Plant basal resistance - Universiteit Utrecht

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10 CHAPTER 1 General Introduction Adapted from: Ahmad S, Gordon-Weeks R, Pickett J, Ton J. Natural variation in priming of basal resistance: from evolutionary origin to agricultural exploitation. Molecular Plant Pathology 11(6), 817-827 (2010).
THE PLANT IMMUNE SYSTEM 11 General introduction Plants are constantly interacting with potentially hostile organisms, such as viruses, bacteria, fungi, oomycetes, nematodes, and insects. Over the course of millions of years of co-evolution, these plant-microbe interactions have shaped the plant immune system. This regulatory system is complex and involves multiple inducible defence mechanisms, which are active at different stages of colonization by the plant attacker (Figure 1; Ton et al., 2009). To establish a successful parasitic interaction, pathogens and herbivores need to penetrate the host tissue. Plant viruses mostly depend on vectors to penetrate plant tissues, but many fungi, oomycetes and aphids can penetrate cell walls directly, whereas pathogenic bacteria often depend on natural openings, such as stomata or wound sites. At this stage of infection, a rapid closure of the stomata can form a first pre-invasive defence barrier (Melotto et al., 2008). After successful entry of the plant tissue, plant attackers often face an early- acting, post-invasive defence barrier that is marked by localized defence responses, such as the accumulation of reactive oxygen species, defence gene induction and deposition of callose-rich papillae (Eulgem et al., 1999; Flors et al., 2005; Torres et al., 2006). Upon further colonization, plants undergo a large-scale transcriptional and metabolic reprogramming that coincides with the biosynthesis of defence regulatory hormones, such as salicylic acid (SA) or jasmonic acid (JA), and complementary long-distance signals to regulate a broad spectrum of local and systemic defence mechanisms (Heil and Ton, 2008). The default mode of the plant immune system: non-host resistance The most common type of disease resistance in plants is non-host resistance, which is effective against a very wide range of attackers and provides the most effective form of plant defence (Mysore and Ryu, 2004). Non-host resistance can result from the fact that the host plant simply does not provide the right environment for the attacking pathogen. However, in addition to this passive form of non-host resistance, research over the past decade has uncovered that non-host resistance also relies on active inducible defence mechanisms (Lipka et al., 2005). This non-host defence response is typically activated by conserved microbial features, such as flagellin, chitin, glycoproteins or lipopolysaccharides, which are referred to as “pathogen-associated molecular patterns” (PAMPs, synonymously called MAMPs for “microbe-associated molecular patterns”). Defence responses to herbivores can be triggered by herbivore-associated molecular patterns (HAMPs; Mithoefer and Boland, 2008), but are more commonly triggered by the perception of endogenous plant elicitors that are released upon tissue damage, which are called damage-associated molecular patterns (DAMPs; Heil, 2009; Heil et al., 2012). Much about the perception machinery of HAMPs remains unknown (Mithoefer and Boland, 2008). PAMPS and DAMPS are thought to be recognised by plasma membrane-localised pattern-recognition receptors
Page 1 and 2: Plant basal resistance: genetics, b
Page 3 and 4: Most of the research described in t
Page 5: Promotor: Prof. dr. Ir. C.M.J. Piet
Page 12 and 13: Chapter 1 (PRRs; Gomez-Gomez and Bo
Page 14 and 15: Chapter 1 by avirulent pathogens (R
Page 16 and 17: Chapter 1 Selective non-pathogenic
Page 18 and 19: Chapter 1 an endogenous plant signa
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Page 22 and 23: Chapter 1 rarely provides complete
Page 24 and 25: Chapter 1 genetic resources for Ara
Page 26 and 27: Chapter 1 metabolites are biosynthe
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Page 30: Chapter 1 latest insights. This Cha
Page 33 and 34: ABSTRACT 33 Genetic dissection of b
Page 35 and 36: 35 Genetic dissection of basal defe
Page 45 and 46: Natural variation in responsiveness
Page 57: 57 Genetic dissection of basal defe
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ABSTRACT 61 Role of benzoxazinoids
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63 Role of benzoxazinoids in maize
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Chemical treatments and callose qua
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Aphid infestation stimulates apopla
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Table S1: Primers used for RT-qPCR
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86 CHAPTER 4 Benzoxazinoids in root
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Chapter 4 INTRODUCTION Plants have
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Chapter 4 Our study presents eviden
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Chapter 4 Maize - P. putida FBC004
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Chapter 4 P. putida is tolerant to
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Chapter 4 Impact of DIMBOA on the P
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Chapter 4 PP5286 dut deoxyuridine 5
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Chapter 4 DIMBOA-producing wild-typ
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Chapter 4 DISCUSSION The rhizospher
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Chapter 4 patterns, we considered t
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108 CHAPTER 5 General Discussion
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Chapter 5 QTL was caused by a polym
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Chapter 5 Figure 1: CYP81D11 regula
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Chapter 5 et al., 2009), and allele
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Chapter 5 defence against different
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Chapter 5 occurred at time-points l
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Chapter 5 rhizospheric signals that
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Chapter 5 glucosinolate profiles. 1
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References References Abramovitch R
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References QTL mapping and characte
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References Gianoli E, Niemeyer HM (
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References Kliebenstein DJ, Kroyman
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References Studies in Natural Produ
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References Geniostoma antherotrichu
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References Todesco M, Balasubramani
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References Walters DR, Paterson L,
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Summary Summary Basal resistance in
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Samenvatting Samenvatting Basale re
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Samenvatting inzichten opgeleverd i
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Acknowledgments Acknowledgements In
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Curriculum vitae Shakoor was born o
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List of Publications Published arti
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