A wheat tandem kinase activates an NLR to trigger immunity.

The role of nucleotide-binding leucine-rich repeat (NLR) receptors in plant immunity is well studied, but the function of a class of tandem kinases (TKs) that confer disease resistance in wheat and barley remains unclear. In this study, we show that the SR62 locus is a digenic module encoding the Sr62TK TK and an NLR (Sr62NLR), and we identify the corresponding AvrSr62 effector. AvrSr62 binds to the N-terminal kinase 1 of Sr62TK, triggering displacement of kinase 2, which activates Sr62NLR. Modeling and mutation analysis indicated that this is mediated by overlapping binding sites (i) on kinase 1 for binding AvrSr62 and kinase 2 and (ii) on kinase 2 for binding kinase 1 and Sr62NLR. Understanding this two-component resistance complex may help engineering and breeding plants for durable resistance. Editor's summary: Plant immunity relies heavily on intracellular nucleotide-binding leucine-rich repeat (NLR) proteins, which can act as either receptors or signal transducers to facilitate disease resistance. In wheat and barley, an alternative class of genes called the tandem kinases also contribute to disease resistance. Two papers in this issue elucidate how tandem kinases work, showing that wheat tandem kinases require an NLR to function. Chen et al. found a pathogen effector that triggers the action of the wheat Sr62 tandem kinase. They demonstrate that the effector interacts with Sr62's active kinase domain, enabling a pseudokinase domain to activate the corresponding NLR. In parallel, Lu et al. found that a different tandem kinase, WTK3, activates the same NLR as Sr62, and that this NLR acts as a calcium ion channel once activated. Together, these studies solidify the role of NLRs as hubs for immune signaling in response to diverse pathogens and will guide breeding efforts for disease-resistant wheat. —Madeleine Seale [ABSTRACT FROM AUTHOR]