Fig. 4.

A model showing the hypothetical evolution and mechanisms of Puccinia graminis f. sp. tritici (Pgt) effector interactions and function to elicit and suppress the barley RMRL-mediated resistance mechanism. The box on the right shows the stepwise evolution of virulence effectors that allows Pgt to become virulent on barley (virulence effector depicted by a red circle) then subsequently repress RMRL mediated resistance through gaining a suppressor of Avr4/5 avirulence. The host immunity evolution model shown in the box on the left was developed based on the genetic and functional analyses of RMRL that shows it represents an integrated sensory domain (ISD) nucleotide binding site-Leucine rich repeat (NLR) resistance locus [58]. The barley NLR Rpg5 contains a Protein Kinase domain that represents an integrated sensory domain (ISD) that recognizes the Avr4/5 avirulence effector that originally evolved as a virulence effector that targets the progenitor Rpg5 protein kinase as a virulence target. Based on the ISD hypothesis we speculate that the Pgt virulence effector targeted the protein kinase in barley to gain effector induced susceptibility (EIS). As these susceptibility targets represent host proteins with a critical function barley was forced to co-evolve by duplicating and translocating this susceptibility hub to the Rpg5 NLR that functions as pathogen “bait” that recognizes the virulence effectors manipulation of the original susceptibility target through its ISD triggering RMRL-mediated resistance. Thus, the original virulence effector is now transformed by host evolution to the avirulence effector Avr4/5. During the molecular arms race, the pathogen may be unable to shed Avr4/5 as it has an essential virulence function, thus evolved a suppressor of RMRL-mediated resistance signaling which includes the heat shock proteins and others (Table 1; Additional file 1: Table S10) to regain EIS