Table of Contents
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Table of Content
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PREFACE
FOREWORD
DEDICATION
ACKNOWLEDGEMENTS
Introduction
Plant Pathogens and Plant Pests
Abstract
INTRODUCTION
1. Subcellular pathogens
1.1. Viruses
1.2. Viroids
2. Cellular pathogens
2.1. Mycoplasmas (also called Mollicutes)
a. Phytoplasmas
b. Spiroplasmas
2.2. Bacteria
2.3. Fungi
2.4. Oomycetes
2.5. Nematodes
2.6. Parasitic Plants
3. Arthropods
3.1. Insects
3.2. Mites
4. THE CONCEPT OF HOST RANGE
CONCLUSION
Plant Diseases
Abstract
INTRODUCTION
1. DEFINITION OF A PLANT DISEASE
2. CLASSIFICATION OF PLANT DISEASES
2.1. Parasitic (Biotic) Diseases
2.2. Noninfectious (Abiotic) Diseases
3. ECONOMIC IMPACT OF PLANT DISEASES
3.1. Quantitative Effect on Production
3.2. Effect on Product Quality
4. DIAGNOSIS AND IDENTIFICATION OF DISEASES
4.1. Diagnosis Based on Symptoms, Landscape, and Agricultural History
a. Symptoms
b. The Agricultural Landscape and History
4.2. Detection and Identification of Pathogens
a. Methods Based on Morphological Observations
b. Methods Based on Biochemical Markers
c. Serological/Immunological-Based Detection Systems
d. Methods Based on Molecular Markers
5. MOLECULAR HOST-PATHOGEN DIALOGUE
5.1. Compatible Reaction
5.2. Incompatible Reaction
a. Non-Host Resistance 5
b. Horizontal Resistance6
c. Vertical Resistance7
6. METHODS OF CONTROLLING PATHOGENS AND PESTS
6.1. Phytosanitary Regulations
6.2. Control by Cultural Practices
6.3. Chemical Control
6.4. Physical Control
6.5. Biological Control
a. The Strategy of Antagonistic Organisms
b. The Strategy of Secondary Plants
6.6. Genetic Resistance
6.7. Integrated Pest Management (IPM)
CONCLUSION
Plant Immunity: An Overview
Abstract
INTRODUCTION
1. COEVOLUTION OF PLANT DEFENSE AND PATHOGEN ATTACK MECHANISMS: THE ZIGZAG MODEL
2. COMPONENTS OF PLANT IMMUNITY
2.1. Innate Immunity
2.2. Acquired Resistance
2.3. Host Versus Nonhost Resistance
a. Nonhost Resistance
b. Host Resistance
3. CONCEPTS OF AVOIDANCE, RESISTANCE AND TOLERANCE
4. COMPARISON BETWEEN IMMUNE SYSTEMS IN PLANTS AND ANIMALS
a. Non-specific Immunity (Plants vs. Animals)
b. Specific Immunity (Plants vs. Animals)
c. Immune Memory (Plants vs. animals)
d. Programmed Cell Death (apoptosis) (Plants vs. animals)
CONCLUSION
Passive Defenses
Abstract
INTRODUCTION
1. PRE-EXISTING MECHANICAL DEFENSES
2. PRE-EXISTING BIOCHIMICAL DEFENSES
2.1. Phenolic Compounds
2.2. Terpenoids
2.3. Alkaloids
2.4. Phytoanticipins
2.5. Nutrient Deprivation
CONCLUSION
Basal or Nonspecific Plant Defense
Abstract
INTRODUCTION
1. PASSIVE (CONSTITUTIVE) DEFENSES
2. ACTIVE (INDUCIBLE) DEFENSES
2.1. Development of the Concept of PAMP from that of Elicitors
2.2. Generic and Conserved Nature of PAMPs
2.3. Pattern Recognition Receptors (PRRs)
2.4. Popular Models of PTI in Plants
2.4.1. Flagellin-Induced Resistance
a. Conservation, Diversity, Evolution
b. Downstream Signaling Cascade
2.4.2. Elongation Factor (Ef-Tu)-Induced Basal Resistance
3. HETEROLOGOUS EXPRESSION OF PRR GENES
CONCLUSION
Pathogen Race-Specific Resistance
Abstract
INTRODUCTION
1. THE FLOR MODEL
2. PATHOGEN EFFECTORS
3. PLANT RESISTANCE (R) GENES
4. ELEMENTS OF DIFFERENTIATION BETWEEN PTI AND ETI
CONCLUSION
Acquired Resistance and Elicitors of Natural Plant Defense Mechanisms
Abstract
INTRODUCTION
1. ACQUIRED RESISTANCE
1.1. Systemic Acquired Resistance (SAR)
1.2. Induced Systemic Resistance (ISR)
1.3. Metabolic Changes Associated with Induced Resistance
2. ELICITORS OF NATURAL PLANT DEFENSE MECHANISMS. CAN PLANTS BE IMMUNIZED?
2.1. Definition of an NDS
2.2. Advantages and Disadvantages of Using NDSs
CONCLUSION
Quantitative Resistance
Abstract
INTRODUCTION
1. MOLECULAR MECHANISMS ASSOCIATED WITH QUANTITATIVE IMMUNITY
2. BREEDING FOR QUANTITATIVE RESISTANCE
3. SPECIFICITY OF QTLS
4. RELATIONSHIP BETWEEN GENES, PROTEINS, METABOLITES AND QTL
5. MOLECULAR MARKERS ASSOCIATED WITH QTLS
6. DURABILITY OF QUANTITATIVE RESISTANCES
CONCLUSION
Molecular Models of Specific Host-Pathogen Recognition
Abstract
INTRODUCTION
1. « RECEPTOR – LIGAND » MODEL
2. The « GUARD » MODEL
3. THE « DECOY » MODEL
4. INTEGRATED DECOY MODEL (NLR-ID MODEL)
4.1. A Remarkable Diversity of Non-Canonical Integrated Sequences in NLRs
4.2. Elucidation of the Function of NLR-IDs
5. Sensor NLRs (sNLRs) and Helper NLRs (hNLRs)
CONCLUSION
PRRs and WAKs: PAMPs and DAMPs Detectors
Abstract
INTRODUCTION
1. PATTERN-RECOGNITION RECEPTORS (PRRs)
1.1. An Overview: Nature of PAMPs and Biochemical Structure of PRRs
1.2. Best Known Examples of Bacterial and Fungal PAMPs and their Cognate Pattern Recognition Receptors
1.3. Focus on FLS2-flg22 Interaction
2. A PARTICULAR PRR CLASS: WALL-ASSOCIATED KINASES (WAKS), DAMPS RECEPTORS
2.1. Nature of DAMPs
2.2. Example of OGs – WAK1 interaction
3. PLANT LECTIN RECEPTORS
CONCLUSION
NLRs: Detectors of Pathogen Effectors
Abstract
INTRODUCTION
1. THE MAIN STRUCTURAL DOMAINS OF NBS-LRR PROTEINS
1.1. The C-terminal Region
1.1.1. Leucine-Rich Repeats (LRR) Domain
1.1.2. Other Domains of the C-Terminal Region
1.2. The Central NOD Region
1.3. N-Terminal Region
1.3.1. TIR (Toll Interleukin Receptor) Domain
1.3.2. Coiled-Coil (CC) Domain
1.3.3. Other Domains of the N-terminal Region
2. GENOMIC ORGANIZATION OF NBS-LRR LOCI
2.1. Simple Locus Organized in Allelic Series
2.2. Complex Clusters of Homologous Resistance Genes
2.3. Complex Clusters of non Homologous Resistance Genes
3. EVOLUTION OF THE NBS-LRR GENE FAMILY
3.1. The Crucial Role of Duplication in the Evolution of R Genes
3.2. Diversification of Resistance Genes by Transposable Elements
CONCLUSION
Molecular Classification of Plant Resistance Genes
Abstract
INTRODUCTION
1. WHY STUDY R GENES?
2. CLASSES OF PLANT DISEASE RESISTANCE GENES BASED ON STRUCTURAL FEATURES
2.1. The Two Classes of Coiled Coil-Nucleotide Binding Site-Leucine Rich Repeat (CNL) and Toll-Interleukin Receptor-Nucleotide Binding Site-Leucine Rich Repeat (TNL)
2.2. The two classes of Receptor-Like Protein (RLP) and Receptor-Like Kinase (RLK)4
2.3. Superclass of Oth-R-Genes
a. Example of Genes Encoding Toxin Reductases
b. Example of Genes Encoding Proteins With CC Domain and a Transmembrane Domain
c. Example of Genes Encoding a Cytoplasmic Protein Kinase
3. CELLULAR LOCALIZATION OF RESISTANCE PROTEINS
4. POSITIONAL CLONING OF PLANT RESISTANCE (R) GENES
CONCLUSION
Strategies and Mechanisms for Plant Resistance Protein Function
Abstract
INTRODUCTION
1. STRATEGY (1): PERCEPTION
1.1. Mode (1.1): Extracellular Perception
a. Mechanism 1: Direct Extracellular Perception
b. Mechanism 2: Indirect Extracellular Perception
1.2. Mode (1.2): Intracellular Perception
c. Mechanism 3: Direct Intracellular Recognition
d. Mechanism 4: Indirect Intracellular Recognition
e. Mechanism 5: NLR-IDs
1.3. Mode (1.3)
f. Mechanism 6: Executor Genes
2. STRATEGY (2): LOSS OF SUSCEPTIBILITY
g. Mechanism 7: Active Loss of Susceptibility
h. Mechanism 8: Passive Loss of Susceptibility due to mutation in a host component targeted by the pathogen
i. Mechanism 9: Passive Loss of Susceptibility by Host Reprogramming
CONCLUSION
Signal Transduction Pathways Activated During Plant Resistance to Pathogens
Abstract
INTRODUCTION
1. PHYTOHORMONE SIGNALING
1.1. Salicylic Acid (SA)
1.2. Jasmonic Acid (JA) and Ethylene
2. CALCIUM SIGNALING
3. MAPK cascades
4. The Oxydative Burst
5. MAIN PATHWAYS TRIGGERED DURING RESISTANCE TO BACTERIA
6. MAIN PATHWAYS TRIGGERED DURING RESISTANCE TO BIOTROPHIC FUNGI
7. MAIN PATHWAYS TRIGGERED DURING RESISTANCE TO NECROTROPHIC FUNGI
8. SIGNALING CROSSTALK BETWEEN PLANT ABIOTIC AND BIOTIC STRESS RESPONSES
CONCLUSION
Transcriptional Reprogramming in Plant Defense
Abstract
INTRODUCTION
1. MAJOR TRANSCRIPTION FACTOR FAMILIES ACTIVE IN PLANT IMMUNITY
1.1. WRKY Transcription Factors
1.2. NAC Transcription Factors
1.3. MYB Transcription Factors
1.4. AP2 / EREBP Transcription Factors
1.5. bZIP Transcription Factors
1.6. NPR1 Transcription Factors
2. REGULATION OF TRANSCRIPTIONAL COMPLEXES
2.1. Direct Regulation of Transcriptional Complexes by Transcription Factors
2.2. Regulation of Transcriptional Complexes by MAPK Cascades
2.3. Regulation of Transcriptional Complexes by Ca2+ signaling
CONCLUSION
Insights into the Role of Epigenetics in Controlling Disease Resistance in Plants
Abstract
INTRODUCTION
1. DNA METHYLATION
1.1. Reduced DNA Methylation and Defense-Related Genes Priming
1.2. Plant Methylation Changes During Pathogen Infection
1.3. Transgenerational Epigenetically Acquired Resistance
2. TRANSPOSABLE ELEMENTS
3. ROLE OF NON-CODING RNAS IN EPIGENETIC CONTROL
CONCLUSION
Plant Defense Gene Expression and Physiological Response
Abstract
INTRODUCTION
1. HYPERSENSIBLE RESPONSE (HR)
2. ENZYMES AND ENZYME INHIBITORS
3. DEFENSINS
4. PHYTOALEXINS
5. PATHOGENESIS-RELATED PROTEINS (PRs)
CONCLUSION
Contribution of Genomics to the Study of Resistance in Cultivated Plants
Abstract
INTRODUCTION
1. PLANT GENOMIC RESEARCH
2. FROM PLANT GENOMES TO PLANT PHENOTYPES: THE ANNOTATION OF PLANT GENOMES AS A FIRST STEP INTO THE IMPROVEMENT OF PLANTS FOR RESISTANCE TO BIOTIC STRESSES
3. GENOME-WIDE IDENTIFICATION OF R GENE ANALOGS (RGAS) FROM PLANT SPECIES
4. TARGETING INDUCED LOCAL LESIONS IN GENOMES (TILLING)
5. TRANSCRIPTOME ANALYSIS
6. CONTRIBUTION OF GENOME-WIDE ASSOCIATION STUDIES (GWAS) TO THE IMPROVEMENT OF PLANTS FOR RESISTANCE TO BIOTIC STRESSES
CONCLUSION
State of the Art and Perspectives of Genetic Engineering of Plant Resistance to Diseases
Abstract
INTRODUCTION
1. GENETICALLY ENGINEERED CROPS
1.1. Broad-Spectrum Resistance Conferred By PRR and Chimeric PRR Transgenes
1.2. Plant Defensins Transformed into Target Plants
1.3. Plant Protease Inhibitors (PI) Transformed into Target Plants
1.4. Bacterial Harpins (hrp) Genes Transformed into Target Plants
1.5. Bacillus thuringiensis Delta-Endotoxin Genes Transformed into Target Plants
1.6. RNA-Based Antiviral Resistance
2. PLANT GENOME EDITING
2.1. Modifying Host Plant Susceptibility Genes By Site-Directed-Mutagenesis and CRISPR-Cas9
CONCLUSION
Durability of Plant Resistance to Pathogens and Pests
Abstract
INTRODUCTION
1. Mechanisms for overcoming specific resistance
2. ASSOCIATION OF QUANTITATIVE AND QUALITATIVE RESISTANCE IN A SINGLE CULTIVAR
3. R GENE DEPLOYMENT STRATEGIES
3.1. One Gene at a Time
3.2. Gene Rotation
3.3. Gene Pyramids
3.4. Cultivar Mixtures
CONCLUSION
References
An Introduction to Plant Immunity
Authored byDhia Bouktila Higher Institute of Biotechnology of Béja, University of Jendouba (Tunisia) &
Higher Institute of Biotechnology of Monastir, University of Monastir (Tunisia)
&
Yosra HabachiIndependent writer
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PREFACE
The world population is increasing day by day, imposing that agricultural production increases proportionally. Unfortunately, the increase in agricultural production is limited due to abiotic and biotic stresses, which have a negative impact on the growth and development of crops and their yields, resulting in considerable economic loss worldwide. In addition, monoculture, which we are witnessing today in agricultural landscapes, and which represents the workhorse of intensive agriculture, weakens plants enormously, while biodiversity protects them. It should be noted that the economic loss attributable to plant diseases and pests, which is estimated at 10-40% of the production potential worldwide, is already being held back by the massive use of phytosanitary products. Although this use of chemicals helps plants to fight against pathogenic microorganisms, it is not without consequences for the environment.
At the sunrise of this new millennium, mankind has an extraordinary chance to enhance development through the scientific improvement of crops and sustainable management of biodiversity. Indeed, advances in Genetics, Molecular Biology and Genomics have evolved to allow what is now called a high-tech plant breeding. Improvements in plant performance can be manifested, among other things, by tolerance or resistance to abiotic and biotic stresses. It follows all the importance that the acquisition of a deep understanding of the genetic mechanisms governing the response of a plant to its invasion by pathogens and pests currently takes. Plants have their own mechanisms for overcoming stress, and activating complex - and sometimes crossed - signal transduction pathways. In recent years, knowledge of the immunogenetic defense mechanisms of plants has improved considerably.
In this perspective, we wanted this book to be an extensive and up-to-date scientific review of the different aspects of knowledge and technologies related to the field of plant immunity. Our goal is to offer a real modern tool for learning and documenting plant immunity for specialist academicians. We hope that students from all over the world will be able to benefit from this informative resource, while allowing teacher-researchers to use it for their teaching and research activities.
Dhia Bouktila
Higher Institute of Biotechnology of Béja
University of Jendouba (Tunisia) &
Higher Institute of Biotechnology of Monastir
University of Monastir (Tunisia)Yosra Habachi
Independent writer
University of Tunis El Manar
Tunisia
FOREWORD
It has often been said that plants have neither nervous nor immune systems. However, they are able to react to certain stimuli in the environment and to different stresses whether they are biotic or abiotic. They can fight or resist the germs that surround them. In fact, if they do not have an immune system per se, neither dedicated organs nor immune cells, plants have defense mechanisms that can be compared to those of so-called innate immunity in the animal kingdom.
First, they have natural physical (cuticles or spines) or chemical (wax or other compounds) barriers that allow them to prevent or limit infections and control pests. From this point of view, they use the same passive defense strategies as animals (skin, mucous membranes, sweat, sebum, acid secretions).
When pathogens cross these barriers, they encounter active defense mechanisms at the cellular level, with the same molecular systems for the perception of microbial aggressions. These systems involve surface and intracellular receptors PRRs (Pathogen Recognition Receptors) that recognize PAMPs (pathogen-associated molecular patterns) or DAMPs (damage-associated molecular pattern molecules) and trigger signaling pathways aimed at carrying out resistance to infection. Interestingly, these recognition molecules are also described for innate immunity cells in animals. While PRRs identified in plants are primarily, in cell membrane, mammalian receptors can be membrane, cytoplasmic or localized in the endosome membrane. This recognition displays certain specificity and there is a diversity of PRRs recognizing PAMPs, which are conserved patterns, common to different germs and pathogenic microorganisms. Some bacterial PAMPs, such as flagellin (Flg), lipopolysaccharides (LPS) and peptidoglycans (PGN) are recognized in both plants and animals. However, if PRR orthologs in animals do not appear to exist in plants, protein domains such as LRRs (leucine-rich repeats) are conserved between the PRRs of the two kingdoms. For example NOD2 (nucleotide-binding oligomerization domain 2), a cytoplasmic PRR whose mutations are associated with Human Crohn disease, is homologous to resistance R proteins in plants.
Similarities between the two kingdoms are also observed in reaction processes including signaling and immune responses. In animals and plants, the perception of PAMPs and DAMPs induces a signaling cascade that leads to the activation of transcription factors and results in the transcription of defense genes. Signal transduction in plants and mammals also involves altering ion flow through membranes, especially Ca2+, as well as producing ROS (reactive oxygen species) or NO (nitrogen monoxide). All of these second messengers also contribute to the expression of a defense transcriptome.
In both cases, pathogen-activated cells have a reprogrammed transcription profile associated with transcription factors (TFs) induced via the signaling pathways. These TFs regulate key genes of the protective response. In plants, the target genes, encode in particular, enzymes involved in the synthesis of phytohormones that amplify the immune response and warn neighbouring cells. This is to be compared with what is observed in animal models in which the recognition of PAMPs by TLRs, for example, leads to transduction pathways regulating the expression of genes encoding mediators of inflammation (e.g. cytokines and chemokines) that allow the recruitment of specialized defense cells. Moreover, plants and animals synthesize antimicrobial compounds, some of which are common to both kingdoms, such as those of the defensin and thionin family.
In some cases, plant immunity can lead to programmed cell death, called hypersensitive response, which helps to limit the spread of microorganisms. It results in the appearance of localized necrotic lesions at the sites of infection. The mechanisms leading to this cell death can be compared in some ways to the apoptosis or pyroptosis that is observed in animals. Several events of programmed cell death are indeed similar between the two kingdoms.
The adaptation of pathogens to their host is essentially manifested by bypassing the host’s immunity. Microbes that infect animals use a variety of escape strategies to reduce the host’s defenses and infect them. As in animals, pathogens that infect plants are able to manipulate the cellular functions of their host through effectors (proteins, toxins, etc.), thus facilitating their spread. These effectors largely target the cellular signaling pathways that lead to the immune response but also those that induce the opening of the stomata.
Another aspect known for several years in plants is cross-protection. This aspect has been described, in the last decade, in vertebrates and explained by a mechanism known as innate memory or trained immunity. Indeed, it is now accepted that activated innate immunity cells can be maintained in their state of activation for several months with a reprogramming of the transcriptional profile determined, not only by transcription factors, but also by epigenetic changes in DNA and histones methylation profiles, as well as in microRNA expression. Thus, the cells of innate immunity induced into memory cells will persist under an activation state for several months during which they will be more receptive and respond to other infections more effectively. Hence is explained the non-specific cross-protection that can be observed in animals and also in plants where epigenetic change associated to immune response are documented.
Thus, plants use defense strategies against biotic aggressions, which are very similar to those of vertebrates. Knowledge of the mechanisms of innate animal immunity could, therefore, guide research to a better understanding of the defense pathways induced by PAMPs and DAMPs in plants. At a time when agro-ecological concerns are guiding us towards reducing inputs in agriculture, this knowledge will lead to the development of new biocontrol strategies based on stimulating the natural defenses of plants.
This book is a basic document for those who want to understand and deepen their knowledge of immunity in plants. All aspects are dealt with in a gradual and clear way, including the basic concepts, and the subject is treated from its multiple facets: microbiological, phytopathological, cellular, biochemical, genetic, evolutionary, biotechnological and agronomic.
Amel Benammar Elgaaïed
Tunisian Academy of Sciences
Tunisia
DEDICATION
To my wife, Rafika, and my kids, May and Marwen: Your support made all of this possible,
To my parents for always loving and supporting me,
To my dear friend and coauthor, Yosra Habachi,
To every student I have taught or advised once in my carreer,
A special dedication to dear friends, Dr. Chokri Belaid, Dr. Anwar Mechri, Dr. Khaled Chatti, Dr. Lotfi Cherni and Dr. Salim Lebbal.
Dhia Bouktila
To my husband, Sami, for his irreplaceable support and his unconditional love.
To my little angels: Seif Allah and Chahed, as a testimony to the attachment, love and affection I have for them.
To my dear friend Dhia Bouktila,
To Dr. Abdelfatteh Zeddini, Head of Laboratory of Pathological Anatomy and Cytology, for his kindness and support.
ACKNOWLEDGEMENTS
Dhia Bouktila,Yosra HabachiThis work was facilitated by a one academic year teaching leave awarded to Dhia Bouktila, Associate Professor at the Higher Institute of Biotechnology of Beja, in order to focus on completing the writing of this book and achieving this publication. For this, the authors thank the Scientific Council of the Higher Institute of Biotechnology of Beja, the University of Jendouba Council, as well as the Tunisian Ministry of Higher Education and Scientific Research.
The authors want to thank everyone who helped them create this book, especially the students Jihen Hamdi for her valuable help in the preparation of chapters 8 and 14, and Narjess Kmeli and Inchirah Bettaieb for their help in formatting bibliographical entries. Special thanks goes to our editor, Bentham Science Publishers who welcomed us into this publishing experience and assisted us with great professionalism.
The authors disclose receipt of the following financial support for the authorship and publication of this book. This work was supported by the Tunisian Association of Psycho-Neuro-Endocrino-Immunology (Association Tunisienne de Psycho-Neuro-Endocrino-Imm unologie) [grant number 2-2020].
CONSENT FOR PUBLICATION
Not applicable.
CONFLICT OF INTEREST
The authors declare no conflict of interest, financial or otherwise.
Introduction
Dhia Bouktila,Yosra HabachiThe survival of most organisms under various environmental conditions depends on the presence of general immune mechanisms, governed by an integrated genetic system. Plants, despite their immobility, have developed various sophisticated and effective mechanisms to recognize and combat pathogens during their attacks. Plant immunity is defined as the ability of plants to contain the damaging effect of a pathogen or pest. Plants contain the genetic information necessary to defend themselves from attack by a multitude of plant pathogens and pests such as viruses, bacteria, insects, nematodes, fungi and oomycetes. This defense can operate at different levels, using either preexisting passive defense systems (cuticle, wax, thorns, chemical compounds, etc.), or active defense systems appearing after the perception of aggression. In most cases, the first line of defense is sufficient to repel the pathogen, but sometimes the constitutive barriers are not sufficient and the second, active, line of resistance will be required.
Cell wall penetration introduces microbes to the plant plasma membrane where they will be confronted with extracellular surface receptors that detect pathogen-associated molecular patterns (PAMPs). This detection of microbes on the cells surface sets up PAMP-triggered immunity (PTI), which hopefully prevents the infection well before the pathogen begins to spread in the plant. That being said, pathogens have evolved strategies to disrupt PTI by secreting specific proteins, called effectors, in the cytosol of plant cells, which affect the efficacy of primary resistance (PTI). Once pathogens have gained the potential to eliminate primary defenses, plants, on the other hand, will establish a more advanced framework for the detection of microbes, termed effector-triggered immunity (ETI). In the scenario of ETI, the products of major resistance (R) genes, normally intracellular receptors, perceive the associated effector molecules released by the pathogen inside the host cell. Interplay between effectors and intracellular receptors activates a dynamic signaling network to gain disease resistance (McDowell and Dangl 2000). In fact, plant disease resistance conferred by R genes is usually supported by an oxidative burst, which is a rapid generation of significant amounts of reactive oxygen species (ROS). This ROS output is necessary for
another component of the resistance process, called hypersensitive response (HR), a form of programmed cell death that is assumed to restrict pathogen access to the plant.
Finally, at the molecular level, the plant coordinates the transcription of a variety of genes whose sole objective is resistance. The success of the plant depends on the intensity and speed of the perception of the pathogen signals and their transmission in it to produce an effective response against the pathogen. In Arabidopsis, the identification of pathogen-responsive genes is the subject of numerous studies. It has been found that no less than 25% of the genes identified in this model plant species have a transcriptional level affected following the attack of a pathogenic agent. In this way, a deeper knowledge of the basic processes involved in defense responses would make it easier to interpret the interactions between plants and pathogens and allow better resistance of plants, especially in species of agronomic interest.
The relationship between a plant and a harmful organism (i.e. pathogen or pest) depends on the environmental conditions, the properties of the harmful organism and the plant’s ability to defend itself. The concomitant evolution at the genetic level, including the plant and its pathogenic organism, is a coevolutionary process, which means a specific reciprocal interaction, between the plant and the pathogen. It obviously follows that a large part of the diversity of the living world comes from this coevolution between plants and pathogens, which seems to be an interminable arms race: a species induces a behavioral response to selection pressure imposed by another antagonistic species and the latter changes its behavior in response to the change in the first species. In all coevolutionary systems, the two partner species seek to stabilize with a balanced genetic structure. However, the structure of the genomes of any living organism is constantly modified according to the evolutionary race, via, both, small (point mutations) or large-scale (whole-genome duplications) events.
When a pathogen colonizes a plant, or a pest chooses it as a food resource, this will exert a selection pressure on the plant, thus reducing its fitness. The plant will react in two ways, either it definitively eliminates the aggressor; it is, in this case, a resistant plant, or it accepts the invasion by activating a compensation process; it is, in this case, a tolerant plant. Thus, in-depth knowledge of the genetic defense mechanisms involving resistance genes against biotic stress in plants is a prerequisite for the implementation of management programs and effective control, taking into account of the concomitant evolution of the two protagonists involved.
Contrary to popular belief, the first study linking the development of a disease to a microorganism was not carried out by Robert Koch on the tuberculosis Bacillus in 1890. Instead, at the beginning of the 19th century, the cause of wheat decay was identified by the Swiss Isaac-Bénédict Prévost (1755-1819). This researcher analyzed the cycle of the microscopic parasite responsible for this disease, and developed a mixture capable of eradicating it. However, this work was forgotten because of the preference, in official scientific circles, for the theory of spontaneous generation1. In 1861, the German Anton de Bary, considered as the father of phytopathology, did the same by proving that the terrible epidemic of potato late blight responsible for the great famine of Ireland of the 19th century was caused by the filamentous pathogen Phytophtora infestans (Matta 2010). More recently, the fungus Helminthosporium oryzae was the cause of one of the most significant famines of the 20th century. In 1943, the destruction of rice crops by this fungus was responsible for the deaths of three million people in Bengal (Padmanabhan 1973). The practice of intensive farming since the late 1970s encouraged the development of epidemics. Indeed, monoculture on very large plots and the shortening of crop rotations have led to a loss of diversity in cultivated plants, which are no longer able to resist pathogenic agents on a long-term basis (Ricci et al. 2011). Control of phytopathogenic agents is, therefore, a major issue to ensure food security for populations.
To limit the damage caused by pathogens in agrosystems, humans have developed various control methods. First of all, cultural practices make it possible to limit the quantities of inoculum, by crop rotation and the burial of residues. Chemical control has also been widely used since the start of the 20th century and has significantly increased yields (Hirooka and Ishii 2013). Chemical treatments of crops effectively fight against phytophagous insects and fungal diseases. However, their possible impact on the environment is a real source of concern. In addition, as it is the case in animals and humans, chemical treatments are powerless against viral plant diseases, except in the rare cases where they attack the organisms that vector them, insects, nematodes or fungi. It is therefore necessary to develop alternative strategies to chemical control, against viruses. Finally, genetic selection is based on the use of cultivar resistance to fight against pathogens.
Two types of cultivar resistance are differentiated. Quantitative resistance is controlled by a large number of genes (polygenic resistance) associated with genome portions called Quantitative Trait Loci (QTLs) that contribute to the expression of resistance. It most often gives the plant partial resistance to a pathogen because the defenses of the plant do not completely prevent the invasion of the disease. It is therefore not blocked but only slowed down in its progression, which causes some visible damage to the plants. On the other hand, qualitative resistance is controlled by one or a few genes called R genes (mono- or oligogenic control). It most often gives the plant complete resistance to a pathogenic agent. The latter is blocked from the early stages of infection and does not cause damage. This resistance is often associated with symptoms of hypersensitivity (HR) and triggered by molecules manipulating the structure or cellular functions of the host, called effectors or virulence factors (Greenberg and Yao 2004).
In this context, the genetic dissection of quantitative resistance to diseases, a priori more durable than monogenic resistance, has progressed considerably over the past fifteen years with the development of molecular tools and genomics. However, even if numerous studies on quantitative resistance in various pathosystems have made it possible to identify QTLs of resistance, their exploitation in cultivar breeding remains difficult because of the complexity of genetic determinisms and the instability of their effects, partly due to their interactions with the genetic background.
1 Theory stating that life may arise from nonliving matter.
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