Pathogens secrete effectors into host cells to promote virulence and often establish disease by interception of basal defence components. One widespread mechanism of disease resistance in plants requires nucleotide-binding oligomerization (NOD)-like receptor (NLR) genes. Recognition of an effector by a cognate NLR prevents pathogen proliferation. A co-evolutionary arms race between the host barley and the pathogenic powdery mildew fungus Blumeria graminis forma specialis hordei
(Bgh) has driven the functional diversification of allelic NLR variants encoded at the MLA disease resistance locus (for Mildew locus A). Recent work revealed that Bgh effectors detected by allelic MLA receptor variants are unexpectedly sequence-unrelated and evolved independently from different ancestors. Additionally, the MLA orthologs in wheat and rye, Sr33 and Sr50, confer isolate-specific resistance to the stem rust pathogen Puccinia graminis forma specialis tritici (Pgt). This is remarkable because rust and mildew fungi belong to different phyla and cannot encode sequence-related effectors. MLA variants can therefore not have diversified to directly bind sequence-related effectors and thus monitor effector-mediated modifications of host targets conserved between different cereals.
To reintegrate into the European scientific community, I wish to perform the “TOPPER” project at the Max-Planck Institute for Plant Breeding Research, Cologne, Germany.
The “TOPPER” project will clarify whether the sequence-unrelated Bgh effectors target the same host protein or converge on a common signalling pathway/complex consisting of related or unrelated host proteins. I hypothesize that the host protein(s), manipulated by Bgh effectors, is/are also targeted by effectors of other plant-associated microorganisms, which will be tested here. The collaboration with the partner ‘2Blades’ will ensure direct deployment of results in agriculture to battle plant disease, where appropriate.
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