Plants and oomycetes, an intimate relationship: co-evolutionary principles and impact on agricultural practice.

Abstract

Plants face continuous attacks from a broad range of pathogens and have evolved effective defence mechanisms that are initiated upon pathogen attack. Invading oomycete pathogens secrete effectors, molecules that manipulate host cell defence and thereby enable colonization. However, plant species evolved resistance (R) genes to most specialized pathogen species. The R proteins can detect effectors, termed avirulence (AVR) proteins, and thus confer immunity to pathogens. Effectors and their interacting genes in the plant play a central role in the co-evolution of pathogens with their hosts. In this review, we discuss the role that effectors play in the pathogenesis and lifestyles of oomycetes. Particularly intriguing features emerge for (hemi-)biotrophic oomycetes, which establish an intimate contact with the host by forming haustoria. At this interface, effectors with an RXLR motif are translocated into the cytoplasm, where they reprogramme the host towards susceptibility. Such interactions between effectors and host targets are highly specific and are considered a result of tight co-evolution. In addition, we elaborate on the Phytophthora infestans-Solanum pathosystem, from which various R and Avr genes were cloned recently. We discuss a rationale for exploiting molecular insights into R-Avr interactions for developing more durable resistance strategies to control late blight in agriculture.

Exploiting Knowledge of Pathogen Effectors to Enhance Late Blight Resistance in Potato

“…This can reveal if the apparently novel resistance is genuinely new, or closely related to previously characterised resistances. For example, the PiAvr2 effector is not only recognised by R2 but also by an R2-like protein, RpiBlb3 and RpiAbpt proteins from S. bulbocastanum and RpiSnk1 from Solanum schenckii (Rietman et al 2010;Gilroy et al 2011a). A similar observation was also made for RpiBlb1, which recognises the PiAvrBlb1 effector (Vleeshouwers et al 2008).…”

Understanding and Exploiting Late Blight Resistance in the Age of Effectors

“…In contrast, the R2 homolog Rpi-mcd1, originating from the Argentinean species S. microdontum, does not show HR when coagroinfiltrated with Avr2 family members, indicating that it may have evolved to recognize a different P. infestans effector (79). This difference could be explained by adaptive evolution of R loci driven by local P. infestans populations in South versus Central America, which may have led to distinct recognition spectra between late blight R genes from the two centers of diversity (77,111).…”

“…These R genes often segregate as quantitative trait loci (QTL) in genetic mapping populations and breeders tend to wrongly assume that their mode of action differs from classical gene-for-gene interactions (reviewed in 35,46,106,111). In these cases, coevolution between pathogen and host may be less advanced than for genes conferring full resistance.…”