Effector biology during biotrophic invasion of plant cells

Chaudhari, Prateek; Ahmed, Bulbul; Joly, David L; Germain, Hugo

Filamentous pathogens have a large suite of predicted, secreted proteins, which could act early during infection to suppress PTI as the pathogens are establishing themselves and, at later stages, to rewire host cellular activities to meet the pathogen's metabolic needs. It has been proposed that protein trafficking from haustoria allows pathogens to hijack host cells for their own purposes. However, the precise mechanism governing effector translocation from the extra-haustorial space to host cells has eluded scientists thus far. 14 For the purpose of this review, we have classified effectors into three types based on the subcellular compartment they target: apoplastic effectors, cytoplasmic effectors and nuclear effectors. Apoplastic effectors can be secreted by appressoria and/ or hyphae invading the intercellular space where they remain outside the cells. This class of effectors includes proteins with inhibitory functions, interfering with plant proteases and peroxidases. For example, the Avr2 effector from the biotrophic fungal pathogen Cladosporium fulvum suppresses basal defense through inhibition of specific host proteases. [15] [16] [17] On the other side, cytoplasmic and nuclear effectors affect host defense mechanisms by Several obligate biotrophic phytopathogens, namely oomycetes and fungi, invade and feed on living plant cells through specialized structures known as haustoria. Deploying an arsenal of secreted proteins called effectors, these pathogens balance their parasitic propagation by subverting plant immunity without sacrificing host cells. Such secreted proteins, which are thought to be delivered by haustoria, conceivably reprogram host cells and instigate structural modifications, in addition to the modulation of various cellular processes. As effectors represent tools to assist disease resistance breeding, this short review provides a bird's eye view on the relationship between the virulence function of effectors and their subcellular localization in host cells.