Plant basal resistance - Universiteit Utrecht

Chapter 1
by avirulent pathogens (Ross, 1961; Hoffland et al., 1996), suggesting that priming can
boost both PTI and ETI mechanisms. Since basal resistance has been defined as the sum of
resistance by PTI and ETI, minus the susceptibility by ETS (Jones and Dangl, 2006), priming
of defence can best be defined as an augmented capacity to express basal resistance
mechanisms (Figure 2A). If the augmented basal defence response precedes the delivery of
pathogen effectors, priming can provide full immunity against otherwise virulent pathogens
(Figures 2B). Indeed, this has been reported for some forms of chemically-induced priming
(Zimmerli et al., 2000; Conrath et al., 2006). In most cases, however, primed defence
expression slows down the colonisation by virulent pathogens to a larger extent than
basal resistance (Conrath et al., 2006). Most priming-inducing stimuli can trigger defence
mechanisms directly if applied in higher doses. For instance, relatively high soil-drench
concentrations of beta-aminobutyric acid (BABA) trigger PR-1 gene induction directly in
Arabidopsis, whereas lower concentrations of BABA merely prime the induction of PR-1
(Van Hulten et al., 2006). Furthermore, transient induction of direct defence can give rise
to longer-lasting priming of defence (Bruce et al., 2007; Heil and Ton, 2008). Hence, many
induced resistance phenomena are based on a combination of direct defence and priming
and their relative contribution depends on the dose of the resistance inducing stimulus and
the time point after induction.
Biologically induced priming of defence
Priming of defence can be induced by various biological agents and is often expressed in plant
parts distal from the initial site of stimulation. For example, localised attack by pathogenic
microbes can elicit a broad-spectrum systemic acquired resistance (SAR) response that is
associated with priming of defence responses (Kohler et al., 2002; Conrath et al., 2006; Jung
et al., 2009; Conrath, 2011). SAR is triggered by localised pathogen attack and develops in
uninfected distal parts of the plant as against a broad spectrum of pathogens (Durrant and
Dong, 2004). During this process, leaves/tissue under pathogen attack produce a systemic
signal which is transported to uninfected distal plant parts, where it primes the tissues
for SA-dependent defences (Jung et al., 2009). The 1 st systemic study of SAR in Nicotiana
benthamiana demonstrated that the phenomenon lasts for up to 20 days after primary
infection (Ross, 1961). Studies in the following decades have mostly focused on the onset of
SAR, which requires accumulation of plant stress hormone, SA and an intact NPR1 protein
(Durrant and Dong, 2004). More recent studies have revealed that SAR establishment
requires additional signals, which precede systemic accumulation of SA, such as jasmonates
(Truman et al., 2007) and indole-derived metabolites (Truman et al., 2010). The exact nature
of the mobile SAR signal, however, remains debatable, even within the same Arabidopsis-
based pathosystem (Attaran et al., 2009). Apart from MeSA (Vlot et al., 2008), glycerolipids
(Chaturvedi et al., 2008), azelaic acid (Jung et al., 2009), and glycerol-3-phosphate (Chanda
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