Plant Pathogen Resistance Biotechnology E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Wissenschaft und neue Technologien
• Sprache: Englisch

Seitenzahl: 1115

Veröffentlichungsjahr: 2016

Beschreibung

Plant pathogens and diseases are among the most significant challenges to survival that plants face. Disease outbreaks caused by microbial or viral pathogens can decimate crop yields and have severe effects on global food supply. Understanding the molecular mechanisms underlying plant immune response and applying this understanding to develop biotechnological tools to enhance plant defense against pathogens has great potential for moderating the impact of plant disease outbreaks. Plant Pathogen Resistance Biotechnology's main focus is an in depth survey of the biological strategies being used to create transgenic disease resistant plants for sustainable plant resistance Plant Pathogen Resistance Biotechnology is divided into four sections. The first section covers biological mechanisms underpinning disease resistance in plants, while the second highlights case studies of important pathogen-crop groups and then considers why the application of important pathogen-crop groups, transgenic-based strategies designed to selectively target pathogens could benefit crop production. The third section provides information on the status of transgenic crops around the world, and finally the last part explores high-tech alternatives to genetic engineering for developing disease resistant traits in plants. Edited and authored by leaders in the field, Plant Pathogen Resistance Biotechnology will be an invaluable resource to those studying or researching plant biotechnology, plant pathology, plant biology, plant and crop genetics, in addition to crop science.

Leseprobe

Table of Contents

Cover

Title Page

List of Contributors

Foreword

Organisation of the book

References

Acknowledgments

Chapter 1: The Status and Prospects for Biotechnological Approaches for Attaining Sustainable Disease Resistance

1.1 Introduction

1.2 Factors to consider when generating disease-resistant crops

1.3 Opportunities to engineer novel cultivars for disease resistance

1.4 Technical barriers to engineering novel cultivars for disease resistance

1.5 Approaches for identification and selection of genes important for disease resistance

1.6 Promising strategies for engineering disease-resistant crops

1.7 Future directions and issues

References

Part I: Biological Strategies Leading Towards Disease Resistance

Chapter 2: Engineering Barriers to Infection by Undermining Pathogen Effector Function or by Gaining Effector Recognition

2.1 Introduction

2.2 Plant defence and effector function

2.3 Strategies for engineering resistance

2.4 Perspective

References

Chapter 3: Application of Antimicrobial Proteins and Peptides in Developing Disease-Resistant Plants

3.1 Introduction

3.2 Biological role of PR-proteins

3.3 Antimicrobial peptides

3.4 Regulation of PR-protein expression

3.5 Biotechnological application of PR-protein genes in developing improved crop plants

3.6 Future directions

Acknowledgement

References

Chapter 4: Metabolic Engineering of Chemical Defence Pathways in Plant Disease Control

4.1 Introduction

4.2 Present status of metabolic engineering in the control of plant disease

4.3 Metabolic engineering: technical challenges and opportunities

4.4 The outlook for metabolically engineering of disease resistance in crops

References

Chapter 5: Arabinan

5.1 Introduction

5.2 Biosynthesis and modification of arabinan

5.3 Distribution of arabinan in different tissues and during development

5.4 Role of arabinan in plant growth and development

5.5 Roles of arabinan degrading enzymes in virulence of phytopathogenic fungi

5.6 Roles of arabinan in pathogen interactions

5.7 Conclusion

References

Chapter 6: Transcription Factors that Regulate Defence Responses and Their Use in Increasing Disease Resistance

6.1 Introduction

6.2 Transcription factors and plant defence

6.3 AP2/ERF transcription factors

6.4 bZIP transcription factors

6.5 WRKY transcription factors

6.6 MYB transcription factors

6.7 Other transcription factor families

6.8 Can the manipulation of specific transcription factors deliver sustainable disease resistance?

6.9 Have we chosen the right transgenes?

6.10 Have we chosen the right expression strategies?

6.11 What new ideas are there for the future of TF-based crop improvement?

References

Chapter 7: Regulation of Abiotic and Biotic Stress Responses by Plant Hormones

7.1 Introduction

7.2 Regulation of biotic stress responses by plant hormones

7.3 Regulation of abiotic stress responses by plant hormones

7.4 Conclusions and further perspectives

References

Part II: Case Studies for Groups of Pathogens and Important Crops. Why Is It Especially Advantageous to use Transgenic Strategies for these Pathogens or Crops?

Chapter 8: Engineered Resistance to Viruses

8.1 Introduction

8.2 Mitigation of viruses

8.3 Biotechnology and virus resistance

8.4 Success stories

8.5 Challenges of engineering RNAi-mediated resistance

8.6 Benefits of virus-resistant transgenic crops

8.7 Conclusions

References

Chapter 9: Problematic Crops: 1. Potatoes

9.1 Potato late blight resistance breeding advocates GM strategies

9.2 GM strategies for late blight resistance breeding

9.3 Late blight-resistant GM varieties

References

Chapter 10: Problematic Crops: 1. Grape

10.1 Introduction

10.2 Introduction to grapevine pathology

10.3 Approaches for the improvement of grapevine disease resistance

10.4 Pierce's disease of grapevines: a case study

References

Chapter 11: Developing Sustainable Disease Resistance in Coffee

11.1 Introduction

11.2 Agronomic aspects of coffee

11.3 Major threats to coffee plantations

11.4 Breeding for disease resistance and pest management

11.5 Various traits targeted for transgenic coffee development

11.6 Bottlenecks in coffee transgenic development

11.7 GM or hybrid joe: what choices to make?

Acknowledgements

References

Webliographies

Chapter 12: Biotechnological Approaches for Crop Protection

12.1 Introduction

12.2 Plant immunity

12.3 Transgenic approaches to engineer disease resistance in rice plants

12.4 Targeted genome engineering

12.5 Safety issues of genetically engineered rice

12.6 Conclusions and future prospects

Acknowledgement

References

Part III: Status of Transgenic Crops Around the World

Chapter 13: Status of Transgenic Crops in Argentina

13.1 Transgenic crops approved for commercialization in Argentina

13.2 Economic impact derived from transgenic crops cultivation

13.3 Local developments

13.4 Perspectives

References

Chapter 14: The Status of Transgenic Crops in Australia

14.1 Introduction

14.2 Government policies

14.3 Field trials

14.4 Crops deregulated

14.5 Crops grown

14.6 Public sentiment toward GM crops

14.7 Value capture

14.8 What is in the pipeline

14.9 Summary

References

Chapter 15: Transgenic Crops in Spain

15.1 Introduction

15.2 Transgenic crops in Europe

15.3 Transgenic crops in Spain

15.4 Future prospects

Acknowledgements

References

Chapter 16: Biotechnology and Crop Disease Resistance in South Africa

16.1 Genetically modified crops in South Africa

16.2 Economic, social and health benefits of GM crops in South Africa

16.3 Biotechnology initiatives for crop disease control in South Africa

16.4 Future prospects

Acknowledgements

References

Part IV: Implications of Transgenic Technologies for Improved Disease Control

Chapter 17: Exploiting Plant Induced Resistance as a Route to Sustainable Crop Protection

17.1 Introduction

17.2 Examples of elicitors of induced resistance

17.3 Priming of induced resistance

17.4 Drivers and barriers to the adoption of plant activators in agriculture and horticulture

17.5 Conclusions and future prospects

References

Chapter 18: Biological Control Using Microorganisms as an Alternative to Disease Resistance

18.1 Introduction

18.2 Getting the right biocontrol organism

18.3 New approaches for studying the biology of BCAs and biocontrol interactions

18.4 Strategy for using biocontrol in IPM

References

Webliography

Chapter 19: TILLING in Plant Disease Control

19.1 Concepts of forward and reverse genetics

19.2 The TILLING procedure

19.3 Mutagenesis

19.4 DNA preparation and pooling of individuals

19.5 Mutation discovery

19.6 Identification and evaluation of the individual mutant

19.7 Bioinformatics tools

19.8 EcoTILLING

19.9 Modified TILLING approaches

19.10 Application of TILLING and TILLING-related procedures in disease resistance

19.11 Perspectives

References

Chapter 20: Fitness Costs of Pathogen Recognition in Plants and Their Implications for Crop Improvement

20.1 The goal of durable resistance

20.2 New ways of using

R

-genes

20.3 Costs of resistance in crop improvement

20.4 Fitness costs of

R

-gene defences

20.5 Phenotypes of

R

-gene over-expression

20.6 Requirements for

R

-protein function

20.7 Necrotic phenotypes of

R

-gene mutants

20.8 Summary of fitness costs of

R

-gene mutations

20.9

R

-genes in plant breeding

20.10 Biotech innovation and genetic diversity

20.11 Conclusion

Acknowledgement

References

Index

End User License Agreement

List of Tables

Chapter 02

Table 2.1 Effector proteins from selected plant pathogens and parasites with their plant target, R-gene and activities.

Chapter 03

Table 3.1 Application of PR-proteins and peptides for crop improvement. The articles were identified by Pubmed searches for articles from the past 5 years.

Chapter 06

Table 6.1 The major transcription factor families that have members shown to play important roles in the responses to pathogens. Examples are given of where alteration of expression may have effects on defence responses and disease resistance.

Chapter 07

Table 7.1 List of abbreviations.

Table 7.2 The role of hormones in stomatal regulation.

Table 7.3 The role of hormones in abiotic stress responses and associated effect on growth and ROS.

Chapter 08

Table 8.1 Examples of strategies used for engineering virus resistance in major vegetable, fruit and field crops.

Chapter 09

Table 9.1 An overview of cloned late blight resistance genes from the potato germplasm and their recognition spectra.

Chapter 12

Table 12.1 Genes used to improve disease resistance in transgenic rice.

Chapter 13

Table 13.1 Transgenic crops approved for commercialization in Argentina.

Table 13.2 Local developments by crop being evaluated for commercialization in Argentina in the last two years.

Chapter 14

Table 14.1 OGTR licenses issued for crops engineered for improved disease resistance.

Table 14.2 Transgenic crops approved for commercial cultivation.

Table 14.3 Largest 5 crops grown in Australia.

Table 14.4 Transgenic potato engineered for disease resistance.

Chapter 15

Table 15.1 Summary of field trials with GM plants carried out in Spain during last five years.

Chapter 16

Table 16.1 GM events approved for general release in South Africa.

Table 16.2 Breakdown of genetically modified (GM) crops grown in South Africa during 2012.

Chapter 17

Table 17.1 Selected chemical elicitors of plant-induced resistance responses.

Chapter 19

Table 19.1 Description of TILLING resources developed in model and crop plants.

List of Illustrations

Chapter 01

Fig. 1.1 Selected plant pathogen interactions illustrating lifestyle and the effects of specific types of pathogenicity factor. (a) The biotrophic pathogen

Blumeria graminis

f.sp.

tritici

(ascomycete) on wheat (

Triticum aestivum

). Note that the plant tissue is largely green and that there is profuse conidial sporulation as well as chasmothecia (cleistothecia). (b) The necrotrophic pathogen

Botrytis cinerea

on raspberry (

Rubus idaeus

). Note tissue collapse. (c) The hemibiotrophic fungal pathogen

Phoma lingam

on oilseed rape (

Brassica napus

). Note chlorosis in advance of necroses as an effect of the toxins. (d) Hydrolytic enzymes: rotting potato tuber tissue. (e) Hormones:

Agrobacterium tumefaciens

(bacteria) on rose (Rosa cultivar). Note tumours. (f) Effectors:

Blumeria graminis

f.sp.

hordei

on barley (

Hordeum vulgare

). Without effectors, the powdery mildew fungus would not be able to establish infection. Note lack of DAB staining (brown colour, Thordal-Christensen et al., 1997) where penetration has been successful and led to haustorial formation.

Fig. 1.2 Pathogenicity factors and regulation of defence. Biotrophic pathogens produce effectors and often hormones as their main pathogenicity factors. Small amounts of enzymes are also produced, but not toxins. The effectors interfere primarily with defence signalling. Stimulation is marked with a block arrow, inhibition by a “T”. some fungal and oomycete biotrophic pathogens develop haustoria as feeding structures. Necrotrophic and hemibiotrophic pathogens generally produce tissue disrupting enzymes and/or toxins to damage host tissues, often remotely from their position. Effectors are also used. Elicitors are molecules of pathogen origin that the host can recognise via receptors. Some of these are specific to special groups or individual pathogen species, whereas others are widely produced. The latter are termed MAMPS (or PAMPS). Host receptors recognising PAMPS are termed pattern recognition receptors (PRRs). They stimulate signal transduction via other protein kinases such as MAP or calmodulin-dependent protein kinases. Likewise, G-proteins and transcription regulators activate defence using transcription factors. Effectors (

sensu stricto

) are proteins of pathogen origin, which are injected/taken up by the host cell where they interfere with the host transcriptional activation of defences or stimulate a biotrophic interaction to provide nutrients for the host, e.g., by establishing a haustorium. It has been proposed that the term “effector” should be considered synonymous with the term ‘pathogenicity factor’ (Hogenhout et al., 2009). For the purpose of assisting comprehension, we retain the original narrow sense meaning for the term effector, i.e., proteins introduced into the host cell to manipulate host defence or availability of nutrition (Chapter 2). Receptors for MAMP-triggered immunity (MTI - or PTI) can be receptor-like proteins, receptor-line protein kinases or nucleotide-binding site leucine-rich repeat proteins (NBS-LRR). Receptors for Effector-Triggered Immunity (ETI) are NBS-LRR proteins. These are the classic resistance genes. The subset of effectors that are documented to interact either directly or indirectly with described resistance genes are the avirulence gene (Avr) products. Hormones include the classic defence hormones salicylic acid (predominately biotrophic interactions) and jasmonic acid/ ethylene (predominately necrotrophic interactions), but it has been discovered that abscisic acid, cytokinins, brassinosteroids and strigolactones also play important roles in regulating defences and pathogenicity. Hormone levels can be modulated by abiotic stress or by pathogens. Pathogens can make or degrade hormones themselves, but also inhibit or stimulate production or degradation in the host. Hormones modulate host growth and defence mechanisms. Reactive oxygen species (ROS) and ions like Ca

2+

play roles in the stimulation and regulation of defences. Enzymes can be used by pathogens to release nutrients and interfere with signal transduction. Their activity can inadvertently release elicitor active fragments from cell walls.

Chapter 02

Fig. 2.1 Strategies for genetically engineering resistance in crops against pathogens and parasites. Genetically engineered immunity in plants might encompass four core combinative strategies: Firstly, transfer of genes between closely or distantly related species (encoding e.g. PRR receptors, R proteins from ‘effectoromics’, insensitive effector targets) can promptly offer resistance to highly adapted pathogens (1). Secondly, chimeric fusions of genes or their promoters can be used to ‘attach’ new functions to known proteins or to alter their expression in space and time (2). In a third strategy, targeted mutations in known components of signalling and regulatory cascades of plant immunity might confer resistance by re-wiring plant metabolism towards resistance (e.g. protein turnover, hormonal imbalance) or render specific insensitivity to pathogenic effectors and their function (e.g. mutagenesis screening for improved

R

genes) (3). Finally, enhancement of plant resistance can be achieved by aiming at

ex situ

targets, that is, targeting directly the pathogen by means of silencing its genes (e.g. RNAi) or shutting down its metabolism (e.g. production of antimicrobial toxins and inhibitors) (4). Truly durable engineered resistance (inner circle) is depicted here as a resulting combination of two or more of these genetic engineering strategies.

Chapter 04

Fig. 4.1 Chemical structures of plant chemical defence compounds mentioned in the text.

Fig. 4.2 Simplified schematic of phenylpropanoid metabolism. Different branches of the pathway lead to the production of stilbenes, isoflavonoids and anthocyanidins. Key enzymes are indicated: stilbene synthase (STS), chalcone synthase (CHS), isoflavone synthase (IFS), dihydroflavonol 4-reductase (DFR), and flavonoid 3'5'hydroxylase (F3'5'H). (Original artwork by Krijn Rook.)

Fig. 4.3 Simplified schematic of the biosynthesis of triterpenes.

Chapter 05

Fig. 5.1 A schematic overview of the primary plant cell wall. Individual changes of cellulose form bundles via hydrogen bonding resulting in highly insoluble microfibrilis which intervene with hemicelluloses creating a strengthening network that is embedded by pectic polymers (Cosgrove, 2005). To penetrate the cell wall and break down the polysaccharides, one strategy used by invading pathogens is to release a cocktail of cell wall degrading enzymes such as glucanases, polygalacturonase (PG), pectin lyase (PL), pectin methyl esterase (PME), pectin acetylesterases (PAEs) and arabinanase (Hematy et al., 2009). Glucanases break down the 1,4-beta-D-glucosidic linkage found in the backbone of cellulose and hemicellulose. PG and PL break the α(1,4) linked galacturonic acid residues by hydrolysis and elimination respectively (Blanco et al., 1999). PME cleave methyl groups of the galacturonic acid residues, thereby making the pectin more accessible for PG, abinanases break down the arabinan side chain of RGII (Cantu et al., 2008; Senechal et al., 2014). Some of the resulting products from these reactions, such as oligosaccharides (OGs), are able to elicit defence responses in the plant via cell wall bound receptors such as WAK1 (Aziz et al., 2004; Aziz et al., 2006; Aziz et al., 2007; Brutus et al., 2010).

Fig. 5.2 An illustration of arabinan structure in plants. Araf, Rha, GalU are arabinofuranose, rhamonose, and galacturonic acid, respectively. Black and white arrow heads indicate linkages targeted by endo-arabinanases and arabinofuranosidases, respectively.

Fig. 5.3 Transcript abundance of arabinan biosynthetic (left) and catabolic (right) genes in Arabidopsis. Relative transcript abundance of the indicated genes in arbitray units (y-axes) across different developmental stages (x-axes) are shown. RGP1 and RGP2 are recognized by the same probe. The data are derived from Genevestigator (Hruz et al., 2008).

Chapter 06

Fig. 6.1 Strategies to produce plants with increased disease resistance using transcription factors. The cartoon shows possible strategies for the manipulation of TFs that function as activators of defence reactions and other strategies for those that act as repressors. Promoters are shown as short solid rectangles and coding regions or RNAi constructs as longer grey rectangles. Transgenic lines with altered TF expression, knockdown of TFs, or knockout of TFs are produced and defined using precision/high throughput phenotyping to identify lines with improved disease resistance.

Fig. 6.2 Overview of different levels of signalling during biotic stress where transcription factors can play roles towards confering disease resistance. (Black) biological questions; (Grey) mechanistic understanding.

Chapter 07

Fig. 7.1 Phytohormonal regulation network of plant immunity integrating CKs as important novel factor and manipulation through pathogen-derived effectors. The model includes recent information of direct and indirect interactions of CKs with phytohormone-based signalling in plant immunity. Furthermore, the regulation of phytohormones by different representative effectors of

P. syringae

(1 to 5) are indicated which efficiently alter defence responses. Arrows indicate positive regulation, circles indicate negative regulation.

Fig. 7.2 Phytohormonal regulation of elicited plant defences. The scheme shows the two major phytohormonal defence signalling cascades of SA (left columns) and JA/ET (right columns) and includes some important signalling components of each branch. After elicitation, signalling follows the accordingly coloured pathways (arrows), which regulate defence against (hemi)biotrophs, necrotrophs or herbivores, respectively. Additional regulations of these central strands by other phytohormones (middle) are indicated by black lines (arrows – positive regulation, circles – negative regulation, square – differential regulation indicated).

Chapter 09

Fig. 9.1 Interaction of potato plants with

Phytophthora infestans.

(a) Two detached potato leaves that were inoculated with a

P. infestans

isolate in the laboratory show a distinct phenotype depending on the presence (on the right) and absence (on the left) of a resistance (

R

) gene. The resistant leaf remains green and has only small hypersensitive cell-death response (HR) spots at the inoculation sites, while the susceptible leaf is completely colonized. (b) The process of infection causing an HR is depicted (Haldar et al., 2006). The germinated cysts (Gc) on the surface of the leaf produce appressoria (Ap) to penetrate the epidermis, and then produce infection vesicles (Iv), intercellular hyphae (Ih) and haustoria (Ha) within the plant tissues. Pathogens secrete effectors to facilitate host colonization. Apoplastic effectors (Ae) are secreted into the extracellular space (apoplast). The cytoplasmic effectors (Ce) are secreted from haustoria and enter the plant cell, where they travel to different subcellular locations like, among others, the nucleus (N). In the absence of recognition, the pathogen can successfully colonize the plant. In case of recognition, HR cell death is induced, as shown in grey. (c) The subcellular view of how

P. infestans

interferes with potato life. Molecules derived from the pathogen’s intracellular hyphae (cell wall material, protease inhibitors, elicitins) are released into the extracellular spaces. If such Pathogen-Associated Molecular Patterns (PAMPs) are recognized by Pattern Recognition Receptors (PRRs), this will lead to PAMP-Triggered Immunity (PTI). Many PRRs interact with accessory proteins like BAK1 to initiate the PTI signalling pathway.

P. infestans

also delivers effectors from haustoria into the potato cell by an intensively studied but still unresolved mechanism (Petre and Kamoun, 2014). These cytoplasmic effectors often act to suppress PTI, but some of them are recognized by intracellular NB-LRR type of receptors encoded by R genes, thereby inducing effector-triggered immunity (ETI). Successively, PTI and ETI comprise a number of cellular signalling events whose sequence is poorly understood but include phospholipid signalling, activation of mitogen-activated protein kinases (MAPKs), reprogramming of gene expression. This results in downstream defence responses which include a burst of reactive oxygen species (ROS), callose deposition at sites of attempted infection and, often, localized cell death which is macroscopically recognized as a HR. Modified after (Dodds and Rathjen, 2010; Haldar et al., 2006).

Fig. 9.2 Durability is relative to the combination of components defined by each counterpart for a R-AVR pair. (Left) A R-AVR pair is shown. The contribution of a plant R protein to durability resides in its recognition spectrum and is reflected by the abundance of functional homologs in the germplasm. As a counterpart of the durable

R

genes, pathogen

Avr

genes with multiple copies in the genome and abundant presence among pathogen isolates are preferred targets for recognition by durable R proteins. (Right) Stacking of different durable R proteins with different resistance spectra recognizes a different suite of pathogen AVR proteins from potentially all pathogen isolates, facilitating the development of durable resistance.

Fig. 9.3 PPASSA multiple cloning site. The PPASSA multiple cloning site was introduced into cloning vectors pCC, pUC and into the binary vectors pBINPLUS, pCAMBIA, and their NPTII free equivalents, that can be used for marker-free transformation. Rare cutting restriction enzymes (eight cutters) recognition sites, indicated using gray highlights, allow the directional cloning and combination of up to five genes.

Fig. 9.4 A cycle for breeding durably late blight resistance potatoes by means of cisgenesis.

Chapter 10

Fig. 10.1 Every organ of a grapevine can be damaged severely by pathogen infections. (a) Grapevine (

V. vinifera

cv. Carignan) leaf showing typical symptoms of powdery mildew infections caused by the biotrophic fungus,

E. necator

. The white, powdery appearance is due to colonization of the leaf surface by mycelia (b) Bunch rot caused primarily by

B. cinerea

infection on ripe grape berries of

V. vinifera

cv. Semillon (c) Section of an arm of a grapevine (

V. vinifera

cv. Flame) showing a wood canker caused by the fungus

Neoscytalidium dimidiatum

Fig. 10.2 Visible symptoms of Pierce’s disease of grapevines normally do not appear before 2-3 months following a needle inoculation with cultured

X. fastidiosa

cells used in most studies of disease development. Panel (a) Leaf “scorch” symptom and (b) another scorched leaf to show that scorching starts at the leaf margin and progresses toward the main veins. (c) “Matchstick” petioles remain after the unusual abscission that occurs between the petiole and the leaf blade. Normally, grape leaf abscission occurs between the petiole and the shoot. (d) A complete cork layer generally forms as young stems develop secondary growth; however, infected vines develop “green islands”, indicating delayed activity of the cork cambium. Not shown: developing berries often dry out, becoming raisins rather than fully-grown fruit.

Fig. 10.3 (a) Shown is the working hypothesis of the steps in Pierce’s disease that follow vector feeding on a grapevine. This shaped our studies of PD development and proved to be relatively correct. The hormone ethylene’s role

vis-a-vis

disease resistance versus susceptibility remains uncertain (Section 4.4). It could contribute to vine death because it can promote tylose development and this occludes vessels and reduces water transport; however, if tyloses form soon after infection, they limit pathogen spread, potentially enhancing resistance (Section 4.4). (b, c, d, e) The progressive breakdown of grapevine intervessel pit membranes (PMs), beginning 4 weeks post-inoculation (P-I, B) and ending 12 weeks P-I (e), when visible symptoms became evident. In intact grapevine xylem, each PM has an arch of secondary wall that forms an open “roof” between the vessel lumen and the primary wall “face” of the PM. However, during sectioning, the knife angle was adjusted in a way that caused the arches to be removed, allowing the full extent of the PM surface to be seen. (d, e) Note the bacteria and their size in relationship to the gaps in the PMs. The narrow slits visible through the disrupted PMs are the openings in the secondary wall arches over the PMs in the adjacent vessel (i.e., the vessel into which the bacteria are moving. (f) A tylose as the PM shared with an adjacent xylem parenchyma cell has just begun to expand into a grapevine vessel. The PM from which it is developing is hidden by the tylose. Note the fibrillar nature of the tylose cell wall. (g) A section through a vessel into which 5 tyloses, each formed from the PM of a different xylem parenchyma cell, have expanded into the same vessel, completely occluding it. Perhaps visible in the sectioned tylose at 5 o’clock is the passageway leading to the “parental” parenchyma cell. Several tyloses have grown into vessels, completely blocking their lumens. The timing of tylose development relative to pathogen introduction can have an important impact on Pierce’s disease spread in a vine. (h, i, j) The value of non-destructive NMR to view changes in grapevine vessel function. (h) is an image of a stem in a well-watered, healthy vine. The xylem tissue (white line) is to the interior of the ring of vascular cambium (white arrow). The bright points in the xylem are water-filled vessels. (i, j) show the progressive loss of water from vessels (vessel cavitation, i.e., bright spots disappear) as PD develops or a vine is exposed to ethylene. Images b-g are courtesy of Professor Q. Sun, Dept of Biology D, U. Wisconsin Stevens Point; b-e and g are from Sun et al. (2011).

Fig. 10.4

V. vinifera

cv “Chardonnay” grapevines (10 per treatment) were needle-inoculated with wild-type

X. fastidiosa

or cells of the

X. fastidiosa

(

pg1A

-

) PG-knockout strain (40μl of 10

8

CFU/ml) or water and then maintained in a greenhouse for 20+ weeks. Vine presentation of Pierce’s disease symptoms was evaluated at intervals. The vines at 18 weeks P-I are shown. At 22 weeks, the wild-type-inoculated vines were dead and the

pg1A

- and water-inoculated vines were indistinguishable.

Chapter 11

Fig. 11.1 World coffee production for the year 2013–2014 (a) and import statistics in the major importing nations for the year 2012-2013 (b) (ICO statistics for 2013).

Chapter 13

Fig. 13.1 Progression of surface area of land cultivated with GM crops in Argentina from 1996/97 until 2013/14 sowing seasons.

Chapter 14

Fig. 14.1 Ownership of transgenic crops approved for commercial cultivation.

Fig. 14.2 Cotton yields in Australia from 1989–2012. Graph and table.

Fig. 14.3 Transgenic traits approved by FSANZ in Australia.

Chapter 15

Fig. 15.1 Hectares of Bt maize cultivated in Spain in the period from 1998 to 2013.

Chapter 16

Fig. 16.1 Increase of GM crops planted in South Africa from 2001 to 2012.

Chapter 17

Fig. 17.1 Plant-induced resistance to biotic stress.Induced resistance responses can be broadly classified as either chemical or structural, and may either augment constitutive defences or be produced

de novo

. The figure shows a cartoon representation of the main features of induced resistance in leaf tissues attacked by herbivores or pathogens. Resistance to feeding by arthropod herbivores is provided by a range of secondary metabolites and defensive proteins which can act either as toxins (T;

e.g

. alkaloids, isothicyanates) or antifeedants (AF;

e.g

. proteinase inhibitors, non-protein amino acids). Herbivory leads to the production of volatile organic compounds (VOCs) that can act as deterrents of feeding and/or oviposition of herbvores, and as attractants for herbivore predators and parasitoids. Herbivory can also trigger morphological defences, such as changes in trichome (Tr) density and type. Infection of leaves by avirulent pathogens is detected by R-genes and triggers the hypersensitive response (HR), which is typically associated with localised cell death and restriction of pathogen spread. Penetration by biotrophic fungal and oomycete pathogens (B) can be blocked by the deposition of callose papillae (C). Invasion by necrotrophic pathogens (N), is achieved by the production phytotoxins and hydrolytic enzymes (E;

e.g

. cutinases, pectinases) that degrade the cuticle and plant cell walls. Induced resistance responses can include the synthesis of inhibitors (I) of these enzymes (

e.g

. polygalacturonase inhibitor proteins), and the plant in turn produces it’s own hydrolytic enzymes to target the pathogen cell wall (

e.g

. glucanases and chitinases). Induced resistance is commonly associated with the synthesis of defensive secondary metabolites, known collectively as phytoalexins (PA), many of which have antimicrobial activities. Bacterial (Ba) pathogens are also targeted by synthesis of antimicrobial peptides (AMP). Another key chemical defense for induced resistance is the production of reactive oxygen species (ROS), which have multiple functions, including direct antimicrobial activity, roles as signalling molecules, and as substrates for cross-linking and polymerisation reactions during cell wall strengthening (CWS), a common structural induced resistance response that takes place around sites of infection. Several facets of resistance responses induced by herbivores and pathogens overlap, such as synthesis of secondary metabolites and cell wall strenthening, such that induced resistance can often provide very broad spectrum protection.

Fig. 17.2 The concept of priming as a memory of stress exposure.Previously unstressed plants exhibit a basal stress resistance phenotype to which constitutive defences contribute. Upon exposure to stress, such as pathogen infection, plants respond by activating induced resistance mechanisms. If induced resistance is successful, and the plant is able to recover from the initial stress, induced defences are switched off and return to basal levels. However, induced defences are maintained in a primed state, such that upon exposure to a second stress episode, induced defences are more rapidly deployed than in a naïve, previously unstressed plant. In the absence of further stress following the initial priming response, it is assumed that the capacity for induced resistance will slowly revert to the original basal level. Biological and chemical priming agents such as PGPR and BABA can switch the plant into a primed state without prior stress.

Chapter 18

Fig. 18.1 There is no scientific evidence to support well-defined protocols to implement either the collection of microorganisms as starting point for selection or to select good antagonists. Selection procedures refer to the collection of microorganisms. Such collections should be implemented taking into account the following issues:What kind of microorganisms should be included? Fast growing microorganisms with simple nutritional requirements should be preferred.Where to search for candidate antagonists? Two possible approaches are possible. Sampling agricultural environments facilitates the isolation of isolates well adapted to the same environment where they will be applied, but in such environments biodiversity is lower; sampling in a less anthropic environment, such as natural parks or not cultivated fields, allows the exploitation of a larger biodiversity but with the risk of collecting isolates less adapted to agricultural use.When to collect samples? Under environmental conditions similar to those of BCA products application (same period of year for field application, same controlled environment for post-harvest application, etc.) searching for actively growing microorganisms.Selection procedures should follow logical steps in succession. Taking into account that usually the first steps (up to the proof of concept) in the search for BCA(s) are performed by public researchers, it should be useful to build up a collection of well-characterized microorganisms to be exploited in selection procedures against different pathogens. “Acceptable” genetics modifications include classical approaches, such as mutagenesis or protoplast fusion, or those following a genetic engineering strategy if, and when, they will be allowed by each country’s legislation.The figure illustrates possible protocols to select antagonists against soil-borne plant pathogens, and takes into account that modifications will be required to adapt the protocol to specific requirements.

Fig. 18.2 (a) Colonization of the rind cells and growth in the cortex of a sclerotium of

Sclerotium rolfsii

by a

T. virens

GFP marked strain (Sarrocco. S & Vannacci. G). (b) Intracellular fungal growth, producing hyphal mats, within the sclerotia cortex (Sarrocco. S & Vannacci. G). (c) Advanced colonization of a tomato root by gfp-expressing

C. rosea

IK726 grown along the junctions of the epidermal cells and forming a net of hyphae around the main root six days after inoculation (with permission reproduced from Karlsson et al., 2015).

Fig. 18.3 Six scenarios for how biological control can be a part of IPM strategies in field crops in which chemical pesticides also are used

in full or reduced dosages

. Several other options are possible and some of the presented scenarios can also be combined depending on the cropping system and plant diseases in focus. For an IPM strategy the use of herbicides, insecticides, etc. should also be looked upon. (a) Seed or soil treatment at sowing: BCA(s) combined with chemical pesticides. The BCA(s) must be tolerant or less sensitive than the pathogen to the pesticide in use. The BCA effect might even last longer than the pesticide, i.e., controlling root diseases after plant establishment. (b) BCA(s) combined with pesticides. Depends on the tolerance of the BCA towards the pesticide(s) in use. The BCA(s) might be effective longer than the chemical pesticide, thus reducing the need for another pesticide spray later. (c) Alternating sprays: BCA sprays can be alternated with pesticide sprays aiming to reduce the number of chemical pesticide sprays used and help avoiding development of fungicide-resistant pathogen populations. (d) Chemical pesticides can only be used until the start of the “pre-harvest interval, PHI”. Use of BCAs is normally accepted after that time point - in the PHI. (e) Post-harvest BCA treatment of commodities like soft fruit, tubers and carrots for avoiding post-harvest spoilage and accumulation of mycotoxins. Treatment with chemical pesticides post-harvest should be very restricted but is used in some countries. (f) BCA treatment of straw or bare soil for reducing survival of pathogens in between crops.

Chapter 19

Fig. 19.1 A schematic representation of the TILLING strategy.

Chapter 20

Fig. 20.1 Agronomic performance in disease-free field trials of pairs of near-isogenic lines of barley cultivar Manchuria differing in the presence or absence of each of ten

R

-genes for resistance to powdery mildew (

Blumeria graminis

f.sp.

hordei

). The lack of a significant difference in any trait within each pair implies that there is no evidence for costs of these

R

-genes.

Mla7

was introgressed from two sources, Long Glumes and Multan. Trials were run over two years in a total of six replicates (data from Jørgensen & Jensen, 1990).

(a)

Grain yield (t ha

−1

).

(b)

Thousand grain mass (g).

(c)

Heading date (days in June).

(d)

Straw length (cm).

(e)

Lodging, where low scores indicate high straw strength (0–10 scale where 0 is no lodging and 10 is complete lodging). Black bars represent the resistant lines and white bars the susceptible ones.

Guide

Cover

Table of Contents

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Plant Pathogen Resistance Biotechnology

Edited byDavid B. Collinge

Copyright © 2016 by John Wiley & Sons, Inc. All rights reserved

Published by John Wiley & Sons, Inc., Hoboken, New Jersey

Published simultaneously in Canada

No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the Publisher, or authorization through payment of the appropriate per-copy fee to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, [phone], fax [phone], or on the web at www.copyright.com. Requests to the Publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, [phone], fax [phone], or online at http://www.wiley.com/go/permissions.

Limit of Liability/Disclaimer of Warranty: While the publisher and author have used their best efforts in preparing this book, they make no representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives or written sales materials. The advice and strategies contained herein may not be suitable for your situation. You should consult with a professional where appropriate. Neither the publisher nor author shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.

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Library of Congress Cataloging-in-Publication Data

Names: Collinge, D.B. (David Brian), editor.Title: Plant pathogen resistance biotechnology / David B. Collinge.Description: Hoboken, New Jersey : John Wiley & Sons, [2016] | Includes bibliographical  references and index.Identifiers: LCCN 2015049842 | ISBN 9781118867761 (cloth)Subjects: LCSH: Plant biotechnology. | Plants–Disease and pest resistance–Molecular aspects. | Phytopathogenic microorganisms.Classification: LCC TP248.27.P55 P568 2016 | DDC 630–dc23LC record available at http://lccn.loc.gov/2015049842

To Andrea,Mikkel and JakobTak for jeres støtte

List of Contributors

Geziel Barbosa AguilarSection for Plant and Soil ScienceDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenCopenhagen, Denmark

Ali Abdurehim AhmedSection for Plant and Soil ScienceDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenCopenhagen, Denmark

Yuling BaiWageningen UR Plant BreedingWageningen University & Research CentreWageningen, The Netherlands

Dave K. BergerDepartment of Plant ScienceForestry and Agricultural Biotechnology Institute (FABI)Genomics Research Institute (GRI)University of PretoriaPretoria, South Africa

Paul R.J. BirchCell and Molecular SciencesDundee Effector ConsortiumDivision of Plant SciencesUniversity of Dundee; at James Hutton InstituteDundee, UK

Fernando F. Bravo-AlmonacidLaboratorio de Biotecnología Vegetal, INGEBI-CONICETBuenos Aires, Argentina

James K.M. BrownJohn Innes CentreNorwich, UK

Dario CantuDepartment of Viticulture and EnologyUniversity of CaliforniaDavis, CA, USA

Maryke CarstensDepartment of Plant ScienceForestry and Agricultural Biotechnology Institute (FABI)Genomics Research Institute (GRI)University of PretoriaPretoria, South Africa

María CocaCentre for Research in Agricultural Genomics (CRAG)CSIC-IRTA-UAB-UBBarcelona, Spain

David B. CollingeSection for Microbial Ecology and BiotechnologyDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenCopenhagen, Denmark

Francesca DesiderioCouncil for Agricultural Research and Economics (CREA)Genomics Research CentreFiorenzuola d’Arda, Italy

Marc FuchsDepartment of Plant Pathology and Plant-Microbe BiologyNew York State Agricultural Experiment StationCornell UniversityGeneva, NY, USA

Aravind GallaDepartment of Biology & MicrobiologySouth Dakota State UniversityBrookings, SD, USA

Michael GilbertAustralian Centre for Plant Functional GenomicsUniversity of Adelaide, Waite CampusUrrbrae, South Australia, Australia

Eric van der GraaffSection for Crop SciencesDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenTaastrup, Denmark

Dominik K. GroßkinskySection for Crop SciencesDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenTaastrup, Denmark

Ingo HeinCell and Molecular SciencesDundee Effector ConsortiumDundee, UK

Ronald C.B. HuttenWageningen UR Plant BreedingWageningen University & Research CentreWageningen, The Netherlands

Evert JacobsenWageningen UR Plant BreedingWageningen University & Research CentreWageningen, The Netherlands

Birgit JensenSection for Microbial Ecology and BiotechnologyDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenCopenhagen, Denmark

Dan Funck JensenDepartment of Forest Mycology and Plant PathologyUppsala BioCenter, Swedish University of Agricultural SciencesUppsala, Sweden

Kwang-Ryong JoWageningen UR Plant BreedingWageningen University & Research CentreWageningen, The Netherlands

Hans J.L. JørgensenSection for Plant and Soil ScienceDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenCopenhagen, Denmark

Magnus KarlssonDepartment of Forest Mycology and Plant PathologyUppsala BioCenter, Swedish University of Agricultural SciencesUppsala, Sweden

Geert J.T. KesselPlant Research International (PRI)Wageningen University & Research Centre,Wageningen, The Netherlands

Avinash KumarPlant Cell Biotechnology DepartmentCSIR-Central Food Technological Research Institute (CFTRI)Karnataka, India

John M. LabavitchDepartment of Plant SciencesUniversity of CaliforniaDavis, CA, USA

Belén López-GarcíaCentre for Research in Agricultural Genomics (CRAG)CSIC-IRTA-UAB-UBBarcelona, Spain

Hazel McLellanCell and Molecular SciencesDundee Effector ConsortiumDivision of Plant SciencesUniversity of Dundee; at James Hutton InstituteDundee, UK

Ewen MullinsDepartment of Crop ScienceTeagasc Crops, Environment and Land Use ProgrammeCarlow, Ireland

Ashis Kumar NandiSchool of Life SciencesJawaharlal Nehru UniversityNew Delhi, India

Giridhar ParvatamPlant Cell Biotechnology DepartmentCSIR-Central Food Technological Research Institute (CFTRI)Karnataka, India

Ann L.T. PowellDepartment of Plant SciencesUniversity of CaliforniaDavis, CA, USA

Roel C. RabaraTexas A&M AgriLife Research and Extension CenterDallas, TX, USA

Søren K. RasmussenSection for Plant and Soil ScienceDepartment of Plant and Environmental SciencesUniversity of CopenhagenCopenhagen, Denmark

Michael R. RobertsLancaster Environment CentreLancaster UniversityLancaster, UK

Thomas RoitschSection for Crop SciencesDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenTaastrup, DenmarkGlobal Change Research CentreCzech Globe AS CRDrásov, Czech Republic

Fred RookDepartment of Plant and Environmental Sciences and VILLUM Research Center for Plant PlasticityUniversity of CopenhagenCopenhagen, Denmark

M. Caroline RoperDepartment of Plant Pathology and MicrobiologyUniversity of CaliforniaRiverside, CA, USA

Paul J. RushtonTexas A&M AgriLife Research and Extension CenterDallas, TX, USA

Yumiko SakuragiDepartment of Plant and Environmental SciencesUniversity of CopenhagenCopenhagen, Denmark

Sabrina SarroccoDepartment of Agriculture, Food and EnvironmentUniversity of PisaPisa, Italy

María Eugenia SegretinLaboratorio de Biotecnología Vegetal, INGEBI-CONICETBuenos Aires, ArgentinaBlanca San SegundoCentre for Research in Agricultural Genomics (CRAG)CSIC-IRTA-UAB-UBBarcelona, Spain

Nandini P. ShettyPlant Cell Biotechnology DepartmentCSIR-Central Food Technological Research Institute (CFTRI)Karnataka, India

Simmi P. SreedharanPlant Cell Biotechnology DepartmentCSIR-Central Food Technological Research Institute (CFTRI)Karnataka, India

Maria StranneDepartment of Plant and Environmental SciencesUniversity of CopenhagenCopenhagen, Denmark

Jane E. TaylorLancaster Environment CentreLancaster UniversityLancaster, UK

Paula TennantDepartment of Life SciencesThe University of the West IndiesMona Jamaica, WI

Hans Thordal-ChristensenSection for Plant and Soil ScienceDepartment of Plant and Environmental Sciences and Copenhagen Plant Science CentreUniversity of CopenhagenCopenhagen, Denmark

Anna Maria TorpSection for Plant and Soil ScienceDepartment of Plant and Environmental SciencesUniversity of Copenhagen,Copenhagen, Denmark

Prateek TripathiMolecular & Computational Biology SectionUniversity of Southern CaliforniaLos Angeles, CA, USA

Giampiero ValèCouncil for Agricultural Research and Economics (CREA)Rice Research UnitGenomics Research CentreVercelli, ItalyCouncil for Agricultural Research and Economics (CREA)Genomics Research CentreFiorenzuola d’Arda, Italy

Giovanni VannacciDepartment of Agriculture, Food and EnvironmentUniversity of PisaPisa, Italy

Richard G.F. VisserWageningen UR Plant BreedingWageningen University & Research CentreWageningen, The Netherlands

Vivianne G.A.A. VleeshouwersWageningen UR Plant BreedingWageningen University & Research CentreWageningen, The Netherlands

Jack H. VossenWageningen UR Plant BreedingWageningen University & Research CentreWageningen, The Netherlands

Suxian ZhuWageningen UR Plant BreedingWageningen University & Research CentreWageningen, The Netherlands

Foreword

It is almost a cliché to point out that the agricultural production systems of the planet are facing a series of unprecedented challenges.

The world population is predicted to grow to more than 8 billion within 20 years, approaching 10 billion in 2050 (http://esa.un.org/wpp/).

Urbanization of the population is reducing the available area of agricultural land by encroachment and affecting adjacent areas with pollution and increased water demand.

The advanced economic growth and social development of regions, especially in Asia, is driving demand for meat-based diets with the knock-on effect of increasing the cultivation of commodity crops (e.g., maize, soybean) for animal feed purposes whilst simultaneously elevating greenhouse gas emissions (Smith et al., 2007).

Climate change is challenging the sustainability of traditional cropping systems via stochastic temperature fluctuations, rising CO2 levels, increased frequency of extreme weather events and by moving climate zones.

Faced with these multiple challenges, global agriculture must adopt more dynamic, efficient and sustainable production methods to increase food and fodder production to feed a growing population with fewer resources (FAO). Finally, climate changes alone present several independent factors affecting the pallette of disease and disease control. In particular, emerging pathogens (and pests) find favourable conditions in new regions and, secondly, the increased unpredictability of the weather is leading to an increase in and unpredictability of abiotic stresses, such as drought, heat and cold, thereby altering risk patterns for specific diseases (Chakraborty and Newton, 2011). In turn, the latter leads to the need to understand the subtle interactions between these abiotic stress factors, the hormones regulating the ability of the plant to adapt to abiotic stress and microorganisms exhibiting different lifestyles. These range from beneficial endophytes and symbionts to harmful pathogens, and indeed there are examples where the same microbe can act as a benign if not beneficial endophyte under some conditions and as a harmful pathogen under others. While plant diseases can devastate crops, they can often be controlled by cultural practice, disease resistance, biological control and the use of pesticides. A level of complexity for the biologist attempting to unravel the nature of plant defence and the influence of abiotic factors, however, lies in the fact that evolution is based on adaptation of the tools available. This means that many of the same tools and their regulators are used in radically different processes in the plant where signal transduction processes regulate, e.g., growth and development as well as responses to biotic and abiotic stress. Examples of genes include those encoding different classes of receptors and components of signal transduction such as protein kinases as well as transcription factors. The regulators include phytohormones such as abscisic acid and cytokinins and ions such as Ca2+. Plants are well capable of defending themselves against most pathogens through innate immunity, as the mechanisms of disease resistance are termed at the cellular level, and disease resistance is the most cost-effective and environmentally friendly way of protecting crops from diseases: the plants themselves do the job. However, successful pathogens overcome the plants’ defences and, indeed, effective natural disease-resistance is often not available for the breeder. This is especially true for some hemibiotrophs and necrotrophs. In these cases, transgenic strategies may afford a viable alternative for crop production. Thus, the main aim of this book is to provide an in-depth overview of the current strategies available to develop transgenic-based disease-resistant plants, whilst also presenting the knowledge gained to date in this area and thus evaluating the potential of such strategies for disease control.

No magic bullet has been developed to combat fungal and bacterial diseases effectively, but an increased understanding of the underlying biology suggests several approaches, which may be combined – pyramided – to provide sustainable resistance. The strategies differ depending both on the organisms to be controlled as well as on the lifestyle strategy used by the pathogen and these are exemplified in the different chapters. Disease resistance (or, at this level, immunity) is triggered by the recognition in the host of molecules produced by the pathogen, or by the perturbations that pathogen molecules have on plant immunity. The response event leads to inhibition of pathogen development through several independent physiological mechanisms which are activated concomitantly. Strategies for developing transgenic disease resistance attempt to exploit the recognition events, the signalling pathways regulating the immune response or the tools actually responsible for pathogen arrest. The different chapters of the first part of the book explore examples of these mechanisms in order to highlight the depth of knowledge gained from research in this field to date and demonstrate the potential for how this information can be exploited for biotechnological purposes for targeted plant breeding.

The second part of the book provides contrasting case studies of globally important crops, namely coffee, grapevine, potato and rice and their diseases, where effective and durable disease resistance to the major pathogens has not been achieved by conventional breeding, and describes the strategies which are being tested to assist pathogen defence of for these diverse crops.

A third section combines national and regional surveys of the actual use of transgenic crops including those conferring disease resistance in the field coupled with those currently in development and regulatory pipelines. This section of the book presents several case studies in which the authors in question were asked to answer the following questions: Which transgenic crops are grown? What is the economic and agronomic impact of these studies? Are there transgenic disease resistant crops among these? In addition, BT maize is grown in many countries to control European Corn Borer (Ostrinia nubilalis) and the corn earworm (Helicoverpa zea), but are there studies from their country showing enhanced resistance to Fusarium and reduced levels of mycotoxins compared to the non-transgenic crop (see (Clements et al., 2003; Duvick 2001))? Is there promising work aiming to introduce disease-resistant crops in the foreseeable future? The reader is also referred to the pro-GM (genetically modified) lobby ISAAA’s (International Service for the Acquisition of Agri-biotech Applications) annual reports http://www.isaaa.org/ where the latest reports that “18 million farmers in 27 countries planted biotech crops in 2013, reflecting a five million, or three percent, increase in global biotech crop hectarage” (James, 2013). The penetration in the domestic market for some of these transgenic varieties exceeds 90% in some countries, according to the IAAA.

Several chapters impinge on the issues perceived by society as being important in relation to the extent that GM technology can be implemented, seen in relation to the approaches taken by those countries who are focused on the need both to thrive agronomically and economically whilst respecting public opinion on an issue of intense debate. It is no secret that there is considerable opposition against GM food amongst consumers worldwide, but the nature of this opposition differs geographically. This means that only about 30 countries use GM crops in commercial agriculture, although many others import GM plant products either for fodder, industrial purposes (including cotton) or other consumer products (e.g., cut flowers). Many more use GM microorganisms in industry for the production of enzymes or medicines, and there is little or no opposition against these applications. Within those countries which have adopted the GM technology, the main crops have often reached a very high level of penetration in the potential market: again, according to ISAAA (ibid), 96% rape (canola) is GM in Canada, in the USA over 90% maize, cotton and soybean are GM. In India and China, over 90% of the cotton is GM and in India 18 million farmers use GM. In other words, 90% of farmers using GM crops are in developing countries (James, 2013). Economy is the driving force. Farmers cannot be expected to plant a crop for more than one season unless it pays – or they are persuaded.

The need to feed populations across the world is not equally distributed. The pressure is greatest in Asia which includes some of the world’s most densely-populated countries. Among these are India and China, which are currently experiencing a rapid economic development that is leading to a shift from being largely vegetarian to omnivore, meaning that the requirement of fodder is increasing accordingly. It is estimated that the demand for rice will at least double by 2050 (see Chapter 12 by San Segundo et al.). Europeans (and North Americans) can (still) afford to import the food and fodder that cannot be produced locally, so the incentive to accept GM food is perhaps therefore lower (Brookes and Barfoot, 2013; Klümper and Qaim, 2014).

The wide and carefully regulated use of GMs in Argentina (see Chapter 13 by Bravo-Almonacid and Segretin) has led to the development of an innovative culture to develop new solutions aimed at local problems. Although all GM crops grown commercially at present originate from well-known international companies, e.g., Monsanto and Syngenta, many new crops (often termed “events”) have been developed and are passing through the regulatory pipeline leading to commercial release (e.g., transgenic lines for PVY resistance in potato). There is a much lower incentive in Europe to develop GM crops; however, although the European moratorium reduces the incentive to look for GM solutions to solve serious problems, it stimulates alternative, more refined technologies, e.g., cisgenics (Holme et al., 2013), and gene targeting approaches such as CRISPR (clustered regularly interspaced short palindromic repeats) (Belhaj et al., 2013) in the host and to target the pathogen using siRNA by HIGS (host-induced gene silencing) (Fairbairn et al., 2007; Ghag et al., 2014; Pliego et al., 2013). The development and potential for these “soft GM” technologies has led to a renewed debate in the EU. These issues are discussed in more detail in Chapters 1 and 4. See also European Academies Science Advisory Council, 2013 (Hartung and Schiemann, 2014).

Much disease resistance has been introduced by crossing in from related plant species. For example, in tomato the Cf genes conferring resistance to Cladosporium fulvum originate from, e.g., Solanum pimpinellifolium (Kruijt et al., 2004), various grasses in the tribe tritici to wheat (Kleinhofs et al., 2009) and Solanum spp (see Chapter 10). Plant breeding by introgression is intrinsically less precise than genetic engineering since many fragments of chromosome from the donor species are introgressed. Of course, errors also occur with genetic engineering, but these can be eliminated for further use by selecting only the verified clean insertion events. What might the consequences be if disease resistance is transferred? Is there any evidence that disease controls the populations of wild relatives? These are among the questions addressed in Chapter 20.

Organisation of the book

An introduction to the problems of diseases, life style strategies and taxonomic groups of pathogens, the nature of plant immunity, and its exploitation for disease resistance.

Biological strategies leading towards disease resistance. Which genes have been used to confer disease resistance and which genes and strategies offer the greatest hope for the future?

Case studies – should certain crops be prioritized or avoided and which special problems are presented by these? Why is it especially advantageous to use transgenic strategies for these pathogens or crops?

Status of transgenic crops around the world. Summaries of the current situation and prospects for the future for four countries on different continents where transgenic strategies are widely used.

Transgenic disease resistance is not the only way of exploiting the knowledge gained from transgenic technology: discussed here is how the status and prospects of how the knowledge gained through experimental molecular genetics and related forms of biotechnology benefit plant protection. The examples chosen represent molecular breeding, induced resistance and biological control.

References

Belhaj K, Chaparro-Garcia A, Kamoun S, Nekrasov V (2013) Plant genome editing made easy: targeted mutagenesis in model and crop plants using the CRISPR/Cas system. Plant Methods 9: 39.

Brookes G, Barfoot P (2013) Key environmental impacts of global genetically modified (GM) crop use 1996–2011. GM Crops & Food: Biotechnology in Agriculture and the Food Chain 4: 109–119.

Chakraborty S, Newton AC (2011) Climate change, plant diseases and food security: an overview. Plant Pathol 60: 2–14.

Clements MJ, Campbell KW, Maragos CM, Pilcher C, Headrick JM, Pataky JK, White DG (2003) Influence of Cry1Ab protein and hybrid genotype on fumonisin contamination and fusarium ear rot of corn. Crop Sci 43: 1283–1293.

Duvick J (2001) Prospects for reducing fumonisin contamination of maize through genetic modification. Environ Health Perspect 109: 337–342.