Plant basal resistance - Universiteit Utrecht

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Chapter 2 accessions. Composite interval mapping of the pooled data did not revealed genetic linkage with basal callose levels in mock-treated seedlings. On the other hand, strong linkage was found between flg22-induced callose and a locus at chromosome III (LOD score = 16.22; Figure 6). An additional weaker influence was detected at a locus on the top of chromosome I (LOD score = 3.01; Figure 6b). The direction of both QTLs suggests opposite effects (Table 1): the major-effect QTL at chromosome III mediates a repressive effect from the Bur-0 parent or a stimulatory effect from the Col-0 parent, whereas the weaker QTL at chromosome I exerts a stimulatory effect from Bur-0 or a repressive effect from Col-0. QTLs regulating defence responsiveness are not associated with reduced growth Induction of defence priming is associated with minor costs on plant growth (Van Hulten et al., 2006; Walters et al., 2008). To examine whether the constitutive defence priming in accession Bur-0 is associated with direct costs on plant growth, we scored rosette sizes of the RILs over a growth period of 4 weeks. Two relatively weak QTLs were identified at the bottom and top of chromosomes III and IV (LOD scores 3.19 and 3.76, respectively), which did not correspond to the QTLs controlling flg22-induced callose or SA-induced PR-1 expression (Figure 6; Table 1). This indicates that the priming-inducing loci from accession Bur-0 are not associated with major costs on plant fitness. Priming by the SA response locus on chromosome IV boosts basal resistance against Pst DC3000 The major callose QTL at chromosome III is based on either a repressive effect by the Bur- 0 alleles, or a stimulatory effect from the Col-0 alleles (Table 1). Because accession Bur- 0 is considerably more resistant against Pst DC3000 than accession Col-0 (Figure 3), it is unlikely that this locus contributes to basal resistance against this pathogen. In contrast, the direction of the SA response locus at chromosome IV is consistent with a positive effect on basal resistance against Pst DC3000. To confirm this, we compared levels of basal resistance between five RILs carrying the Bur-0 alleles of the SA response locus, five RILs carrying the Col-0 alleles of this locus, and the two parental accessions. Basal resistance assays were performed using a bioluminescent luxCDABE-tagged P. syringae pv. tomato DC3000 strain (Pst DC3000-lux), which enable in planta quantification of bacterial colonization (Fan et al., 2008). At 3 days after dipping the leaves in a bacterial suspension, Pst DC3000-lux colonisation in leaves of the Bur-0 lines was consistently lower than in leaves of the Col- 0 lines (Figure 7a). Furthermore, bacterial growth values in all genotypes were inversely related to levels of SA-induced PR-1 transcription (Figures 7b and 7c). Multiple regression analysis of the bacterial growth values confirmed a statistically significant effect of the SA response locus (P < 0.001), whereas variation between lines with similar genotypes for this locus had no significant influence on bacterial growth (P = 0.258). These results indicate 48
49 Genetic dissection of basal defence responsiveness that constitutive priming of the SA response by the locus on chromosome IV boosts basal resistance against Pst DC3000. DISCUSSION Figure 7: Basal resistance against Pst DC3000-lux and SA-induced PR1 expression in 5 RILs with the Col-0 alleles of the SA response QTL (lines #15, #17, #62, #80 #371), 5 RILs with the Bur-0 alleles of this locus (lines #22, #116, #292, #440, #511) and the parental accessions Col-0 and Bur-0. Black and white bars/symbols indicate genotypes carrying the Bur-0 and Col-0 alleles of the locus, respectively. (a) Colonization by Pst DC3000-lux at 3 days after dip-inoculation of the leaves. Bacterial titres were based on in planta bioluminescence by the bacteria. Data shown represent average values (n=12; ± SEM) of bioluminescence-corresponding pixels in leaves relative to the number of pixels covering total leaf material in each plant. (b) Transcriptional levels of PR-1 expression at 7 h after treatment of the leaves with 0.5 mM. Data presented are average fold-change values (n=3; ± SEM) standardised to the mean expression value between Col-0 and Bur-0. (c) Correlation between bacterial colonisation and SAinduced PR-1 expression. Plant resistance to biotic stress largely depends on inducible defence mechanisms. However, induced defence can be costly due to allocation of resources or toxicity to the plant’s own metabolism. These contrasting benefits provide a classic trade-off between plant defence
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 18 and 19: Chapter 1 an endogenous plant signa
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
Page 28 and 29: Chapter 1 constitutively produced i
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 47: 47 Genetic dissection of basal defe
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 67 and 68: Chemical treatments and callose qua
Page 69 and 70: Aphid infestation stimulates apopla
Page 81 and 82: Table S1: Primers used for RT-qPCR
Page 86 and 87: 86 CHAPTER 4 Benzoxazinoids in root
Page 88 and 89: Chapter 4 INTRODUCTION Plants have
Page 90 and 91: Chapter 4 Our study presents eviden
Page 92 and 93: Chapter 4 Maize - P. putida FBC004
Page 94 and 95: Chapter 4 P. putida is tolerant to
Page 96 and 97: 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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106
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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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