Induced resistance for plant disease control - Disease Control in Crops - page 80

4.4 Trade-offs associated with induced resistance

4.4.1 Trade-offs between pathogens with different lifestyles

In plantpathogen interactions, distinct defence responses are activated, depending on
the lifestyle of the attacking pathogen. As indicated earlier in this chapter, SA and JA
play important signalling roles in these responses. It appears that SA induces defence
against biotrophic pathogens, while JA mediates defences against necrotrophic patho-
gens (Glazebrook, 2005). Cross-talk between the two signalling pathways might help
to fi ne-tune defence responses against a particular pathogen according to its mode of
infection (Beckers & Spoel, 2006). Little is known however, about cross-talk between
defence signalling in response to attempted infection by more than one pathogen. In some
interesting recent work, Spoel et al. (2007) found that infection with the biotrophic patho-
gen Pseudomonas syringae, which induces SA-mediated defence, rendered Arabidopsis
thaliana more susceptible to the necrotrophic pathogen Alternaria brassicicola. They
found that this trade-off was restricted to plant tissue adjacent to the site of initial infec-
tion, since A. brassicicola infection in systemic tissue was not affected. Further, the trade-
off only occurred with a virulent strain of P. syringae , and avirulent strains that induced
programmed cell death (PCD), did not cause suppression of JA-dependent defence. The
authors suggested that this might be advantageous to the plant by preventing growth of
necrotrophic pathogens in tissue undergoing PCD.

4.4.2 Trade-offs with resistance to insects

Insect herbivory results in the induction of a series of events, including the generation
and release of specifi c signals, the subsequent perception and transduction of those
signals and, fi nally, activation of wound-related defence mechanisms (Figure 4.2) (Leon
et al., 2001). Thereafter, secondary signals are generated, leading to the further activation
of local and systemic defences. These secondary signals include oxylipins (oxygen-
ated fatty acids), including JA and its volatile methyl ester (MeJA), both of which, as
indicated above, play an important role in regulating induced resistance to insect attack
(Figure 4.2) (Bostock, 2005; Walters et al., 2006). However, the situation is considerably
more complex than the simple split between JA regulation of defence against insects and
SA regulation of pathogen defence. For example, it is known that the nature of the acti-
vated signalling pathway depends on the particular plant/insect combination (Bostock,
2005), since both SA- and JA-responsive gene expression can be elicited by aphids and
whitefl ies, while methyl salicylate is generated by aphid attack in maize (Bernascone
et al., 1998; Walling, 2000). There are, nevertheless, several examples of negative cross-
talk between the SA and JA signalling systems, especially for SA-mediated suppression
of JA-inducible gene expression (Figure 4.2) (Van Wees et al. , 1999; Glazebrook et al. ,
2003). Thus, activation of SA-dependent SAR has been shown to suppress JA signalling,
thereby compromising the plants' ability to induce defences to insect attack (Stout et al.,
1999; Thaler et al. , 1999, 2002). For example, tobacco plants expressing TMV-induced
SAR were more susceptible to grazing by the tobacco hornworm Manduca sexta than
non-induced plants (Preston et al. , 1999), while application of the chemical activator
acibenzolar- S -methyl (ASM) to fi eld-grown tomato plants reduced resistance to the beet
armyworm Spodoptera exigua (Thaler et al. , 1999). Interestingly, JA has also been shown