The zig-zag-zig in oomycete-plant interactions

Abstract

In addition to a range of preformed barriers, plants defend themselves against microbial invasion by detecting conserved, secreted molecules, called pathogen-associated molecular patterns (PAMPs). PAMP-triggered immunity (PTI) is the first inducible layer of plant defence that microbial pathogens must navigate by the delivery of effector proteins that act to suppress or otherwise manipulate key components of resistance. Effectors may themselves be targeted by a further layer of defence, effector-triggered immunity (ETI), as their presence inside or outside host cells may be detected by resistance proteins. This 'zig-zag-zig' of tightly co-evolving molecular interactions determines the outcome of attempted infection. In this article, we consider the complex molecular interplay between plants and plant pathogenic oomycetes, drawing on recent literature to illustrate what is known about oomycete PAMPs and elicitors of defence responses, the effectors they utilize to suppress PTI, and the phenomenal molecular 'battle' between effector and resistance (R) genes that dictates the establishment or evasion of ETI.

Figure 1

The zig‐zag‐zig in oomycete–plant interactions (modified from Jones and Dangl, 2006). Shown are the characterized oomycete pathogen‐associated molecular patterns (PAMPs) and other elicitors of PAMP‐triggered immunity (PTI) and necrosis [represented by a dotted arrow extending PTI beyond the threshold for host programmed cell death (PCD)]; examples of oomycete effectors that contribute to effector triggered susceptibility (ETS); and examples of host resistance proteins that detect oomycete effectors to trigger immunity (ETI). The amplitude of defence is shown on the y axis, and the threshold for activation of host PCD is also indicated. CBEL, cellulose‐binding elicitor lectin; CRN, crinkling and necrosis; NLP, Nep1‐like protein; PRR, pattern recognition receptor; R, resistance; SCR, small cysteine‐rich.