Plant immune receptors detect pathogen-secreted effector proteins to trigger robust disease resistance. Understanding which effector–receptor interactions drive immunity enables targeted discovery and deployment of resistance genes for crop protection. This study examined why the wild tomato relative Solanum americanum is resistant to the bacterial spot pathogen Xanthomonas euvesicatoria, with the objective of identifying the pathogen effectors and corresponding plant receptors that mediate effector-triggered immunity (ETI).
The authors screened X. euvesicatoria type III effectors (T3Es) by transiently expressing individual effectors in S. americanum leaves to detect host responses. Several effectors produced visible cell death when expressed in leaf tissue, indicating recognition by host immune systems. The screening approach established a set of candidate T3Es that provoke defense-associated cell death in the S. americanum accession SP2273.
Using quantitative assessment of immune responses in S. americanum SP2273 challenged with X. euvesicatoria multiple-T3E knockout mutants, the study demonstrated that at least nine effectors collectively contribute to ETI. The nine identified T3Es are AvrBs2, XopAP, XopAU, XopE1, XopJ3, XopM, XopN, XopX, and XopZ1. Loss of subsets of these effectors in the pathogen reduced the measured immune response, supporting a model in which multiple recognition events combine to produce strong resistance in the host.
Among the nine T3Es, AvrBs2 and XopJ3 were singled out as the principal contributors to the ETI phenotype. When delivered naturally into plant cells by the bacterium, these two effectors elicited the most robust cell death and induction of defense genes in S. americanum. These observations indicate that AvrBs2 and XopJ3 are dominant elicitors of immune signaling in this host–pathogen interaction.
To test the genetic basis of recognition, the authors created S. americanum lines with concomitant edits at the loci corresponding to Bs2 and ZAR1 immune receptors. The edited line is referred to as SP2273-bz. Editing these receptor loci allowed functional interrogation of whether recognition of specific effectors depends on the corresponding receptor genes in the host.
Genetic complementation of the SP2273-bz edited line established the specific pairing of effectors and receptors. Complementation data confirmed that the four SaBs2 homologs present in S. americanum specifically recognize AvrBs2, while SaZAR1 mediates recognition of XopJ3. These results map the primary effector–receptor relationships that underlie the dominant ETI responses observed in SP2273.
Functional tests on the characterized SP2273-bz line revealed that X. euvesicatoria growth was enhanced when the host receptors were disrupted, indicating that both AvrBs2 and XopJ3 are required for restraining bacterial multiplication in S. americanum. This finding supports the conclusion that recognition of these effectors by SaBs2 and SaZAR1 is biologically relevant for limiting pathogen success on the wild host.
The study provides a clear framework linking specific effector molecules from X. euvesicatoria to corresponding immune receptors in S. americanum that collectively produce strong ETI. Identification of primary drivers (AvrBs2 and XopJ3) and their cognate receptors (SaBs2 homologs and SaZAR1) supplies candidate genes and molecular pairs that could be leveraged for breeding or engineering disease resistance in cultivated solanaceous crops. The multi-effector recognition model also highlights the potential advantage of deploying multiple resistance genes to achieve durable protection.
The abstract reports experimental findings, accession identifiers (SP2273 and SP2273-bz), lists of contributing T3Es, and conclusions about effector–receptor specificity and effects on bacterial growth. However, the abstract does not report full experimental protocols, quantitative values, statistical analyses, or detailed methods for screening, editing, complementation assays, and pathogen growth measurements. Those procedural and numerical details were not reported in the abstract and require consultation of the full preprint for replication or deeper evaluation.