Aleksandra Wawryk-Khamdavong

Plants encounter diverse pathogens and have evolved a 2-layered innate immune system to detect pathogen molecules and activate defense mechanisms that restrict infection. Most cloned plant Resistance (R) genes encode NLR immune receptors. NLR genes are often found in clusters of paralogs with sequence and copy number variation; whether these NLR clusters evolve in response to single or multiple pathogens has been unclear. We report here the isolation of a Phytophthora capsici resistance gene, Rpc2, along with a novel P. infestans resistance gene, Rpi-amr5, from 2 Solanum americanum accessions. These orthologous genes reside in the Rpi-amr1 cluster, which has previously been associated with resistance to P. infestans. By screening RXLR effector libraries of P. infestans and P. capsici, we identified multiple effectors recognized by both NLRs. Our findings highlight the complexity of NLR clusters and evolution driven by interactions with multiple pathogens. This work will underpin efforts to elevate resistance against Phytophthora pathogens and enhances our understanding of NLR evolution.

Plants and animals respond to pathogen attack by mounting innate immune responses that require intracellular nucleotide-binding leucine-rich repeat (NLR) proteins. These immune receptors detect pathogen infection by sensing virulence effector proteins. However, how receptors evolve new recognition specificities remains poorly understood. We found that the plant NLR MLA3 (Mildew locus a 3) has evolved to recognize a pathogen effector by acting as a molecular mimic of an effector virulence target, thereby triggering an immune response. By introducing the mimic’s binding interface into the wheat stem rust resistance protein SR50, we bioengineered a chimeric receptor with dual recognition activities that conferred resistance to two major cereal pathogens in barley transgenic lines. These results demonstrate that molecular mimicry by immune receptors can be harnessed to engineer multiple disease resistance.