Plant basal resistance - Universiteit Utrecht

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Chapter 1 an endogenous plant signalling metabolite, or that it activates a plant regulatory protein controlling multiple immune responses simultaneously. Indeed, research on BABA-induced defence priming in Arabidopsis revealed that BABA not only mimics SAR-related priming of SA-dependent defences, but it also primes for pathogen-induced deposition of callose- containing papillae (Zimmerli et al., 2000; Ton et al., 2005). This priming of cell wall defence functions independently of SA and JA, but requires intact biosynthesis and perception of the plant hormone ABA (Ton and Mauch-Mani, 2004; Van der Ent et al., 2009) Table I. Chemicals that trigger priming of defence in plants after exogenous application. Chemical Stimulus Primed defence response Plant Species Reference Benzothiadiazole (BTH) PAL gene induction Arabidopsis (Kohler et al., 2002) Probenazole SA-inducible genes Rice (Iwai et al., 2007) Saccharin Cinnamyl alcohol dehydrogenase activity Beta amino butyric acid (BABA) Thiamine (Vitamin B1) SA-inducible genes and callose deposition ROS accumulation, callose deposition, and SAinduced expression 18 Barley (Boyle and Walters, 2006) Arabidopsis (Zimmerli et al., 2000; Ton and Mauch-Mani, 2004) Arabidopsis (Ahn et al., 2007) Cytokinins SA-inducible genes Arabidopsis (Choi et al., 2011) JA-inducible genes Poplar (Dervinis et al., 2010) Scopoletin and Capsidiol Tobacco (Großkinsky et al., 2011) Azelaic acid SA-inducible genes Arabidopsis (Jung et al., 2009) Quercetin ROS accumulation, callose deposition, and PR1 gene induction Molecular mechanisms of priming Arabidopsis (Jia et al., 2010) In contrast to research on innate plant defences that are directly responsive to pathogens and herbivores, the majority of research on priming of defence has remained limited to a description of the phenomenon after treatment with resistance-inducing agents, along with an assessment of its effectiveness in terms of disease resistance (Conrath et al., 2006; Frost et al., 2008). Only a few research groups have begun to address the mechanistic basis of defence priming (Conrath, 2011). Consequently, there are still many open questions about defence priming in plants, particularly with respect to the signalling mechanisms controlling the onset and long-term maintenance of the phenomenon.
19 General introduction enhanced accumulation of signalling proteins. One common hypothesis postulates that priming is based on an increased accumulation of inactive defence signalling proteins, thereby providing enhanced defence signalling capacity (Conrath et al., 2006). Subsequent exposure to environmental stress would then lead to a faster and stronger defence signalling cascade, ultimately resulting in the augmented defence response. Indeed, SAR- related priming is associated with an increased accumulation of two inactive MAP protein kinases, MPK3 and MPK6, which show enhanced kinase activity upon secondary stress application (Beckers et al., 2009). Simultaneously, a genome-wide profiling of transcription factor (TF) genes was performed, which demonstrated that induction of ISR-related priming is associated with augmented expression of JA-regulatory TF genes (Van der Ent et al., 2009). The same study showed that BABA-induced priming was associated with enhanced expression of WRKY transcription factor genes, which encode transcription factors that regulate SA-induced defence gene transcription (Van Verk et al., 2011). Although enhanced accumulation of defence-related signalling TFs can contribute to a faster and stronger transcriptional activation of defence genes after pathogen attack, these signalling proteins typically have a limited half-life. Hence, their enhanced accumulation after application of a single priming stimulus does not provide a satisfactory explanation for the long-lasting nature of priming phenomena. epigenetic mechanisms. A recent study showed that SAR-related priming in Arabidopsis is associated with post-translational changes of histone H3 and H4 tails at gene promoters of defence-regulatory transcription factor genes (Jaskiewicz et al., 2011). Although these chromatin modifications were monitored relatively shortly after SAR induction, such epigenetic regulatory mechanism provides an attractive explanation for the long-lasting nature of the priming phenomenon. Indeed, recent evidence demonstrated that priming is an epigenetic phenomenon. Three independent research groups demonstrated that the primed defence state in Arabidopsis can be transmitted to following generations from iso- genic plant lines (Luna et al., 2012; Rasmann et al., 2012; Slaughter et al., 2012). Moreover, expression of trans-generational priming of SA-dependent defence genes was associated with chromatin remodelling at the corresponding gene promoters (Luna et al., 2012), whereas priming of JA-dependent defence requires intact biogenesis of small interfering RNAs (Rasmann et al., 2012). glycolylation of secondary metabolites. It is also conceivable that secondary metabolites contribute to long-lasting priming of defence. The chemical defence capacity of plants can be enhanced by an increased accumulation of inactive defence metabolite conjugates, such as glucosinolates and plant hormone-glucosides. Consequently, pathogen- or wounding-induced activity of hydrolytic glucosidase enzymes would lead to a faster and greater release of active aglycone metabolites. signalling cross-talk. Priming can also result from a shift in the cross-talk balance
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 10 and 11: 10 CHAPTER 1 General Introduction A
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 20 and 21: Chapter 1 between defence signallin
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 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
Page 61 and 62: ABSTRACT 61 Role of benzoxazinoids
Page 63 and 64: 63 Role of benzoxazinoids in maize
Page 65 and 66: 65 Role of benzoxazinoids in maize
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Aphid infestation stimulates apopla
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71 Role of benzoxazinoids in maize
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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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