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.

Abstract

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 can also bind Arabidopsis thaliana SRF3 and A. thaliana AVRa13-lines mimic srf3 mutants in iron signaling. In barley, srf3 mutants and AVRa13 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.