Plant basal resistance - Universiteit Utrecht

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General discussion
For a successful parasitic interaction, pathogens and insects have to cope with a plethora
of plant defence mechanisms. Some of these defences are pre-existing, while others are
inducible by the attacking organism. As was outlined in the General Introduction of this thesis
(Figure 1; Chapter 1), induced defence in plants is based on sequentially activated defence
layers that are active at different stages of the parasitic interaction. In general terms, these
layers of the plant immune system can be separated between pre-invasive defence barriers,
such as PAMP-induced closure of stomata (Melotto et al., 2006), early-acting post-invasive
defence, such as localised deposition of ROS and callose (Luna et al., 2011), and late-acting
post-invasive defences that are under control by de novo produced defence hormones, such
as salicylic acid (SA; Heil and Ton, 2008). The overarching objective of the work presented in
this thesis was to study the contribution of post-invasive defence barriers to basal resistance
(Chapters 2 and 3) and their impact on the interactions with plant-beneficial microbes, such
as rhizosphere-colonizing Pseudomonas putida bacteria (Chapter 4).
NATURAL OCCURRING VARIATION IN BASAL RESISTANCE
The vast majority of studies on natural variation in plant defence have focussed on ETI (De
Meaux and Mitchell-Olds, 2003; Holub, 2007; Van Poecke et al., 2007), which is likely due to
the robustness and reproducibility of the ETI phenotype. There are also numerous studies
about natural variation in basal resistance against pathogens and herbivores, many of which
are based on the genetic model plant species Arabidopsis (Koornneef et al., 2004). However,
relatively few of these have linked this variation to actual resistance mechanisms. The natural
variation in basal resistance of Arabidopsis to insects often originates from differences
in pre-existing pools of glucosinolates (Kliebenstein et al., 2001; Koornneef et al., 2004).
Glucosinolates enable a rapid production of biocidal isothiocyanates after herbivore attack
and could therefore, be viewed as a constitutively primed defence mechanism. Natural
variation in basal resistance of Arabidopsis against pathogens, on the other hand, seems to
stem from more diverse mechanisms than from glucosinolates. For instance, Denby et al.,
(2004) reported that natural variation in basal resistance against the necrotroph Botrytis
cinerea correlates with responsiveness of pathogen- and acifluorfen-induced camalexin, an
indole-derived phytoalexin. Further genetic dissection of this basal resistance in a mapping
population of recombinant inbred lines (RILs) revealed multiple small-to-medium-effect
quantitative trait loci (QTLs), but it remained unclear to what extent these loci influence
the responsiveness of camalexin induction itself. Similarly, Llorente et al. (2005) used a RIL
population to dissect natural variation in basal resistance against the necrotrophic fungus
Plectosphaerella cucumerina, which identified three different QTLs. The most influential