Targeting of the barley cell-surface receptor SRF3 by the Blumeria hordei effector AVR A13 overlaps with AVR A13 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 ) 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 can also bind Arabidopsis thaliana SRF3 and A. thaliana AVR a13 -lines mimic srf3 mutants in iron signaling. In barley, srf3 mutants and AVR a13 expression desensitize iron-induced restriction of Bh growth, suggesting that AVRA13 facilitates fungal proliferation by manipulating SRF3-mediated changes to iron homeostasis. Together, these findings identify SRF3 as molecular link between pathogen virulence and iron-related processes. In addition, our data demonstrates that MLA specifically detects the residues that underlie Bh effector neo-functionalization and intrinsic AVRA virulence functions.