Blumeria hordei (Bh) causes the powdery mildew disease of barley. In resistant barley lines, the RNase-like Bh AVRA effectors are recognized by immune receptors encoded at the barley Mildew locus a (Mla). The maintenance of AVRa effector genes in the Bh population despite the detection of the gene products by MLA receptors suggests that the effectors' intrinsic function is crucial for Bh virulence. However, these virulence functions are currently entirely unknown.
To identify the AVRA virulence function we isolate the AVRA targets inside barley host cells. For this, we applied in vivo proximity-dependent protein labelling (BioID) using AVRA-expressing stable transgenic barley lines. We identified that one specific AVRA effector targets a member of the barley Strubbelig Receptor Family (SRF).
Using chimeric AVRa constructs, we demonstrate that the AVRA domains required for interaction with the intracellular domain of the host target are the same domains that the matching MLA immune receptor has evolved to detect for resistance. Together our data suggests that a) the intrinsic virulence functions of individual Bh AVRA effectors differ despite the fact that the effectors are structurally related; b) that at MLA immune receptors may have evolved to specifically detect the residues of effectors that are required for the effectors' virulence functions and c) that members of the SRF may modulate immunity towards powdery mildew and potentially other pathogens.