References

112 M.D. Stefano, A. Ferrarini, M. Delledonne
8.2
Activation of the Defense Response
Plants exhibit a wide array of both passive and active defense strategies
against pathogen attack. Preformed physical barriers (e.g., the cuticle and
the cell wall) and biochemical defenses (e.g., antimicrobial toxins) are often
insufficient to avoid spread of infection. Therefore, after recognition
of the invading pathogen, plants activate a very effective arsenal of inducible
defense responses (hypersensitive response, HR) characterized by
hypersensitive cell death, tissue reinforcement and production of antimicrobial
metabolites (McDowell and Woffenden 2003; Dangl et al. 1996;
Hammond-Kosack and Jones 1996). The rapid recognition of pathogen
infection is supported by a sophisticated surveillance system that is capable
of distinguishing between self-generated signals and those emitted by
pathogens (Holub 2001). It is followed by the establishment of systemic
acquired resistance (SAR), a salicylic acid dependent long-lasting immunity
against a broad spectrum of pathogens (Ryals et al. 1996). The HR
requires active host protein synthesis and is kept under tight genetic control,
being activated only if the plant detects a potential invader (Baker et
al. 1997). In this way, plant cells autonomously maintain constant vigilance
against pathogens by expressing large arrays of “R genes” (R, resistance).
R genes encode putative receptors that respond to the product of “Avr
genes” (Avr, avirulence) expressed by a pathogen during infection (Mc-
Dowell and Woffenden 2003). This gene-for-gene interaction results from
either direct or indirect interaction between the R gene and Avr gene
products depending on the R–Avr gene pair. Evidence is emerging that
RproteinsoftendonotrecognizeAvrproteinsdirectly.Inthe“guard
hypothesis,” R proteins activate resistance by interacting with another
plant protein that is modified by the pathogen (McDowell and Woffenden
2003).
R-gene-mediated activation of HR triggers a number of rapid cellular
responses, including perturbations in ion fluxes and the pattern of protein
phosphorylation, which precede the accumulation of ROS (mainly O − 2 and
H2O2) and NO as well as the transcriptional activation of defense-related
genes (McDowell and Dangl 2000; Cohn et al. 2001) (Fig. 8.1). These initial
responses are followed by the production of phytoalexins, transcriptional
activation of defense genes and hypersensitive cell death, which is a form
of programmed cell death having regulatory and mechanistic features that
are similar to apoptosis in animal cells, such as membrane dysfunction,
cytoplasmic vacuolization, chromatin condensation and endonucleolytic
cleavage of DNA (Gilchrist 1998). The interplay between ROS and NO
contributes to the establishment of the HR and to the potentiation of defense
responses (Blume et al. 2000). Downstream events are inhibited by some