Targeting of the barley cell-surface receptor SRF3 by the Blumeria hordei effector AVRA13 overlaps with AVRA13 recognition by MLA and the induction of NLR-mediated cell death.

Pathogens secrete effector proteins to promote virulence. Despite their recognition by barley Mla resistance genes, the structurally-related Blumeria hordei (Bh) AVRA effectors are maintained in the Bh genome, suggesting virulence functions critical for fungal pathogenicity. Using proximity-dependent protein labelling in transgenic barley, we detected distinct host protein interactomes for five AVRAs despite their structural homology and convergence on MLAs. We report the specific interaction of the highly conserved AVRA13 effector with the barley cell-surface receptor SRF3. AVRA13 disrupts HvSRF3-HvBAK1 interaction and alters HvSRF3 plasma membrane levels. AVRa13-expression desensitizes iron-induced restriction of Bh growth, suggesting that AVRA13 facilitates fungal proliferation by manipulating SRF3-mediated iron homeostasis. Our results suggest that MLAs have diversified to specifically detect the residues that underly Bh effector neo-functionalization and intrinsic AVRA virulence functions. Together, these findings identify SRF3 as molecular link between pathogen virulence, immune recognition, and iron homeostasis.