2026/01/09 by Wei Shi, Merle Bilstein-Schloemer, Sara Christina Stolze +5 · 1 voice
Agricultural and Biological Sciences · Biochemistry, Genetics and Molecular Biology · #Effector #Fungal and yeast genetics research #Homology (biology) #Immune system #Pathogen #Plant-Microbe Interactions and Immunity #Receptor #Secretion #Signal transduction #Transgene #Virulence #Wheat and Barley Genetics and Pathology
paper · pdf · doi:10.64898/2026.01.08.698370
openalex publication_date 2026/01/09 · openalex created_date 2026/01/10 · openalex updated_date 2026/08/01
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.