTANCE GENES.............. 224 3.9.6 SUPPRESSOR GENES
225 3.10 CONCLUSION 225 REFERENCES : 227 CHAPTER 4 CELL DEATH PROGRAMS
DURING FUNGAL PATHOGENESIS 243 4.1 INTRODUCTION 243 4.2 CELL DEATH IN
RESISTANT INTERACTIONS 243 4.2.1 PROGRAMMED CELL DEATH 243 4.2.2
HYPERSENSITIVE CELL DEATH 244 4.2.3 SPONTANEOUS CELL DEATH 244 4.2.4
RUNAWAY CELLDEATH 245 4.2.5 CELL DEATH-INDUCING SYSTEMIC ACQUIRED
RESISTANCE 245 4.3 MOLECULAR MECHANISM OF INDUCTION OF HYPERSENSITIVE
CELL DEATH 245 4.3.1 MEDIATORS, REGULATORS, AND EXECUTIONERS OF CELL
DEATH 245 4.3.2 R GENE SIGNALS INVOLVED IN TRIGGERING CELL DEATH 246
4.3.3 REACTIVE OXYGEN SPECIES IN CELL DEATH.......... 246 4.3.4 NITRIC
OXIDE IN CELL DEATH 249 4.3.5 BAX FAMILY OF PROTEINS 250 4.3.6
ION-CONDUCTING CHANNELS 251 4.3.7 FUNCTION OF MITOCHONDRION IN INDUCTION
OF CELL DEATH 251 4.3.8 PROTEOLYTIC ENZYMES 251 4.3.8.1 PLANT CASPASES
251 4.3.8.2 VACUOLAR PROCESSING ENZYMES (VPES) 252 4.5 4.6 4.7 4.8 XV
4.3.8.3 METACASPASES 252 4.3.8.4 OTHER TYPES OF PROTEOLYTIC ENZYMES 253
4.3.9 PROBABLE SEQUENCE IN INDUCTION OF HYPERSENSITIVE CELL DEATH 253
4.4 MOLECULAR MECHANISM OF INDUCTION OF SPONTANEOUS CELL DEATH 253 4.4.1
SPONTANEOUS CELL DEATH-REGULATING GENES.......... 253 4.4.2 SALICYLIC
ACID 255 4.4.3 ETHYLENE 255 4.4.4 PHOSPHATIDIC ACID .. 255 MOLECULAR
MECHANISM OF INDUCTION OF RUNAWAY CELL DEATH 256 ROLE OF CELL DEATH IN
INDUCTION OF SYSTEMIC ACQUIRED RESISTANCE 257 SUSCEPTIBILITY-RELATED
CELL DEATH 258 MOLECULAR MECHANISMS IN INDUCTION OF CELL DEATH IN
SUSCEPTIBLE INTERACTIONS 258 4.8.1 MEDIATORS, REGULATORS, AND
EXECUTIONERS OF SUSCEPTIBILITY-RELATED PLANT CELL
DEATH....................................... 258 4.8.2 REACTIVE OXYGEN
SPECIES 259 4.8.3 PROTEOLYTIC ENZYMES 259 4.8.4 CALCIUM ION : 260 4.8.5
SALICYLATE, ETHYLENE, AND JASMONATE 260 4.8.6 SPHINGOLIPID METABOLISM
262 4.8.7 EXTRACELLULAR ATP LEVELS.......... 262 4.9 WHAT IS THE
FUNCTION OF CELL DEATH IN FUNGAL PATHOGENESIS? 262 4.10 CONCLUSION 264
REFERENCES 264 CHAPTER 5 CELL WALL DEGRADATION AND FORTIFICATION 275 5.1
INTRODUCTION 275 5.2 STRUCTURE OF CUTICLE 275 5.3 PENETRATION OF
EPICUTICULAR WAXY LAYER BY PATHOGENS 276 5 .4 PRODUCTION OF CUTINASES TO
BREACH CUTICLE BARRIER.......................................... 276 5
.5 GENES ENCODING
CUTINASES.....................................................................
................. 277 5.6 PLANT SIGNALS TRIGGERING FUNGAL CUTINASES 278
5.7 IMPORTANCE OF CUTINASES IN PENETRATION OF CUTICLE 279 5.8 CUTINASES
AS VIRULENCE/PATHOGENICITY FACTORS 280 5.9 MELANINS IN FUNGAL
PENETRATION OF CUTICLE
BARRIER................................................. 281 5.9.1
BIOSYNTHESIS OF MELANINS 281 5.9.2 MELANINS AID IN PENETRATION OF
CUTICLE BARRIER BY FUNGAL PATHOGENS 283 5.10 DEGRADATION OF PECTIC
POLYSACCHARIDES 285 5.10.1 TYPES OFPECTIC POLYSACCHARIDES 285 5.10.2
TYPES OF PECTIC ENZYMES 285 5.10.3 FUNGAL PATHOGENS PRODUCE MULTIPLE
PECTIC ENZYMES 286 5.10.4 GENES ENCODING PECTIC ENZYMES 287 5.10.5
EVIDENCES TO SHOW THAT PECTIC ENZYMES AID PATHOGENS TO PENETRATE CELL
WALL 288 5.10.5.1 IMMUNOCYTOCHEMICAL EVIDENCES 288 5.10.5.2 EVIDENCES BY
SHOWING PROTECTION OF THE HOST BY INHIBITION OF PECTIC ENZYMES WITH
SPECIFICANTIBODIES 289 5.10.5.3 EVIDENCES SHOWING PROTEETION OF HOST
PLANTS BY INHIBITION OF PECTIC ENZYMES WITH
SELECTIVEINHIBITORS.............................. 290 5.10.5.4 EVIDENCES
USING PECTIC ENZYME-DEFICIENT FUNGAL ISOLATES ....... 290 XVI 5.10.5.5
EVIDENCES SHOWING CORRE1ATION BETWEEN THE LEVEL OF PECTIC ENZYMES AND
VIRU1ENCE 291 5.10.5.6 EVIDENCES SHOWING ENHANCEMENT OF VIRU1ENCE BY
GENE TRANSFER........................................... 291 5.10.5.7
EVIDENCES SHOWING DECREASE IN VIRULENCE BY GENE DISRUPTION 291 5.10.6
PLANT SIGNALS TO INDUCE PECTIC ENZYMES 291 5.10.7 HOST CELLWALL DIFFERS
IN ITS SUSCEPTIBILITY TO PECTIC ENZYMES 292 5.10.8 CELLWALL PROTEINS
MODULATE PECTIC ENZYME ACTIVITY 292 5.11 PATHOGENS PRODUCE CELLULOLYTIC
ENZYMES TO BREACH.CELL WALL BARRIER.. 294 5.12 FUNGAL HEMICELLU1ASES IN
PLANT CELLWALL J?EGRADATLON 295 5.13 DEGRADATION OF CELL WALL STRUCTURAL
PROTE~NS 296 5.14 REQUIREMENT OF SEVERAL CELL WALL-DEGRADMG ENZYMES TO
DEGRADE THE COMPLEX-NATURED CELL WALL 297 5.15 PRODUCTION OF
SUITABLEENZYMES IN APPROPRIATE SEQUENCE BY FUNGAL PATHOGENS 297 5.16
REINFORCEMENT OF HOST CELL WALL DURING FUNGAL INVASION 298 5.17 PAPILLAE
SUPPRESS FUNGA1 PENETRATION 298 5.18 CALLOSE DEPOSITIONIN CELLWALL 300
5.19 HOW DO PATHOGENS OVERCOME THE PAPILLAE AND CALLOSE BARRIERS? 301
5.19.1 PATHOGEN DELAYS PAPILLAE FORMATION 301 5.19.2 PATHOGENS MAY
SUPPRESS CALLOSE SYNTHESIS IN SUSCEPTIBLE INTERACTIONS 302 5.19.3
PATHOGENS MAY BE ABLE TO PENETRATE THE PAPILLAE BARRIER. 303 5.19.4
PATHOGENS MAY DEGRADE CALLOSE BY PRODUCING SS-1,3-G1UCANASE 303 5.20
ACCUMULATION OF HYDROXYPROLINE-RICH G1YCOPROTEINS IN PLANT CELLWALLS 304
5.20.1 HOST CELL WALL RESPONDS TO FUNGAL INVASION BY ACCUMULATING HRGP
.. 304 5.20.2 SIGNALS TRIGGERING ACCUMULATION OF HRGPS 304 5.20.3 HOST
CELL WALL RESPONDS TO FUNGAL INVASION BY STRENGTHENING ITS HRGPS BY
GLYCOSYLATION 305 5.20.4 INSOLUBILIZATION OF HRGPS IN HOST CELL
WALL....... 305 5.20.5 ENRICHMENT OF HRGPS BY LIGNIN DEPOSITION 305
5.20.6 SOMEHRGPS MAY IMMOBILIZE PLANT PATHOGENS 306 5.20.7 HOW DOES
PATHOGEN OVERCOME HRGP BARRIER? 306 5.20.7.1 LESS ACCUMULATION OF HRGPS
IN COMPATIB1E INTERACTIONS 306 5.20.7.2 PATHOGEN OVERCOMES HRGP BARRIER
BY DELAYING ACCUMULATION OF HRGPS IN HOST CELL WALL 306 5.21 CELL
WALL-BOUND PHENOLICS AND LIGNINS 307 5.21.1 FORTIFICATION OF PLANT CELL
WALL BY PHENOLICS AND LIGNIN 307 5.21.2 BIOSYNTHESIS OF PHENOLICS AND
LIGNINS 308 5.21.3 PHENOLIC DEPOSITION IN HOST CELL WALL IN RESPONSE TO
FUNGAL INVASION 308 5.21.4 HOST CELL WALL
RES;~~D~ ~~ F~~~I I~~~I~~ B; A~~ I ~~TI~ ~ E~~;~~~ INVOLVED IN
SYNTHESIS OF WALL-BOUND PHENOLICS 310 5.21.5 HOW DOESTHE PATHOGEN
OVERCOME THE CELL WALL-BOUND PHENOLICS TO CAUSE DISEASE? 311 5.21.5.1
PATHOG~~S~~~;~~~~~A~~~~I~TI~~~FPH~~II~~I~ . HOSTCELL WALL
5..21..5.2 PATHOGEN
DELA;~ S;~TH~ I~ ~F CII WII~B~~~D PH~~II~~ ::::::: ~G 5.21.6
LLGMFICATLON DURING FUNGAL PATHOGENESIS 312 XVII 5.21.6.1 HOST CELL WALL
RESPONDS TO FUNGAL INVASION BY INCREASING LIGNIFICATION PROCESS 312
5.21.6.2 PATHOGEN SUPPRESSES LIGNIN DEPOSITION 313 5.21.6.3 PATHOGEN
SUPPRESSES ENZYMES INVO1VED IN LIGNIN BIOSYNTHESIS 314 5.21.6.4 HOW DOES
PATHOGEN SUPPRESS LIGNIFICATION IN HOST CELL WALL? 315 5.22 SUBERIZATION
DURING FUNGAL PATHOGENESIS 316 5.22.1 HOST CELL WALL RESPONDS TO FUNGAL
INVASION BY SUBERIZATION 316 5.22.2 BIOSYNTHESIS OF SUBERIN IN
PATHOGEN-INOCULATED HOST CELL WALL 316 5.22.3 PATHOGEN DE1AYS SUBERIN
ACCUMULATION 317 5.22.4 PATHOGEN MAY SUPPRESS SUBERIN-SYNTHESIZING
ENZYMES 317 5.22.5 PATHOGENS MAY PENETRATE THE SUBERIZED WALLS OFHOST
CELLS 318 5.23 DEPOSITION OF MINERAL ELEMENTS IN HOST CELL WALL IN
RESPONSE TO FUNGAL
INVASION..............................................................................
318 5.23.1 SILICON DEPOSITION 318 5.23.2 CALCIUM DEPOSITION IN PAPILLAE
318 5.23.3 MANGANESE ACCUMULATION IN PAPILLAE 319 5.24 CONCLUSION 319
REFERENCES 320 CHAPTER 6 INDUCTION AND EVASION OF PATHOGENESIS-RE1ATED
PROTEINS 345 6.1 INTRODUCTION 345 6.2 MULTIPLICITY OF PR PROTEINS 346
6.3 CLASSIFICATION OF PR PROTEINS 347 6.3.1 PR-1 PROTEINS 347 6.3.2 PR-2
PROTEINS 348 6.3.3 PR-3 PROTEINS 349 6.3.4 PR-4 PROTEINS 350 6.3.5 PR-5
PRO TEINS 351 6.3.6 PR-6 PROTEINS 351 6.3.7 PR-7 PROTEINS 352 6.3.8 PR-8
PROTEINS 352 6.3.9 PR-9 PROTEINS 352 6.3.10 PR-LO PROTEINS 353 6.3.11
PR-LI PROTEINS 353 6.3.12 PR-12 PROTEINS 353 6.3.13 PR-13 PROTEINS 354
6.3.14 PR-14 PROTEINS 354 6.3.15 PR-15 PROTEINS 354 6.3.16 PR-16
PROTEINS 355 6.3.17 PR-17PROTEIL1S 355 6.3.18 CHITOSANASES 355 6.4
INDUCTION OF PR PRO TEINS DURING FUNGAL PATHOGENESIS 355 6.5 GENES
ENCODING PR PROTEINS 356 6.6 TRANSCRIPTION OF PR GENES 357 6.7 SIGNALS
INVOLVED IN TRANSCRIPTIONAL INDUCTION OF PR GENES 358 6.7.1 INDUCTION OF
PR GENES BY ELICITORS 358 6.7.2 INDUCTION OF PR GENES BY SALICYLIC ACID
359 6.7.3 6.7.4 6.7,5 XVIII INDUCTION OFPR GENES BY ETHYLENE * 360
INDUCTION OFPR GENES BY JASMONIC ACIDJJASMONATE ,. ,.. 362 INDUCTION
OF PR PROTEINS MAY REQUIRE DIFFERENT SIGNAL TRANSDUCTION SYSTEMS , , **
363 6.7.6 SYNERGISTIC EFFECT OFDIFFERENT SIGNALS *.. 364 6.7.7
ANTAGONISTICEFFECT OFDIFFERENT SIGNALS * 364 6.8 PR PROTEINS ARE
SYNTHESIZED AS LARGER PRECURSORS .. 364 6.9 SECRETION OFPR PROTEINS ,
,.., , ., ,. 365 6.9.1 SECRETORYPATHWAYS .. , , , ,,.., , 365 6.9.2
SITE OF ACCUMULATION OF PR PROTEINS , , 366 6,10 PR PROTEINS MAY BE
INVOLVED IN INHIBITION OF PATHOGEN DEVELOPMENT.. 367 6.10.1 INHIBITION
OF FUNGAL GROWTH BY PR PROTEINS IN VITRO 367 6.10.2 INHIBITION OFFUNGAL
GROWTH BY PR PROTEINS IN VIVO 369 6.10,3 SOME PR PROTEINS MAY BE
INVOLVED IN RELEASE OF ELICITOR MOLEEULES IN PLANTA , ,., , 370 6.10.4
SOME PR PROTEINS MAY BE INVOLVED IN REINFORCEMENT OF CELL WALL
STRUCTURES , , . , , 370 6.11 PR PROTEINS MAY BE INVOLVED IN
TRIGGERING DISEASE RESISTANCE 370 6.11.1 DEMONSTRATION OF THE ROLE OF
PR PROTEINS IN DISEASE RESISTANCE USING CHEMICAL OR BIOLOGICAL ELICITORS
, 370 6.11.2 DEMONSTRATION OF ROLE OF PR PROTEINS IN DISEASE
RESISTANCE BY INDUCING MUTATION , 371 6.11.3 DEMONSTRATION OF ROLE OF PR
PROTEINS IN DISEASE RESISTANCE BY DEVELOPING TRANSGENIE PLANTS , , 371
6.11.4 DEMONSTRATION OF THE ROLE OF PR PROTEINS BY DEVELOPING TRANSGENIE
PLANTS WITH ANTISENSE SUPPRESSION OF PR GENES 373 6.12 HOW DO PATHOGENS
OVERCOME FUNGITOXIC PR PROTEINS OFTHE HOST? 373 6.12.1
SLOWERACCUMULATION OF PR PROTEINS MAY ENABLE PATHOGENS TO ESCAPE THE
ANTIFUNGAL ACTION OF PR PROTEINS 373 6.12.2 PATHOGENS MAY SHED AWAY FROM
THEIR CELL WALL THE SUBSTRATE FOR THE PR PROTEINS OF ENZYMATIC NATURE
AND AVOID THEIR LYTIC ENZYME ACTION , , , , ,.. , 379 6.12,3
PATHOGENS MAY PRODUCE ENZYMES THAT PROTECT THEM FROM FUNGITOXIC ACTION
OF PR-3 PROTEINS 380 6.12.4 PATHOGENS MAY PRODUCE ENZYMES TO INHIBIT
ACTIVITY OF SOME PR PROTEINS , 381 6.12.5 LESS ELICITOR IS
RELEASED FROM PATHOGEN S CELL WALL TO ACTIVATE SYNTHESIS OF PR PROTEINS
381 6.12.6 PR PROTEINS ARE DEGRADED QUICKLY IN THE SUSCEPTIBLE HOST
TISSUES 382 6.12.7 SITE OF ACCUMULATION OF SOME PR PROTEINS MAY
DETERRNINE SUSCEPTIBILITY OR RESISTANCE 382 6.12.8 ADAPTATION OF
PATHOGENS TO PR PROTEINS 384 6.12.9 SOMEPR PROTEINS MAY NOT BE INVO1VED
IN DISEASE RESISTANCE 385 6.13 CONCLUSION , , 385 REFERENCES , , ,
386 CHAPTER 7 EVASION AND DETOXIFICATION OF SECONDARY METABOLITES 411
7.1 INTRODUCTION , , , ,., 411 7.2 CHEMICAL STRUCTURAL CLASSES OF
PHYTOALEXINS , 412 XIX 7.3 BIOSYNTHESIS OF ISOFLAVONOID PHYTOALEXINS 414
7.3.1 PHASEOLLIN AND RELATED COMPOUNDS 414 7.3.2 GLYCEOLLINS 418 7.3.3
MEDIEARPIN 420 7.3.4 PISATIN 423 7.4 BIOSYNTHESIS OF FLAVANONE
PHYTOALEXINS 424 7.5 BIOSYNTHESIS OF COUMARIN PHYTOALEXINS 424 7.6
BIOSYNTHESIS OF STILBENE PHYTOALEXINS 426 7.7 BIOSYNTHESIS OF TERPENOID
PHYTOALEXINS 426 7.8 BIOSYNTHESIS OF INDOLE-BASED SULFUR-CONTAINING
PHYTOALEXINS 430 7.9 BIOSYNTHESIS OF ALKALOID PHYTOALEXINS 431 7.10 SITE
OF SYNTHESIS OFPHYTOALEXINS 432 7.11 PHYTOALEXINS ARE FUNGITOXIC 432
7.12 HOW DO PATHOGENS OVEREOME THE ANTIFUNGAL PHYTOALEXINS? 433 7.12.1
PATHOGENS MAY DETOXIFY PHYTOALEXINS 433 7.12.2 INDUCTION OF PHYTOALEXINS
MAY BE DELAYED IN SUSCEPTIBLE INTERACTIONS 436 7.12.3 PATHOGEN MAY
SUPPRESS AECUMULATION OF PHYTOALEXINS IN SUSEEPTIBLE
HOSTS................ 438 7.12.4 AMOUNT OF ACCUMULATION OF PHYTOALEXINS
MAY BE LESS IN SUSCEPTIBLE INTERAETIONS COMPARED WITH RESISTANT
INTERAETIONS 439 7.12.5 HIGHLY TOXIE PHYTOALEXINS MAY NOT ACCUMULATE IN
SUSEEPTIBLE INTERACTIONS 439 7.12.6 SOME PHYTOALEXINS MAY NOT BE
PRODUCED IN SUSCEPTIBLE INTERAETIONS 439 7.12.7 SOME PHYTOALEXINS MAY
NOT HAVE ANY ROLE IN DEFENSE MECHANISMS OF PLANTS.....................
440 7.13 CHEMICAL STRUCTURAL CLASSES OF PHYTOANTICIPINS 440 7.14
PHENOLICS AS PHYTOANTICIPINS 440 7.15 TOXICITY OF PHENOLICS TO PATHOGENS
441 7.16 HOW DOES PATHOGEN OVERCOME THE ANTIFUNGAL PHENOLICS? 441 7.16.1
PATHOGEN MAY DEGRADE PHENOLICS TO NONTOXIC PRODUCTS 441 7.16.2 PATHOGEN
MAY SUPPRESS INCREASED SYNTHESIS OF PHENOLICS IN PLANTS 443 7.16.3
PATHOGEN MAY SUPPRESS PHENOL BIOSYNTHETIC ENZYMES 443 7.16.4 PATHOGEN
MAY SUPPRESS PHENOLIC METABOLISM BY ITS SUPPRESSOR MOLEEULE .. 443
7.16.5 PATHOGEN MAY SUPPRESS PHENOLIC METABOLISM BY PRODUCING TOXINS 443
7.16.6 PATHOGEN MAY SUPPRESS OXIDATION OFPHENOLICS BY INHIBITING
POLYPHENOL OXIDASE *** ************** ..* ** 444 7.16.7 PHENOLICS ARE
FUNGITOXIC BUT THEY MAY NOT AECUMULATE TO FUNGITOXIC LEVEL DURING
PATHOGENESIS IN SOME PLANT-PATHOGEN INTERACTIONS 444 7.17 SAPONINS AS
PHYTOANTICIPINS 445 7.18 GLUCOSINOLATES AS PHYTOANTICIPINS 447 7.18.1
BIOSYNTHESIS OFGLUCOSINOLATES 447 7.18.2 TOXICITY OF GLUCOSINOLATES TO
FUNGAL PATHOGENS 448 7.18.3 HOW DOES THE PATHOGEN OVERCOME TOXICITY OF
GLUCOSINOLATES? 448 7.18.3.1 CONCENTRATION OF GLUCOSINOLATES MAY BE LESS
IN SUSCEPTIBLE TISSUES 448 XX 7.18.3.2 GLUCOSINOLATES MAY NOT BE
INVOLVED IN DISEASE RESISTANCE UNLESS THE TISSUE IS DAMAGED 448 7.19
CYANOGENIC GLUCOSIDES 450 7.20 DIERIES 450 7.21 CONCLUSION 450
REFERENCES 451 CHAPTER 8 TOXINS IN DISEASE SYMPTOM DEVELOPMENT 469 8.1
INTRODUCTION 469 8.2 IMPORTANCE OF TOXINS IN DISEASE DEVELOPMENT.. 471
8.3 TOXINS SUPPRESS HOST-DEFENSE MECHANISMS 472 8.4 TOXINS CAUSE CELL
MEMBRANE DYSFUNCTION 473 8.4.1 PERMEABILITY CHANGES 473 8.4.2 CHANGES IN
MERNBRANE-BOUND ATPASES 474 8.4.2.1 H+-A TPASE IS STIMULATED 474 8.4.2.2
H+-A TPASE IS INHIBITED 477 8.4.3 INHIBITION OF CALMODULIN ACTIVITY 477
8.4.4 ALTERATION IN MEMBRANE POTENTIAL 477 8.4.5 TOXINS FORM ION
CHANNELS IN PLANT CELL MEMBRANES 479 8.4.6 MODIFICATION OF MEMBRANE
PHOSPHOLIPIDS 479 8.4.7 TOXIN-INDUCED ACTIVE OXYGEN SPECIES INDUCE
MEMBRANE DYSFUNCTION 480 8.4.8 MITOCHONDRIAL MEMBRANE DYSFUNCTION 481
8.5 HOW DO PATHOGENS INDUCE MEMBRANE DYSFUNCTION ONLY IN SUSCEPTIBLE
HOSTS? 483 8.5.1 DETOXIFICATION OF PHYTOTOXINS, WHICH OCCURS IN
RESISTANT HOSTS, DOES NOT OCEUR IN SUSCEPTIBLE HOSTS 483 8.5.2
SUSCEPTIBLE TISSUES MAY HAVE TOXIN RECEPTORS WHICH MAY BE ABSENT IN
RESISTANT TISSUES 484 8.5.3 SUSCEPTIBLE TISSUESMAY BE MORE SENSITIVE TO
TOXINS 486 8.5.4 SPECIFIC PROTEIN SYNTHESIZED AFTER TOXIN EXPOSURE MAY
CONFER HOST SPECIFICITY 487 8.5.5 PROTEINS OF SUSCEPTIBLE HOSTS MAY
ENHANCE POTENTIAL OFPATHOGENS TO PRODUCE TOXINS 487 8.5.6 SUCROSE INFLUX
MAY HAVE CORRELATION WITH SENSITIVITY TO TOXIN 487 8.5.7 TRANSPORT OF
TOXIN TO CYTOPLASM MAY OCCUR ONLY IN SUSCEPTIBLE INTERACTIONS 488 8.6
CONCLUSION 488 REFERENCES 489 INDEX 499
|
| adam_txt |
CONTENTS PREFACE XXI AUTHOR XXIII CHAPTER 1 PERCEPTION AND TRANSDUCTION
OF PLANT SIGNALS IN PATHOGENS. 1 1.1 INTRODUCTION ,. 1 1.2 SIGNALING
AND TRANSDUCTION SYSTEMS IN "FIRST TOUCH" AND ADHESION OF FUNGAL
SPORES.
1 1.2.1 FIRST TOUCH OR INITIAL CONTACT TRIGGERS THE INFECTION PROEESS 1
1.2.2 ADHESION OR CLOSE CONTACT TRIGGERS FUNGAL INFECTION PROCESS 3
1.2.3 ADHESION OF SPORES DUE TO HYDROPHOBIE INTERAETION 3 1.2.4 ADHESION
OF SPORES IS ACEOMPANIED BY RELEASE OF EXTRAEELLULAR MATERIAL. 4 1.2.5
INVOLVEMENT OF CUTINASES IN SPORE ADHESION 5 1.2.6 SOME PLANT SIGNALS
MAY BE NEEDED FOR ADHESION OF SPORES 5 1.3 SIGNALING IN FUNGAL SPORE
GERMINATION.
. 6 1.3.1 PLANT SIGNALS TRIGGER STRUCTURAL CHANGES IN SPORES BEFORE
GERMINATION 6 1.3.2 PLANT-SURFAEE SIGNALS TRIGGER SPORE GERMINATION 7
1.3.3 FLAVONOIDS SIGNALING SPORE GERMINATION 8 1.4 SIGNALING IN
DIFFERENTIATION OF GERM TUBES INTO INFECTION STRUCTURES 8 1.4.1 ADHESION
OF GERMLINGS AND INFECTION
STRUCTURES. 8 1.4.2
EXTRAEELLULAR MATRIX IN GERMLING ADHESION 9 1.4.3 EXTRAEELLULAR MATRIX
IN APPRESSORIAL ADHESION 11 1.4.4 TOPOGRAPHIE SIGNALS IN APPRESSORIUM
FORMATION. 11 1.4.5 PLANT-SURFACE WAX SIGNALS APPRESSORIUM FORMATION 13
1.4.6 CUTIN MONOMERS AS SIGNAL MOLECULES 14 1.4.7 ETHYLENE SIGNALS
APPRESSORIUM FORMATION 14 1.4.8 FUNGAL SIGNALS IN INDUCTION OF
APPRESSORIUM FORMATION 15 1.5 SIGNAL TRANSDUETION IN FUNGAL PATHOGENESIS
16 1.5.1 TRANSMEMBRANE REEEPTOR FOR EXTRACELLULAR SIGNALS 16 1.5.2
G-PROTEINS 17 1.5.3 CALCIUM/CALMODULIN-DEPENDENT SIGNALING 20 1.5.4
CAMPJPROTEIN KINASE SIGNALING PATHWAY 21 1.5.5 MITOGEN-ACTIVATED PROTEIN
KINASE SIGNALING CASCADES 24 1.5.6 LIPID-INDUEED PROTEIN KINASE
SIGNALING 28 1.5.7 PAKSIGNALING 28 1.5.8 PHOSPHORYLATION AND
DEPHOSPHORYLATION CASCADES 29 1.5.9 P-TYPE ADENOSINE TRIPHOSPHATASE
SIGNALING 29 1.6 GENES INVOLVED IN FORMATION OF INFECTION STRUETURES 30
1.7 SIGNALS IN FUNGAL INFECTION PROCESS 32 1.7.1 MAGNAPORTHE GRISEA 32
1.7.2 BLUMERIA GRAMINIS 34 IX X 1.7.3 COLLETOTRICHUM
GLOEOSPORIOIDES. 35 1.7.4 USTILAGO MAYDIS 36 1.7.5 FUSARIUM
OXYSPORUM 37 1.8 CONCLUSION 37 REFERENCES 38 CHAPTER 2 PERCEPTION AND
TRANSDUCTION OF PATHOGEN SIGNALS IN PLANTS 55 2.1 INTRODUCTION 55 2.2
WHAT ARE ELICITORS? 56 2.3 OLIGOSACCHARIDE ELICITORS 57 2.3.1
CHITOOLIGOSACCHARIDE ELICITORS 57 2.3.2 CHITOSAN ELICITORS 58 2.3.3
OLIGOGLUCAN ELICITORS 58 2.3.4 OTHER CARBOHYDRATE ELICITORS 60 2.4
PROTEIN/PEPTIDE ELICITORS 60 2.4.1 ELICITINS. 60 2.4.2 XYLANASE
ELICITOR 64 2.4.3 PANIE213 ELICITOR. 64 2.4.4 NEPL ELICITOR 64
2.4.5 NIP1 ELICITOR 64 2.4.6 PB90 ELICITOR 65 2.5 GLYCOPROTEIN ELICITORS
65 2.5.1 CARBOHYDRATE MOIETY IN THE GLYCOPROTEIN ELICITOR MAY CONFER
ELICITOR ACTIVITY 65 2.5.2 PROTEIN MOIETY IN GLYCOPROTEIN ELICITORS MAY
CONFER ELICITOR ACTIVITY 66 2.5.3 FUNCTIONS OF GLYCOPROTEIN ELICITORS 67
2.6 LIPID ELICITORS 67 2.6.1 SPHINGOLIPIDS 67 2.6.2 ARACHIDONIC AND
EICOSAPENTAENOIC ACIDS 68 2.6.3 ERGOSTEROLS 68 2.7 TOXINS AS ELICITOR
MOLEEULES 69 2.8 PLANT CELL WALL-DEGRADING ENZYMES AS ELICITORS 69 2.9
RACE-SPECIFIC AND CULTIVAR-SPECIFIC ELICITORS 70 2.10 SPECIFICITY OF
GENERAL ELICITORS 72 2.11 ENDOGENOUS OLIGOGALACTURONIDE ELICITORS 73
2.12 MULTIPLE ELICITORS MAY BE NEEDED TO ACTIVATE DEFENSE RESPONSES 74
2.12.1 ELICITOR COMPLEX 74 2.12.2 NETWORK OF ELICITOR MOLECU1ES 74 2.13
AVAILABILITY OF FUNGAL ELICITORS AT THE SITE OF FUNGAL INVASION IN
PLANTS 75 2.14 RECEPTORS FOR ELICITOR SIGNALS IN PLANT CELL MEMBRANE 76
2.14.1 RECEPTOR SITES FOR BINDING OLIGOSACCHARIDE ELICITORS 76 2.14.2
RECEPTOR SITES FOR BINDING PROTEINACEOUS ELICITORS 77 2.14.3 PROTEIN
KINASES AS RECEPTOR SITES 78 2.14.4 LRR-TYPE RECEPTORS 78 2.14.5 LEETINS
AS RECEPTORS 79 2.14.6 RESISTANCE GENE PRODUCTS AS RECEPTORS 79 2.15
CALCIUM ION MAY ACT AS SECOND MESSENGER 79 2.15.1 FUNCTION OF CALCIUM
ION AS SECOND MESSENGER 79 2.15.2 UPSTREAM EVENTS OF CA 2 + SIGNALING 81
2.15.3 DOWNSTREAM EVENTS OF CA 2 + SIGNALING 82 XI 2.16 PHOSPHORYLATION
OF PROTEINS AS A COMPONENT IN SIGNAL TRANSDUCTION SYSTEM 83 2.16.1
PHOSPHORY1ATIONJDEPHOSPHORYLATION EVENTS. 83 2.16.2 CALCIUM ION
IN PHOSPHORYLATION 83 2.17 MITOGEN-ACTIVATED PROTEIN KINASE CASCADES IN
SIGNAL TRANSDUCTION 84 2.18 PHOSPHOLIPID-SIGNALING SYSTEM 85 2.18.1
PLANT CELL MEMBRANE PHOSPHOLIPIDS AS SIGNAL
MOLECULES. 85 2.18.2 ROLE OFPHOSPHOLIPASE A IN
PHOSPHOLIPID-SIGNALING SYSTEM 86 2.18.3 PHOSPHOLIPASE C IN
PHOSPHOLIPID-SIGNALING SYSTEM 87 2.18.4 PHOSPHOLIPASE D IN
PHOSPHOLIPID-SIGNALING SYSTEM 89 2.19 ANION CHANNELS IN SIGNAL
TRANSDUCTION 90 2.19.1 ANION CHANNELS IN THE SIGNALING SYSTEM 90 2.19.2
UPSTREAM EVENTS OF ANION CHANNEL-SIGNALING SYSTEM 91 2.19.3 DOWNSTREAM
OF ANION CHANNEL-SIGNALING SYSTEM 91 2.20 EXTRACELLULAR ALKALINIZATION
AND CYTOPLASMIC ACIDIFICATION IN SIGNALING SYSTEM 91 2.21 REACTIVE
OXYGEN SPECIES IN SIGNAL TRANSDUCTION 92 2.21.1 OXIDATIVE
BURST.
92 2.21.2 MECHANISMS OF PRODUCTION OF REACTIVE OXYGEN SPECIES 93
2.21.2.1 PRODUCTION OF 02 93 2.21.2.2 PRODUCTION OF H2 0 2 94 2.21.2.3
PRODUCTION OF"OH RADICAL. 95 2.21.2.4 PRODUCTION OF SINGLET OXYGEN
E02) 95 2.21.3 UPSTREAM OF ROS SIGNALING 96 2.21.4 DOWNSTREAM OF ROS
SIGNALING 96 2.22 NITRIC OXIDE IN SIGNAL TRANSDUCTION 97 2.22.1
INCREASES IN NITRIC OXIDE. 97 2.22.2 BIOSYNTHESIS OF
NITRIC OXIDE 97 2.22.3 UPSTREAM EVENTS OF NITRIC OXIDE SIGNALING 98
2.22.4 DOWNSTREAM EVENTS OF NITRIC OXIDE SIGNALING. 99 2.23
SALICYLICACID-SIGNALING SYSTEM. 100 2.23.1 SALICYLIC
ACID IN SIGNALING DEFENSE RESPONSE IN PLANTS 100 2.23.2 BIOSYNTHESIS OF
SALICYLIC ACID 101 2.23.3 SIGNAL PERCEPTION 102 2.23.4 UPSTREAM SIGNALS
FOR INDUCTION OF SYNTHESIS OF SALICYLIC ACID 102 2.23.5 DOWNSTREAM OF
SALICYLIC ACID SIGNALING 103 2.23.6 METHYL SALICYLATE 104 2.23.7
SALICYLATE-INDEPENDENT SIGNALING SYSTEMS 105 2.24 JASMONATE-SIGNALING
PATHWAY 105 2.24.1 JASMONATE SIGNALING IN INDUCTION OF DEFENSE
RESPONSES. 105 2.24.2 BIOSYNTHESIS OF
JASMONATES.
106 2.24.3 PERCEPTION OF JASMONATE SIGNALS 108 2.24.4
JASMONATE-SIGNALING SYSTEM MAY BEHAVE DIFFERENTLY IN PROTECTING PLANTS
AGAINST VARIOUS PATHOGENS 108 2.24.5 INDUCTION OF INTERCELLULAR AND
INTERPLANT SYSTEMIC TRANSDUCTION OF JASMONATE
SIGNALS.
. 109 2.24.6 UPSTREAM OF JASMONATE SIGNALING 109 2.24.7
DOWNSTREAM OF JASMONATE SIGNALING 109 2.24.8 TRANSCRIPTIONAL REGULATION
OF JA-RESPONSIVE GENES 109 2.24.9 JASMONIC ACID, METHYL JASMONATE, AND
CYCLIC PRECURSORS AND DERIVATIVES OF JASMONIC ACID AS SIGNAL MO1ECU1ES
110 2.25 ROLE OF SYSTEMIN IN SIGNAL TRANSDUCTION SYSTEM 111 2.26
ETHYLENE-DEPENDENT SIGNALING PATHWAY 112 XII 2.26.1 ETHY1ENE-SIGNALING
SYSTEM INDUCING DISEASE RESISTANCE OR SUSCEPTIBILITY 112 2.26.2
BIOSYNTHESIS OF ETHY1ENE. 112 2.26.3 UPSTREAM SIGNALS IN INDUCTION
OF SYNTHESIS OF ETHYLENE 113 2.26.4 ETHY1ENE SIGNAL PERCEPTION 114
2.26.5 DOWNSTREAM EVENTS IN ETHYLENE SIGNALING 114 2.27 ABSCISICACID
SIGNALING.
115 2.28 FATTY ACIDS AS SYSTEMIC SIGNAL MOLECULES 116 2.29 OTHER
SIGNALING SYSTEMS. 116 2.30 NETWORK AND INTERPLAY OF SIGNALING
PATHWAYS 116 2.30.1 REGULATORY INTERACTION AND COORDINATION AMONG
SALICYLATE-, JASMONATE-, AND ETHYLENE-SIGNALING PATHWAYS 116 2.30.2
CCORDINATED REGULATION OF ETHYLENE- AND JASMONATE-SIGNALING PATHWAYS.,
117 2.30.3 INTERPLAY BETWEEN SALICYLATE- AND JASMONATE-SIGNALING
PATHWAYS 118 2.30.4 INTERPLAY BETWEEN SALICYLATE AND ETHYLENE PATHWAYS
118 2.30.5 CROSS TALK BETWEEN SALICYLATE AND JASMONATE/ETHYLENE PATHWAYS
119 2.30.6 CROSS TALK BETWEEN ABSCISIC ACID-, JASMONATE-, AND ETHYLENE-
DEPENDENT SIGNALING PATHWAYS 120 2.30.7 REGULATORY SWITCHES TO FINE-TUNE
SIGNALING PATHWAYS 121 2.31 INDUCTION OF DEFENSE GENES MAY REQUIRE
DIFFERENT SIGNAL TRANSDUCTION SYSTEMS 121 2.32 PERCEPTION AND
TRANSDUCTION OF PATHOGEN SIGNALS IN PLANTS LEADING TO
SUSCEPTIBILITY.
123 2.32.1 DIFFERENTIAL EXPRESSION OF SIGNALING SYSTEM LEADING TO
SUSCEPTIBILITY OR RESISTANCE 123 2.32.2 SLOWER ACCUMULATION OF
ELICITOR-RELEASING ENZYMES IN SUSCEPTIBLE INTERACTIONS 124 2.32.3
SUSCEPTIBLE VARIETIES MAY RELEASE LESS AMOUNT OF ELICITORS FROM FUNGAL
PATHOGEN CELL WALLS 124 2.32.4 DE1AYED RELEASE OF ELICITORS IN
SUSCEPTIBLE INTERACTIONS 127 2.32.5 ELICITOR OF COMPATIBLE PATHOGENS
INDUCES LESS DEFENSE-RE1ATED ACTIONS THAN THAT OFINCOMPATIBLE PATHOGENS
127 2.32.6 DEGRADATION OF FUNGAL ELICITORS BY PLANT ENZYMES IN PLANT
TISSUES MAY LEAD TO SUSCEPTIBILITY. 128 2.32.7
FUNGAL PATHOGENS MAY DEGRADE HOST E1ICITORS DURING SUSCEPTIB1E
INTERACTIONS 129 2.32.8 ELICITORS MAY BE RELEASED DURING PATHOGENESIS
BUT MAY NOT BE ACTIVE OR LESS ACTIVE IN SUSCEPTIBLE PLANTS 130 2.32.9
SOMEELICITORS DO NOT ACT OR SHOW LITTLE ACTIVITY ON SUSCEPTIBLE
CUITIVARS 132 2.32.10 SPEED OF EXPRESSION OF SIGNAL TRANSDUCTION SYSTEM
MAY DETERMINE SUSCEPTIBILITY OR RESISTANCE 134 2.32.11 REDUCED
ACCUMULATION OF SIGNALS MAY LEAD TO SUSCEPTIBILITY 134 2.32.12 ELICITORS
MAY INDUCE GENES INVO1VED IN SUPPRESSION OF DEFENSE-RELATED GENES IN
SUSCEPTIBLE INTERACTIONS. 135 2.32.13 SUPPRESSORS NEGATING
ELICITOR-INDUCED DEFENSE RESPONSES IN SUSCEPTIBLE INTERACTIONS . 137
2.32.14 SUSCEPTIBLE P1ANTS MAY HAVE SUPPRESSORS TO SUPPRESS ACTION OF
FUNGAL ELICITORS ;. 140 2.32.15 DOWNREGULATION
OF FUNCTIONS OF ELICITORS IN SUSCEPTIBLE INTERACTIONS . 140 XIII
2.32.16 ACTIVATION OF AN UNSUITAB1E SIGNA1ING SYSTEM FOR INDUCTION OF
DEFENSE RESPONSES MAY LEAD TO SUSCEPTIBILITY 141 2.33 SIGNA1ING SYSTEMS
IN SUSCEPTIBLE INTERACTIONS 143 2.33.1 ABSCISIC ACID-SIGNALING SYSTEM
143 2.33.2 ETHY1ENE-SIGNALING SYSTEM. 144 2.33.3 SIGNAL
TRANSDUCTION SYSTEMS MAY INDUCE SUSCEPTIBILITY-RELATED RESPONSES 144
2.34 CONCLUSION 144 REFERENCES 147 CHAPTER 3 DISEASE RESISTANCE AND
SUSCEPTIBILITY GENES IN SIGNAL PERCEPTION AND EMISSION. 193
3.1 INTRODUCTION 193 3.2 MO1ECU1AR STRUCTURE OF RESISTANCE GENES 195
3.2.1 LRR DOMAINS 195 3.2.2 NBS DOMAINS 195 3.3 C1ASSIFICATION OF
RESISTANCE GENES BASED ON MO1ECU1AR STRUCTURE OF R GENE-ENCODED PROTEINS
196 3.3.1 RESISTANCE GENES ENCODING TIR-NBS-LRR PROTEINS 196 3.3.2
RESISTANCE GENES ENCODING NON-TIR-NBS-LRR PRO TEINS 197 3.3.3 RESISTANCE
GENES ENCODING LRR PROTEINS LACKING NBS DOMAIN 199 3.3.4 RESISTANCE
GENES ENCODING PROTEINS LACKING LRR DOMAIN 200 3.3.4.1 LRD PROTEINS 200
3.3.4.2 INTRACELLU1AR PROTEIN KINASES 200 3.3.4.3 TRANSMEMBRANE PROTEINS
201 3.3.4.4 LEETIN-TYPE PROTEINS 202 3.3.4.5 BEAT SHOCK PROTEIN-LIKE
PROTEINS 202 3.3.4.6 NADPB-DEPENDENT REDUCTASE-TYPE PROTEIN 202 3.3.4.7
PLANT ER GENES ENCODING PHOTORESPIRATORY PEROXISOMAL ENZYME PROTEINS 202
3.4 MO1ECU1AR STRUCTURE OF RECESSIVE GENES 202 3.4.1 BARLEY MLO
GENE.
. 202 3.4.2 ARABIDOPSIS PMR6 GENE 203 3.4.3 ARABIDOPSIS
RRS1-R GENE 203 3.4.4 ARABIDOPSIS SSI4 GENE 203 3.5 PERCEPTION OF
PATHOGEN SIGNALS BY RESISTANCE GENES 204 3.5.1 FUNCTIONS OF DIFFERENT
DOMAINS OF R PROTEINS IN PATHOGEN RECOGNITION 204 3.5.1.1 LRR DOMAIN 204
3.5.1.2 NBS DOMAIN 204 3.5.1.3 TIR DOMAIN 205 3.5.1.4 CC DOMAIN 205
3.5.1.5 C-TERMINA1 NON-LRR REGION 206 3.5.1.6 C-TERMINUS TRANSCRIPTIONA1
ACTIVATION DOMAIN 206 3.5.1.7 PROTEIN KINASE DOMAIN 206 3.5.1.8
TRANSMEMBRANE DOMAIN 206 3.5.1.9 CALMODULIN-BINDING PROTEIN 207 3.5.1.10
LEETIN-TYPE PROTEIN 207 3.5.1.11 BEAT SHOCK PROTEIN (BSP)-LIKE PROTEIN
207 3.5.2 R GENE PRODUCT MAY ACT AS A RECEPTOR THAT RECOGNIZES AN A VR
GENE
PRODUCL.
207 3.7.2 3.7.3 3.7.4 XIV 3.5.3 R PROTEIN MAY DETECT BINDING OF AN AVR
PROTEIN TO A DIFFERENT PROTEIN IN THE PLANT 208 3.6 ACTIVATION OF R
PROTEIN AND EMISSION OF SIGNALS TO OTHER COMPONENTS IN THE CELLO 209 3.7
DOWNSTREAM COMPONENTS OF R GENE-SIGNALING SYSTEMS 211 3.7.1 REGULATORY
GENES (OR COMPLEMENTARY GENES OR R GENE-SIGNALING COMPONENTS) 211
EDSI-PAD4 PROTEINS 212 NDRI PROTEINS 213 RAR1-SGTL-HSP90 PROTEINS 214
3.7.4.1 RARI 214 3.7.4.2 SGTI 215 3.7.4.3 RAR1/SGTI COMPLEX 217 3.7.4.4
INTERACTION OF RAR1/SGTL WITH HSP90 217 3.7.5 NPR1 218 3.7.6 PRF-PTO-PTI
SIGNALING SYSTEM 219 3.7.7 OTHERREGUIATORY GENES * 219 3.8 DOWNSTREAM
SIGNALINGEVENTS IN R GENE-MEDIATED RESISTANCE 221 3.9
SUSCEPTIBILITYGENES IN SIGNAL TRANSDUCTION 222 3.9.1 SUSCEPTIBILITY
ALLELES OFRESISTANCE GENES 222 3.9.2 SUSCEPTIBILITY GENES 222 3.9.3
RESISTANCE GENE MAY ACT AS SUSCEPTIBILITY GENE AGAINST SOME PATHOGENS
223 3.9.4 LOW EXPRESSION OF RESISTANCE GENES MAY LEAD TO SUSCEPTIBILITY
224 3.9.5 SUSCEPTIBILITY ALLELES OF RESISTANCE GENES MAY NEGATE THE
FUNCTION OF RESISTANCE GENES. 224 3.9.6 SUPPRESSOR GENES
225 3.10 CONCLUSION 225 REFERENCES : 227 CHAPTER 4 CELL DEATH PROGRAMS
DURING FUNGAL PATHOGENESIS 243 4.1 INTRODUCTION 243 4.2 CELL DEATH IN
RESISTANT INTERACTIONS 243 4.2.1 PROGRAMMED CELL DEATH 243 4.2.2
HYPERSENSITIVE CELL DEATH 244 4.2.3 SPONTANEOUS CELL DEATH 244 4.2.4
RUNAWAY CELLDEATH 245 4.2.5 CELL DEATH-INDUCING SYSTEMIC ACQUIRED
RESISTANCE 245 4.3 MOLECULAR MECHANISM OF INDUCTION OF HYPERSENSITIVE
CELL DEATH 245 4.3.1 MEDIATORS, REGULATORS, AND EXECUTIONERS OF CELL
DEATH 245 4.3.2 R GENE SIGNALS INVOLVED IN TRIGGERING CELL DEATH 246
4.3.3 REACTIVE OXYGEN SPECIES IN CELL DEATH. 246 4.3.4 NITRIC
OXIDE IN CELL DEATH 249 4.3.5 BAX FAMILY OF PROTEINS 250 4.3.6
ION-CONDUCTING CHANNELS 251 4.3.7 FUNCTION OF MITOCHONDRION IN INDUCTION
OF CELL DEATH 251 4.3.8 PROTEOLYTIC ENZYMES 251 4.3.8.1 PLANT CASPASES
251 4.3.8.2 VACUOLAR PROCESSING ENZYMES (VPES) 252 4.5 4.6 4.7 4.8 XV
4.3.8.3 METACASPASES 252 4.3.8.4 OTHER TYPES OF PROTEOLYTIC ENZYMES 253
4.3.9 PROBABLE SEQUENCE IN INDUCTION OF HYPERSENSITIVE CELL DEATH 253
4.4 MOLECULAR MECHANISM OF INDUCTION OF SPONTANEOUS CELL DEATH 253 4.4.1
SPONTANEOUS CELL DEATH-REGULATING GENES. 253 4.4.2 SALICYLIC
ACID 255 4.4.3 ETHYLENE 255 4.4.4 PHOSPHATIDIC ACID . 255 MOLECULAR
MECHANISM OF INDUCTION OF RUNAWAY CELL DEATH 256 ROLE OF CELL DEATH IN
INDUCTION OF SYSTEMIC ACQUIRED RESISTANCE 257 SUSCEPTIBILITY-RELATED
CELL DEATH 258 MOLECULAR MECHANISMS IN INDUCTION OF CELL DEATH IN
SUSCEPTIBLE INTERACTIONS 258 4.8.1 MEDIATORS, REGULATORS, AND
EXECUTIONERS OF SUSCEPTIBILITY-RELATED PLANT CELL
DEATH. 258 4.8.2 REACTIVE OXYGEN
SPECIES 259 4.8.3 PROTEOLYTIC ENZYMES 259 4.8.4 CALCIUM ION : 260 4.8.5
SALICYLATE, ETHYLENE, AND JASMONATE 260 4.8.6 SPHINGOLIPID METABOLISM
262 4.8.7 EXTRACELLULAR ATP LEVELS. 262 4.9 WHAT IS THE
FUNCTION OF CELL DEATH IN FUNGAL PATHOGENESIS? 262 4.10 CONCLUSION 264
REFERENCES 264 CHAPTER 5 CELL WALL DEGRADATION AND FORTIFICATION 275 5.1
INTRODUCTION 275 5.2 STRUCTURE OF CUTICLE 275 5.3 PENETRATION OF
EPICUTICULAR WAXY LAYER BY PATHOGENS 276 5 .4 PRODUCTION OF CUTINASES TO
BREACH CUTICLE BARRIER. 276 5
.5 GENES ENCODING
CUTINASES.
. 277 5.6 PLANT SIGNALS TRIGGERING FUNGAL CUTINASES 278
5.7 IMPORTANCE OF CUTINASES IN PENETRATION OF CUTICLE 279 5.8 CUTINASES
AS VIRULENCE/PATHOGENICITY FACTORS 280 5.9 MELANINS IN FUNGAL
PENETRATION OF CUTICLE
BARRIER. 281 5.9.1
BIOSYNTHESIS OF MELANINS 281 5.9.2 MELANINS AID IN PENETRATION OF
CUTICLE BARRIER BY FUNGAL PATHOGENS 283 5.10 DEGRADATION OF PECTIC
POLYSACCHARIDES 285 5.10.1 TYPES OFPECTIC POLYSACCHARIDES 285 5.10.2
TYPES OF PECTIC ENZYMES 285 5.10.3 FUNGAL PATHOGENS PRODUCE MULTIPLE
PECTIC ENZYMES 286 5.10.4 GENES ENCODING PECTIC ENZYMES 287 5.10.5
EVIDENCES TO SHOW THAT PECTIC ENZYMES AID PATHOGENS TO PENETRATE CELL
WALL 288 5.10.5.1 IMMUNOCYTOCHEMICAL EVIDENCES 288 5.10.5.2 EVIDENCES BY
SHOWING PROTECTION OF THE HOST BY INHIBITION OF PECTIC ENZYMES WITH
SPECIFICANTIBODIES 289 5.10.5.3 EVIDENCES SHOWING PROTEETION OF HOST
PLANTS BY INHIBITION OF PECTIC ENZYMES WITH
SELECTIVEINHIBITORS. 290 5.10.5.4 EVIDENCES
USING PECTIC ENZYME-DEFICIENT FUNGAL ISOLATES . 290 XVI 5.10.5.5
EVIDENCES SHOWING CORRE1ATION BETWEEN THE LEVEL OF PECTIC ENZYMES AND
VIRU1ENCE 291 5.10.5.6 EVIDENCES SHOWING ENHANCEMENT OF VIRU1ENCE BY
GENE TRANSFER. 291 5.10.5.7
EVIDENCES SHOWING DECREASE IN VIRULENCE BY GENE DISRUPTION 291 5.10.6
PLANT SIGNALS TO INDUCE PECTIC ENZYMES 291 5.10.7 HOST CELLWALL DIFFERS
IN ITS SUSCEPTIBILITY TO PECTIC ENZYMES 292 5.10.8 CELLWALL PROTEINS
MODULATE PECTIC ENZYME ACTIVITY 292 5.11 PATHOGENS PRODUCE CELLULOLYTIC
ENZYMES TO BREACH.CELL WALL BARRIER. 294 5.12 FUNGAL HEMICELLU1ASES IN
PLANT CELLWALL J?EGRADATLON 295 5.13 DEGRADATION OF CELL WALL STRUCTURAL
PROTE~NS 296 5.14 REQUIREMENT OF SEVERAL CELL WALL-DEGRADMG ENZYMES TO
DEGRADE THE COMPLEX-NATURED CELL WALL 297 5.15 PRODUCTION OF
SUITABLEENZYMES IN APPROPRIATE SEQUENCE BY FUNGAL PATHOGENS 297 5.16
REINFORCEMENT OF HOST CELL WALL DURING FUNGAL INVASION 298 5.17 PAPILLAE
SUPPRESS FUNGA1 PENETRATION 298 5.18 CALLOSE DEPOSITIONIN CELLWALL 300
5.19 HOW DO PATHOGENS OVERCOME THE PAPILLAE AND CALLOSE BARRIERS? 301
5.19.1 PATHOGEN DELAYS PAPILLAE FORMATION 301 5.19.2 PATHOGENS MAY
SUPPRESS CALLOSE SYNTHESIS IN SUSCEPTIBLE INTERACTIONS 302 5.19.3
PATHOGENS MAY BE ABLE TO PENETRATE THE PAPILLAE BARRIER. 303 5.19.4
PATHOGENS MAY DEGRADE CALLOSE BY PRODUCING SS-1,3-G1UCANASE 303 5.20
ACCUMULATION OF HYDROXYPROLINE-RICH G1YCOPROTEINS IN PLANT CELLWALLS 304
5.20.1 HOST CELL WALL RESPONDS TO FUNGAL INVASION BY ACCUMULATING HRGP
. 304 5.20.2 SIGNALS TRIGGERING ACCUMULATION OF HRGPS 304 5.20.3 HOST
CELL WALL RESPONDS TO FUNGAL INVASION BY STRENGTHENING ITS HRGPS BY
GLYCOSYLATION 305 5.20.4 INSOLUBILIZATION OF HRGPS IN HOST CELL
WALL. 305 5.20.5 ENRICHMENT OF HRGPS BY LIGNIN DEPOSITION 305
5.20.6 SOMEHRGPS MAY IMMOBILIZE PLANT PATHOGENS 306 5.20.7 HOW DOES
PATHOGEN OVERCOME HRGP BARRIER? 306 5.20.7.1 LESS ACCUMULATION OF HRGPS
IN COMPATIB1E INTERACTIONS 306 5.20.7.2 PATHOGEN OVERCOMES HRGP BARRIER
BY DELAYING ACCUMULATION OF HRGPS IN HOST CELL WALL 306 5.21 CELL
WALL-BOUND PHENOLICS AND LIGNINS 307 5.21.1 FORTIFICATION OF PLANT CELL
WALL BY PHENOLICS AND LIGNIN 307 5.21.2 BIOSYNTHESIS OF PHENOLICS AND
LIGNINS 308 5.21.3 PHENOLIC DEPOSITION IN HOST CELL WALL IN RESPONSE TO
FUNGAL INVASION 308 5.21.4 HOST CELL WALL
RES;~~D~'~~'F~~~I'I~~~I~~'B;'A~~'I'~~TI~'~'E~~;~~~"'''' INVOLVED IN
SYNTHESIS OF WALL-BOUND PHENOLICS 310 5.21.5 HOW DOESTHE PATHOGEN
OVERCOME THE CELL WALL-BOUND PHENOLICS TO CAUSE DISEASE? 311 5.21.5.1
PATHOG~~S~~~;~~~~~A~~~~I~TI~~~FPH~~II~~I~ . HOSTCELL WALL
5.21.5.2 PATHOGEN
DELA;~"S;~TH~'I~"~F'CII'WII~B~~~D'PH~~II~~'::::::: ~G 5.21.6
LLGMFICATLON DURING FUNGAL PATHOGENESIS 312 XVII 5.21.6.1 HOST CELL WALL
RESPONDS TO FUNGAL INVASION BY INCREASING LIGNIFICATION PROCESS 312
5.21.6.2 PATHOGEN SUPPRESSES LIGNIN DEPOSITION 313 5.21.6.3 PATHOGEN
SUPPRESSES ENZYMES INVO1VED IN LIGNIN BIOSYNTHESIS 314 5.21.6.4 HOW DOES
PATHOGEN SUPPRESS LIGNIFICATION IN HOST CELL WALL? 315 5.22 SUBERIZATION
DURING FUNGAL PATHOGENESIS 316 5.22.1 HOST CELL WALL RESPONDS TO FUNGAL
INVASION BY SUBERIZATION 316 5.22.2 BIOSYNTHESIS OF SUBERIN IN
PATHOGEN-INOCULATED HOST CELL WALL 316 5.22.3 PATHOGEN DE1AYS SUBERIN
ACCUMULATION 317 5.22.4 PATHOGEN MAY SUPPRESS SUBERIN-SYNTHESIZING
ENZYMES 317 5.22.5 PATHOGENS MAY PENETRATE THE SUBERIZED WALLS OFHOST
CELLS 318 5.23 DEPOSITION OF MINERAL ELEMENTS IN HOST CELL WALL IN
RESPONSE TO FUNGAL
INVASION.
318 5.23.1 SILICON DEPOSITION 318 5.23.2 CALCIUM DEPOSITION IN PAPILLAE
318 5.23.3 MANGANESE ACCUMULATION IN PAPILLAE 319 5.24 CONCLUSION 319
REFERENCES 320 CHAPTER 6 INDUCTION AND EVASION OF PATHOGENESIS-RE1ATED
PROTEINS 345 6.1 INTRODUCTION 345 6.2 MULTIPLICITY OF PR PROTEINS 346
6.3 CLASSIFICATION OF PR PROTEINS 347 6.3.1 PR-1 PROTEINS 347 6.3.2 PR-2
PROTEINS 348 6.3.3 PR-3 PROTEINS 349 6.3.4 PR-4 PROTEINS 350 6.3.5 PR-5
PRO TEINS 351 6.3.6 PR-6 PROTEINS 351 6.3.7 PR-7 PROTEINS 352 6.3.8 PR-8
PROTEINS 352 6.3.9 PR-9 PROTEINS 352 6.3.10 PR-LO PROTEINS 353 6.3.11
PR-LI PROTEINS 353 6.3.12 PR-12 PROTEINS 353 6.3.13 PR-13 PROTEINS 354
6.3.14 PR-14 PROTEINS 354 6.3.15 PR-15 PROTEINS 354 6.3.16 PR-16
PROTEINS 355 6.3.17 PR-17PROTEIL1S 355 6.3.18 CHITOSANASES 355 6.4
INDUCTION OF PR PRO TEINS DURING FUNGAL PATHOGENESIS 355 6.5 GENES
ENCODING PR PROTEINS 356 6.6 TRANSCRIPTION OF PR GENES 357 6.7 SIGNALS
INVOLVED IN TRANSCRIPTIONAL INDUCTION OF PR GENES 358 6.7.1 INDUCTION OF
PR GENES BY ELICITORS 358 6.7.2 INDUCTION OF PR GENES BY SALICYLIC ACID
359 6.7.3 6.7.4 6.7,5 XVIII INDUCTION OFPR GENES BY ETHYLENE * 360
INDUCTION OFPR GENES BY JASMONIC ACIDJJASMONATE ",." ,." 362 INDUCTION
OF PR PROTEINS MAY REQUIRE DIFFERENT SIGNAL TRANSDUCTION SYSTEMS , , **
363 6.7.6 SYNERGISTIC EFFECT OFDIFFERENT SIGNALS " *. 364 6.7.7
ANTAGONISTICEFFECT OFDIFFERENT SIGNALS " * 364 6.8 PR PROTEINS ARE
SYNTHESIZED AS LARGER PRECURSORS ". 364 6.9 SECRETION OFPR PROTEINS ,
,., " , '.,',. 365 6.9.1 SECRETORYPATHWAYS .", , , ,,., , 365 6.9.2
SITE OF ACCUMULATION OF PR PROTEINS , , 366 6,10 PR PROTEINS MAY BE
INVOLVED IN INHIBITION OF PATHOGEN DEVELOPMENT. 367 6.10.1 INHIBITION
OF FUNGAL GROWTH BY PR PROTEINS IN VITRO 367 6.10.2 INHIBITION OFFUNGAL
GROWTH BY PR PROTEINS IN VIVO 369 6.10,3 SOME PR PROTEINS MAY BE
INVOLVED IN RELEASE OF ELICITOR MOLEEULES IN PLANTA , ,., , 370 6.10.4
SOME PR PROTEINS MAY BE INVOLVED IN REINFORCEMENT OF CELL WALL
STRUCTURES , , "." , , 370 6.11 PR PROTEINS MAY BE INVOLVED IN
TRIGGERING DISEASE RESISTANCE " 370 6.11.1 DEMONSTRATION OF THE ROLE OF
PR PROTEINS IN DISEASE RESISTANCE USING CHEMICAL OR BIOLOGICAL ELICITORS
" , 370 6.11.2 DEMONSTRATION OF ROLE OF PR PROTEINS IN DISEASE
RESISTANCE BY INDUCING MUTATION , 371 6.11.3 DEMONSTRATION OF ROLE OF PR
PROTEINS IN DISEASE RESISTANCE BY DEVELOPING TRANSGENIE PLANTS , , 371
6.11.4 DEMONSTRATION OF THE ROLE OF PR PROTEINS BY DEVELOPING TRANSGENIE
PLANTS WITH ANTISENSE SUPPRESSION OF PR GENES 373 6.12 HOW DO PATHOGENS
OVERCOME FUNGITOXIC PR PROTEINS OFTHE HOST? 373 6.12.1
SLOWERACCUMULATION OF PR PROTEINS MAY ENABLE PATHOGENS TO ESCAPE THE
ANTIFUNGAL ACTION OF PR PROTEINS 373 6.12.2 PATHOGENS MAY SHED AWAY FROM
THEIR CELL WALL THE SUBSTRATE FOR THE PR PROTEINS OF ENZYMATIC NATURE
AND AVOID THEIR LYTIC ENZYME ACTION" , , , , ,." """" " , 379 6.12,3
PATHOGENS MAY PRODUCE ENZYMES THAT PROTECT THEM FROM FUNGITOXIC ACTION
OF PR-3 PROTEINS 380 6.12.4 PATHOGENS MAY PRODUCE ENZYMES TO INHIBIT
ACTIVITY OF SOME PR PROTEINS , " ' ' 381 6.12.5 LESS ELICITOR IS
RELEASED FROM PATHOGEN'S CELL WALL TO ACTIVATE SYNTHESIS OF PR PROTEINS
" 381 6.12.6 PR PROTEINS ARE DEGRADED QUICKLY IN THE SUSCEPTIBLE HOST
TISSUES 382 6.12.7 SITE OF ACCUMULATION OF SOME PR PROTEINS MAY
DETERRNINE SUSCEPTIBILITY OR RESISTANCE 382 6.12.8 ADAPTATION OF
PATHOGENS TO PR PROTEINS 384 6.12.9 SOMEPR PROTEINS MAY NOT BE INVO1VED
IN DISEASE RESISTANCE " 385 6.13 CONCLUSION " , , 385 REFERENCES " , , ,
386 CHAPTER 7 EVASION AND DETOXIFICATION OF SECONDARY METABOLITES " 411
7.1 INTRODUCTION "" " , , , ,., 411 7.2 CHEMICAL STRUCTURAL CLASSES OF
PHYTOALEXINS , 412 XIX 7.3 BIOSYNTHESIS OF ISOFLAVONOID PHYTOALEXINS 414
7.3.1 PHASEOLLIN AND RELATED COMPOUNDS 414 7.3.2 GLYCEOLLINS 418 7.3.3
MEDIEARPIN 420 7.3.4 PISATIN 423 7.4 BIOSYNTHESIS OF FLAVANONE
PHYTOALEXINS 424 7.5 BIOSYNTHESIS OF COUMARIN PHYTOALEXINS 424 7.6
BIOSYNTHESIS OF STILBENE PHYTOALEXINS 426 7.7 BIOSYNTHESIS OF TERPENOID
PHYTOALEXINS 426 7.8 BIOSYNTHESIS OF INDOLE-BASED SULFUR-CONTAINING
PHYTOALEXINS 430 7.9 BIOSYNTHESIS OF ALKALOID PHYTOALEXINS 431 7.10 SITE
OF SYNTHESIS OFPHYTOALEXINS 432 7.11 PHYTOALEXINS ARE FUNGITOXIC 432
7.12 HOW DO PATHOGENS OVEREOME THE ANTIFUNGAL PHYTOALEXINS? 433 7.12.1
PATHOGENS MAY DETOXIFY PHYTOALEXINS 433 7.12.2 INDUCTION OF PHYTOALEXINS
MAY BE DELAYED IN SUSCEPTIBLE INTERACTIONS 436 7.12.3 PATHOGEN MAY
SUPPRESS AECUMULATION OF PHYTOALEXINS IN SUSEEPTIBLE
HOSTS. 438 7.12.4 AMOUNT OF ACCUMULATION OF PHYTOALEXINS
MAY BE LESS IN SUSCEPTIBLE INTERAETIONS COMPARED WITH RESISTANT
INTERAETIONS 439 7.12.5 HIGHLY TOXIE PHYTOALEXINS MAY NOT ACCUMULATE IN
SUSEEPTIBLE INTERACTIONS 439 7.12.6 SOME PHYTOALEXINS MAY NOT BE
PRODUCED IN SUSCEPTIBLE INTERAETIONS 439 7.12.7 SOME PHYTOALEXINS MAY
NOT HAVE ANY ROLE IN DEFENSE MECHANISMS OF PLANTS.
440 7.13 CHEMICAL STRUCTURAL CLASSES OF PHYTOANTICIPINS 440 7.14
PHENOLICS AS PHYTOANTICIPINS 440 7.15 TOXICITY OF PHENOLICS TO PATHOGENS
441 7.16 HOW DOES PATHOGEN OVERCOME THE ANTIFUNGAL PHENOLICS? 441 7.16.1
PATHOGEN MAY DEGRADE PHENOLICS TO NONTOXIC PRODUCTS 441 7.16.2 PATHOGEN
MAY SUPPRESS INCREASED SYNTHESIS OF PHENOLICS IN PLANTS 443 7.16.3
PATHOGEN MAY SUPPRESS PHENOL BIOSYNTHETIC ENZYMES 443 7.16.4 PATHOGEN
MAY SUPPRESS PHENOLIC METABOLISM BY ITS SUPPRESSOR MOLEEULE . 443
7.16.5 PATHOGEN MAY SUPPRESS PHENOLIC METABOLISM BY PRODUCING TOXINS 443
7.16.6 PATHOGEN MAY SUPPRESS OXIDATION OFPHENOLICS BY INHIBITING
POLYPHENOL OXIDASE *** ************** .* ** 444 7.16.7 PHENOLICS ARE
FUNGITOXIC BUT THEY MAY NOT AECUMULATE TO FUNGITOXIC LEVEL DURING
PATHOGENESIS IN SOME PLANT-PATHOGEN INTERACTIONS 444 7.17 SAPONINS AS
PHYTOANTICIPINS 445 7.18 GLUCOSINOLATES AS PHYTOANTICIPINS 447 7.18.1
BIOSYNTHESIS OFGLUCOSINOLATES 447 7.18.2 TOXICITY OF GLUCOSINOLATES TO
FUNGAL PATHOGENS 448 7.18.3 HOW DOES THE PATHOGEN OVERCOME TOXICITY OF
GLUCOSINOLATES? 448 7.18.3.1 CONCENTRATION OF GLUCOSINOLATES MAY BE LESS
IN SUSCEPTIBLE TISSUES 448 XX 7.18.3.2 GLUCOSINOLATES MAY NOT BE
INVOLVED IN DISEASE RESISTANCE UNLESS THE TISSUE IS DAMAGED 448 7.19
CYANOGENIC GLUCOSIDES 450 7.20 DIERIES 450 7.21 CONCLUSION 450
REFERENCES 451 CHAPTER 8 TOXINS IN DISEASE SYMPTOM DEVELOPMENT 469 8.1
INTRODUCTION 469 8.2 IMPORTANCE OF TOXINS IN DISEASE DEVELOPMENT. 471
8.3 TOXINS SUPPRESS HOST-DEFENSE MECHANISMS 472 8.4 TOXINS CAUSE CELL
MEMBRANE DYSFUNCTION 473 8.4.1 PERMEABILITY CHANGES 473 8.4.2 CHANGES IN
MERNBRANE-BOUND ATPASES 474 8.4.2.1 H+-A'TPASE IS STIMULATED 474 8.4.2.2
H+-A'TPASE IS INHIBITED 477 8.4.3 INHIBITION OF CALMODULIN ACTIVITY 477
8.4.4 ALTERATION IN MEMBRANE POTENTIAL 477 8.4.5 TOXINS FORM ION
CHANNELS IN PLANT CELL MEMBRANES 479 8.4.6 MODIFICATION OF MEMBRANE
PHOSPHOLIPIDS 479 8.4.7 TOXIN-INDUCED ACTIVE OXYGEN SPECIES INDUCE
MEMBRANE DYSFUNCTION 480 8.4.8 MITOCHONDRIAL MEMBRANE DYSFUNCTION 481
8.5 HOW DO PATHOGENS INDUCE MEMBRANE DYSFUNCTION ONLY IN SUSCEPTIBLE
HOSTS? 483 8.5.1 DETOXIFICATION OF PHYTOTOXINS, WHICH OCCURS IN
RESISTANT HOSTS, DOES NOT OCEUR IN SUSCEPTIBLE HOSTS 483 8.5.2
SUSCEPTIBLE TISSUES MAY HAVE TOXIN RECEPTORS WHICH MAY BE ABSENT IN
RESISTANT TISSUES 484 8.5.3 SUSCEPTIBLE TISSUESMAY BE MORE SENSITIVE TO
TOXINS 486 8.5.4 SPECIFIC PROTEIN SYNTHESIZED AFTER TOXIN EXPOSURE MAY
CONFER HOST SPECIFICITY 487 8.5.5 PROTEINS OF SUSCEPTIBLE HOSTS MAY
ENHANCE POTENTIAL OFPATHOGENS TO PRODUCE TOXINS 487 8.5.6 SUCROSE INFLUX
MAY HAVE CORRELATION WITH SENSITIVITY TO TOXIN 487 8.5.7 TRANSPORT OF
TOXIN TO CYTOPLASM MAY OCCUR ONLY IN SUSCEPTIBLE INTERACTIONS 488 8.6
CONCLUSION 488 REFERENCES 489 INDEX 499 |
| any_adam_object | 1 |
| any_adam_object_boolean | 1 |
| author | Vidhyasekaran, P. |
| author_facet | Vidhyasekaran, P. |
| author_role | aut |
| author_sort | Vidhyasekaran, P. |
| author_variant | p v pv |
| building | Verbundindex |
| bvnumber | BV021626311 |
| callnumber-first | S - Agriculture |
| callnumber-label | SB733 |
| callnumber-raw | SB733 |
| callnumber-search | SB733 |
| callnumber-sort | SB 3733 |
| callnumber-subject | SB - Plant Culture |
| classification_rvk | WN 9350 |
| classification_tum | LAN 244f |
| ctrlnum | (OCoLC)255959352 (DE-599)BVBBV021626311 |
| dewey-full | 632.4 |
| dewey-hundreds | 600 - Technology (Applied sciences) |
| dewey-ones | 632 - Plant injuries, diseases, pests |
| dewey-raw | 632.4 |
| dewey-search | 632.4 |
| dewey-sort | 3632.4 |
| dewey-tens | 630 - Agriculture and related technologies |
| discipline | Biologie Agrarwissenschaft Agrar-/Forst-/Ernährungs-/Haushaltswissenschaft / Gartenbau Pflanzenbau |
| discipline_str_mv | Biologie Agrarwissenschaft Agrar-/Forst-/Ernährungs-/Haushaltswissenschaft / Gartenbau Pflanzenbau |
| edition | 2. ed. |
| format | Book |
| fullrecord | <?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>02086nam a2200541 c 4500</leader><controlfield tag="001">BV021626311</controlfield><controlfield tag="003">DE-604</controlfield><controlfield tag="005">20070917 </controlfield><controlfield tag="007">t</controlfield><controlfield tag="008">060622s2008 d||| |||| 00||| eng d</controlfield><datafield tag="020" ind1=" " ind2=" "><subfield code="a">9780849398674</subfield><subfield code="9">978-0-8493-9867-4</subfield></datafield><datafield tag="020" ind1=" " ind2=" "><subfield code="a">0849398673</subfield><subfield code="9">0-8493-9867-3</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(OCoLC)255959352</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)BVBBV021626311</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-604</subfield><subfield code="b">ger</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1="0" ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="049" ind1=" " ind2=" "><subfield code="a">DE-M49</subfield><subfield code="a">DE-1029</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">SB733</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">632.4</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">WN 9350</subfield><subfield code="0">(DE-625)151120:</subfield><subfield code="2">rvk</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">23</subfield><subfield code="2">ssgn</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">LAN 244f</subfield><subfield code="2">stub</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Vidhyasekaran, P.</subfield><subfield code="e">Verfasser</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Fungal pathogenesis in plants and crops</subfield><subfield code="b">molecular biology and host defense mechanisms</subfield><subfield code="c">P. Vidhyasekaran</subfield></datafield><datafield tag="250" ind1=" " ind2=" "><subfield code="a">2. ed.</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Boca Raton, Fla. [u.a.]</subfield><subfield code="b">CRC Press</subfield><subfield code="c">2008</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">XXIII, 509 S.</subfield><subfield code="b">graph. Darst.</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="b">n</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="b">nc</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="490" ind1="0" ind2=" "><subfield code="a">Books in soils, plants, and the environment</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Fungal diseases of plants</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Plant molecular biology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Plant-pathogen relationships</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Plants</subfield><subfield code="x">Disease and pest resistance</subfield><subfield code="x">Molecular aspects</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Wirtspflanzen</subfield><subfield code="0">(DE-588)4444525-8</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Phytopathogene Pilze</subfield><subfield code="0">(DE-588)4045992-5</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Pathogenese</subfield><subfield code="0">(DE-588)4115512-9</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Abwehrreaktion</subfield><subfield code="0">(DE-588)4416206-6</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="689" ind1="0" ind2="0"><subfield code="a">Phytopathogene Pilze</subfield><subfield code="0">(DE-588)4045992-5</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="0" ind2="1"><subfield code="a">Pathogenese</subfield><subfield code="0">(DE-588)4115512-9</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="0" ind2=" "><subfield code="5">DE-604</subfield></datafield><datafield tag="689" ind1="1" ind2="0"><subfield code="a">Phytopathogene Pilze</subfield><subfield code="0">(DE-588)4045992-5</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="1" ind2="1"><subfield code="a">Wirtspflanzen</subfield><subfield code="0">(DE-588)4444525-8</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="1" ind2="2"><subfield code="a">Abwehrreaktion</subfield><subfield code="0">(DE-588)4416206-6</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="1" ind2=" "><subfield code="5">DE-604</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="m">OEBV Datenaustausch</subfield><subfield code="q">application/pdf</subfield><subfield code="u">http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=014841284&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA</subfield><subfield code="3">Inhaltsverzeichnis</subfield></datafield><datafield tag="999" ind1=" " ind2=" "><subfield code="a">oai:aleph.bib-bvb.de:BVB01-014841284</subfield></datafield></record></collection> |
| id | DE-604.BV021626311 |
| illustrated | Illustrated |
| index_date | 2024-07-02T14:55:22Z |
| indexdate | 2024-07-09T20:40:14Z |
| institution | BVB |
| isbn | 9780849398674 0849398673 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-014841284 |
| oclc_num | 255959352 |
| open_access_boolean | |
| owner | DE-M49 DE-BY-TUM DE-1029 |
| owner_facet | DE-M49 DE-BY-TUM DE-1029 |
| physical | XXIII, 509 S. graph. Darst. |
| publishDate | 2008 |
| publishDateSearch | 2008 |
| publishDateSort | 2008 |
| publisher | CRC Press |
| record_format | marc |
| series2 | Books in soils, plants, and the environment |
| spelling | Vidhyasekaran, P. Verfasser aut Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms P. Vidhyasekaran 2. ed. Boca Raton, Fla. [u.a.] CRC Press 2008 XXIII, 509 S. graph. Darst. txt rdacontent n rdamedia nc rdacarrier Books in soils, plants, and the environment Fungal diseases of plants Plant molecular biology Plant-pathogen relationships Plants Disease and pest resistance Molecular aspects Wirtspflanzen (DE-588)4444525-8 gnd rswk-swf Phytopathogene Pilze (DE-588)4045992-5 gnd rswk-swf Pathogenese (DE-588)4115512-9 gnd rswk-swf Abwehrreaktion (DE-588)4416206-6 gnd rswk-swf Phytopathogene Pilze (DE-588)4045992-5 s Pathogenese (DE-588)4115512-9 s DE-604 Wirtspflanzen (DE-588)4444525-8 s Abwehrreaktion (DE-588)4416206-6 s OEBV Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=014841284&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Vidhyasekaran, P. Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms Fungal diseases of plants Plant molecular biology Plant-pathogen relationships Plants Disease and pest resistance Molecular aspects Wirtspflanzen (DE-588)4444525-8 gnd Phytopathogene Pilze (DE-588)4045992-5 gnd Pathogenese (DE-588)4115512-9 gnd Abwehrreaktion (DE-588)4416206-6 gnd |
| subject_GND | (DE-588)4444525-8 (DE-588)4045992-5 (DE-588)4115512-9 (DE-588)4416206-6 |
| title | Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms |
| title_auth | Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms |
| title_exact_search | Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms |
| title_exact_search_txtP | Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms |
| title_full | Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms P. Vidhyasekaran |
| title_fullStr | Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms P. Vidhyasekaran |
| title_full_unstemmed | Fungal pathogenesis in plants and crops molecular biology and host defense mechanisms P. Vidhyasekaran |
| title_short | Fungal pathogenesis in plants and crops |
| title_sort | fungal pathogenesis in plants and crops molecular biology and host defense mechanisms |
| title_sub | molecular biology and host defense mechanisms |
| topic | Fungal diseases of plants Plant molecular biology Plant-pathogen relationships Plants Disease and pest resistance Molecular aspects Wirtspflanzen (DE-588)4444525-8 gnd Phytopathogene Pilze (DE-588)4045992-5 gnd Pathogenese (DE-588)4115512-9 gnd Abwehrreaktion (DE-588)4416206-6 gnd |
| topic_facet | Fungal diseases of plants Plant molecular biology Plant-pathogen relationships Plants Disease and pest resistance Molecular aspects Wirtspflanzen Phytopathogene Pilze Pathogenese Abwehrreaktion |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=014841284&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
| work_keys_str_mv | AT vidhyasekaranp fungalpathogenesisinplantsandcropsmolecularbiologyandhostdefensemechanisms |