Poster
Merle Bilstein-Schloemer
PhD student
Institute for Plant Sciences, University of Cologne
Cologne, Nordrhein-Westfalen, Germany
Wei Shi
PostDoc
Institute for Plant Sciences, University of Cologne
Cologne, Nordrhein-Westfalen, Germany
Sara Stolze
Max Planck Institute for Plant Breeding Research, Proteomics Group
Koeln, Nordrhein-Westfalen, Germany
Maike Hofmann
Institute for Plant Sciences, University of Cologne
Cologne, Nordrhein-Westfalen, Germany
Hirofumi Nakagami
Group leader
Max Planck Institute for Plant Breeding Research
Koeln, Nordrhein-Westfalen, Germany
Isabel Saur
Group leader
University of Cologne, CEPLAS
Cologne, Nordrhein-Westfalen, Germany
The Blumeria hordei (Bh) AVRA13 effector is highly conserved despite activating host resistance via the barley MLA13 NLR receptor. To understand why AVRa13 has not diversified to escape host recognition, we set out to understand AVRA13 virulence function. By performing proximity-dependent protein labelling on stable transgenic AVRa13 barley lines, we identified the receptor-like kinase HvSRF3 as specific AVRA13 interactor. An extensive set of chimeric and mutant AVRA13 variants demonstrates that a central AVRA13 loop region mediates both, association of AVRA13 with the SRF3 cytoplasmic domain and activation of MLA13 cell death. Thus, MLA13 has evolved to specifically recognise the residues of AVRA13 that the effector requires to bind SRF3, suggesting that AVRA13 cannot escape MLA13 recognition without compromising its virulence function on SRF3. In Arabidopsis, SRF3 regulates iron homeostasis and underlays temperature-dependent hybrid incompatibility, which is executed by the Dm2h NLR. We demonstrate that stable AVRa13-expressing Arabidopsis lines exhibit temperature-dependent Dm2h autoimmunity. In the absence of Dm2h, we detected AVRA13- and SRF3-dependent modulation of iron homeostasis. Collectively these findings demonstrate that pathogens target SRF3 activity for virulence, and that Arabidopsis and barley have evolved the Dm2h and MLA13 NLRs, respectively, to detect pathogen-mediated modulation of SRF3 activity.