Regulation of pathogen-inducible volatile compounds in Arabidopsis and their role in plant defense [Elektronische Ressource] / vorgelegt von Elham Attaran

Thomas Carlyle

Informations

• Publié par: julius-maximilians-universitat_wurzburg
• Publié le: 01 janvier 2010
• Nombre de lectures: 8
• Langue: English
• Poids de l'ouvrage: 2 Mo

Extrait

Regulation of pathogen-inducible volatile
compounds in Arabidopsis and their role in
plant defense




Dissertation zur Erlangung des
naturwissenschaftlichen Doktorgrades
der Julius-Maximilians-Universität Würzburg






vorgelegt von

Elham Attaran

aus dem Iran




Würzburg 2010







Eingereicht am: .............................................




Mitglieder der Promotionskommission:


Vorsitzender: .............................................

Gutachter 1: PD Dr. Jürgen Zeier

Gutachter 2: Prof. Dr. Werner Kaiser




Tag des Promotionskolloquiums: .............................................



Doktorurkunde ausgehändigt am: .............................................




















This thesis is dedicated to my wonderful parents
And my always supportive brother





Acknowledments
First and foremost, I would like to express my deep and sincere gratitude to
my supervisor PD. Dr. Jürgen Zeier for giving me the opportunity to work in
his lab and I will be forever grateful for the guidance, ideas, encouragement;
his excellent supervision over these years have been invaluable.
I highly appreciate Prof Dr. Werner Kaiser for his support during my work in
Würzburg.
I wish to express my gratitude to the head of our department Prof. Dr.
Markus Riederer.
I would like to thank Dr. Tatiana Zeier (Mishina) and Mr.Thomas Griebel as
my colleagues for helpful assistance and contributing to the friendly
atmosphere in our laboratory where make there a nice place to work in.
I wish to extend my warmest thanks to my colleagues in the Department of
Botany II and the Julius-von-Sachs-Institute supporting me during my work.
I am very grateful to German Academic Exchange Service (DAAD) and the
DFG (Graduiertenkolleg 1342) for financial support.
Finally, I owe special gratitude to my family for continuous and unconditional
support: To my parents for the interest they showed in my studies and the
motivation they gave me during those tiring times. Also, to my brother whose
help and encourgenemt is always helping me. I would like to dedicate my
thesis to my family. List of Abbreviations
Avr Avirulence
BSMT1 BENZOIC ACID/SALICYLIC ACID METHYLTRANSFERASE 1
BTH benzo[1,2,3]thiadiazole-7carbothioic acid-S-methyl ester
+2 2+
[Ca ]cyt cytosolic Ca
coi1 coronatine insensitive 1
COR coronatine
dde2 delayed-dehiscence 2
DMNT (E)-4,8-dimethyl-1,3,7-nonatriene
EDS enhanced disease susceptibility
ET ethylene
Flg22 flagellin 22 (22-amino-acid, elicitor-active flagellin peptide)
FLS2 FLAGELLIN-SENSITIVE 2
GLV green leaf volatile
H O hydrogen peroxide 2 2
HR Hypersensitive response
hrc hypersensitive response conserved
hrp hypersensitive response and pathogenicity
ICS1 ISOCHORISMATE SYNTHASE 1
INA 2, 6-dichloroisonicotinic acid
ISR induced systemic resistance
JA jasmonic acid
jar1 jasmonic acid methylester resistant 1
jin1 jasmonate insensitive 1
LPS lipopolysaccharide
LRR leucine-rich repeat
MAPK mitogen-activated protein kinase
MeSA methyl salicylate NADPH nicotinamide adenine dinucleotide phosphate
NB-LRR nucleotide binding, leucine-rich repeat
NPR non-expressor of pathogenesis-related genes
NO nitric oxide
NDR nonrace-specific disease resistance
-
O superoxide 2
OPDA 12-oxophytodienoic acid
OPR3 OPDA-reductase 3
PAD phytoalexin-deficient
PAMP pathogen-associated molecular pattern
PR pathogenesis-related
PRR pattern recognition receptor
PCR polymerase chain reaction
ROS reactive oxygen species
SA salicylic acid
SABP SA binding protein
SAG salicylic acid glucoside
SAR systemic acquired resistance
SID SA induction-deficient
T-DNA Transposon-DNA
TIR Toll and interleukin-1 receptor
TMTT (E,E)-4,8,12-trimethyltrideca-1,3,7,11-tetraene
TPS terpene synthase
TTSS type III secretion system
VOC volatile organic compoundTable of Contents

1 INTRODUCTION 1
1.1 PLANT-PATHOGEN INTERACTIONS 1
PHYTOPATHOGENIC BACTERIA 2
1.2 PLANT DEFENCES 3
1.2.1 PREFORMED DEFENSE RESPONSES 3
1.2.2 INDUCED DEFENSE RESPONSES 4
1.2.2.1 PAMP-triggered immunity 4
1.2.2.2 Effector-triggered immunity 8
1.3 DEFENSE SIGNALING 12
1.3.1 SA-DEPENDENT SIGNALING 13
1.3.2 JA/ET-DEPENDENT SIGNALING 16
1.3.3 SYSTEMIC ACQUIRED RESISTANCE 18
1.3.4 INDUCED SYSTEMIC RESISTANCE (ISR) 22
1.4 VOLATILE ORGANIC COMPOUNDS (VOCS) 23
1.5 THE PSEUDOMONAS-ARABIDOPSIS INTERACTION AS A MODEL SYSTEM 27
1.5.1 ARABIDOPSIS THALIANA AS MODEL PLANT 27
1.5.2 PSEUDOMONAS SYRINGAE AS A PATHOGEN FOR ARABIDOPSIS 28
2 AIMS OF THE WORK 31
3 OWN RESEARCH 32
3.1 PSEUDOMONAS SYRINGAE ELICITS EMISSION OF THE TERPENOID (E,E)-4,8,12-
TRIMETHYL-1,3,7,11-TRIDECATETRAENE IN ARABIDOPSIS LEAVES VIA JASMONATE
SIGNALING AND EXPRESSION OF THE TERPENE SYNTHASE TPS4 32
3.2 METHYL SALICYLATE PRODUCTION AND JASMONATE SIGNALING ARE NOT
ESSENTIAL FOR SYSTEMIC ACQUIRED RESISTANCE IN ARABIDOPSIS 51
4 DISCUSSION 73
4.1 TERPENOID PRODUCTION IN THE ARABIDOPSIS-PSEUDOMONAS INTERACTION 73
4.2 REGULATION OF P. SYRINGAE-INDUCED MESA PRODUCTION AND ITS ROLE IN
LOCAL RESISTANCE 78
4.3 SYSTEMIC ACQUIRED RESISTANCE IN ARABIDOPSIS AGAINST P. SYRINGAE 81
5 SUPPLEMENTAL FIGURES 85 6 SUMMARY AND PERSPECTIVES 89
7 SUPPLEMENT 97
LIST OF PUBLICATIONS 97
POSTER PRESENTATIONS 97
7.1 CURRICULUM VITAE 98
8 REFERENCES 99


















1 INTRODUCTION

1.1 Plant-pathogen interactions
Above- and below-ground parts of plants continuously interact with various
microorganisms, including bacteria, fungi, oomycetes, and viruses. Plant-
microbe interactions can be beneficial for the plant. They might positively
affect agricultural productivity and stimulate plant growth or the activation of
natural plant defenses (Smith and Read, 1996). Nevertheless, many
microbes are pathogenic and in principle able to cause disease on the plant.
Plant pathogens can be broadly divided into two categories, such with a
biotrophic and such with a necrotrophic lifestyle. Biotrophs require a living
host to complete their life cycle, whereas necrotrophs kill host tissue and
feed on the remains (Dangl and Jones, 2001; Glazebrook, 2005).
When a pathogen can overcome plant defense, the interaction is compatible
(Jones and Dangl, 2006). However, plant disease is rare, and the majority of
plant species are resistant to the attack of a potential pathogen. To combat
disease, plants are armed with a variety of preformed and inducible
defences. Such a multiple layered defense system is effective enough to
resist to the attack of the majority of pathogens. Many pathogens are not
able to overcome the first defense barriers that prevent colonization of the
plant, and this form of resistance is termed non-host resistance (NHR,
Thordal-Christensen, 2003; Mysore and Ryu, 2004). For instance,
pathogenic microbes must access the plant interior and penetrate preformed
mechanical barriers, such as the cuticle and the plant cell wall. Moreover,
they must be able to detoxify antimicrobial compounds which are
constitutively produced in the plant, so-called phytoanticipins (Agrios, 2005).
Finally, when a pathogen has an avirulence (avr) gene, and a plant host has
the corresponding disease resistance (R ) gene, the plant can react to the
pathogen by activating a battery of defense responses that interfere with its
multiplication and prevent disease.This interaction becomes incompatible,
and this type of resistance is called specific resistance (Kim et al., 2008).
Phytopathogenic Bacteria
In terms of the mode of pathogenesis, phytopathogens can be divided into
three classes: Necrotrophic pathogens such as Pectobacterium
carotovorum (previously Erwinia carotovora) or the fungus Botrytis cinerea
kill host cells as the main strategy for obtaining nutrients, causing host cell
death during early stages of the infection. By contrast, biotrophic
pathogens obtain nutrients from living host cells withough causing host cell
death (Mole et al., 2007; Melotto et al., 2008). Powdery mildews, downy
mildews and rust fungi are known as biotrophic pathogen (Perferct and
Green, 2001). Similarly, hemibiotrophic pathogens have the most
aggressive phase of population increase in the absence of apparent host cell
death. However, at later stages of pathogenesis, host cells die and infected
tissues show extensive necrosis. Pseudomonas syringae, Ralstonia
solanacearum and Xanthomonas campestris pv. campestris are best
described as hemi