From gene-for-gene to NLRome-for-effectorome: decoding the dynamic interplay between phytopathogenic effector...

Phytopathogenic bacteria rely on type III effectors to suppress host immunity and facilitate colonization. While necessary for virulence, effectors can also trigger effector-triggered immunity (ETI) if hosts have appropriate NLR immune receptors, resulting in a coevolutionary arms races driving high diversity in both the pathogen "effectorome" and the host "NLRome." Here, we synthesize current knowledge of effectoromes into an "interconnected module model", that emphasizes how functional redundancy among effectors organizes them into modules targeting shared host processes; how low target specificity creates interconnections between these modules; how effector-effector interactions can modify infection outcomes; and how the cumulative presence of multiple ETI-eliciting effectors within a repertoire generates an overall ETI load that constrains pathogen fitness. This systems-level perspective reframes the classical gene-for-gene model into a dynamic NLRome-effectorome model characterized by quantitative ETI responses whose magnitude and ultimate outcome is a dynamic balance between ETI load and suppression. Advancing disease resistance requires strategies that exploit this equilibrium, including rational stacking of NLRs targeting core, conserved effectors. Such approaches highlight the potential of network-based frameworks for designing durable, broad-spectrum crop immunity.