Abstract: Blumeria hordei (Bh) causes the powdery mildew disease of barley. In resistant barley lines, the RNase-like Bh AVR_A effectors are recognized by immune receptors encoded at the barley Mildew locus a (Mla). The maintenance of AVR_a 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 AVR_A virulence function we isolate the AVR_A targets inside barley host cells. For this, we applied in vivo proximity-dependent protein labelling (BioID) using AVR_A-expressing stable transgenic barley lines. We identified that one specific AVR_A effector targets a member of the barley Strubbelig Receptor Family (SRF).

Using chimeric AVR_a constructs, we demonstrate that the AVR_A 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 AVR_A 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.

Biography: Isabel Saur is an ANU graduate who did her Honours in the group of Michael Djordjevic followed by a PhD with John Rathjen. She then moved to the Max-Planck Institute for Plant Breeding Research in Cologne to continue her research as a postdoc, funded by EMBO short term, long-term and Marie-Curie fellowships. She currently has an independent position at the University of Cologne, supported by a prestigious Emmy Noether Programme fellowship.