Figure 1.

Diagram showing effectors from non‐gene‐for‐gene ectomycorrhizal, necrotrophic and biotrophic fungi, and from gene‐for‐gene biotrophic fungi, interacting with host targets and resistance proteins. (A) Non‐gene‐for‐gene interactions. Ectomycorrhizal fungi: putative effectors of (ecto)mycorrhizal fungi interact with host targets to facilitate symbiosis and suppress or avoid host defence responses. Necrotrophic fungi: effectors of necrotrophic fungi interact with host targets, eventually causing necrosis of host plant cells to facilitate disease. Biotrophic fungi: effectors of biotrophic fungi interact with host targets and facilitate disease without killing host plant cells. (B) Gene‐for‐gene interactions. It is assumed that, as a result of co‐evolution with their host plants, biotrophic fungi have evolved further. Direct interaction: it is assumed that effectors have two domains, one of which interacts with the virulence target, leading to host susceptibility, whereas the other is recognized by the R protein present in resistant plants, leading to the hypersensitive response (HR) and resistance. Indirect interaction: the effectors interact with the virulence target leading to susceptibility. Resistant plants have developed resistant proteins that do not interact directly with effectors, but guard the virulence target, and HR is triggered after sensing manipulation of the virulence target by the effector. Interaction between effectors and host targets (virulence targets and R proteins) can take place on the plasma membrane, in the cytoplasm or in the nucleus.