Targeting of the barley cell-surface receptor SRF3 by the <i>Blumeria hordei</i> effector AVR _A13 overlaps with AVR _A13 recognition by MLA and the induction of NLR-mediated cell death

Abstract Pathogens secrete effector proteins to promote virulence. Despite their recognition by barley Mla resistance genes, the structurally-related Blumeria hordei ( Bh ) AVR A 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 AVR A s despite their structural homology and convergence on MLAs. We report the specific interaction of the highly conserved AVR A13 effector with the barley cell-surface receptor SRF3. AVR A13 disrupts HvSRF3-HvBAK1 interaction and alters HvSRF3 plasma membrane levels. AVR a13 -expression desensitizes iron-induced restriction of Bh growth, suggesting that AVR A13 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 AVR A virulence functions. Together, these findings identify SRF3 as molecular link between pathogen virulence, immune recognition, and iron homeostasis.