This study compares the ability of the cytokinin (CK) trans ‐zeatin ( t Z) and the CK sugar conjugate 6‐(3‐methoxybenzylamino)purine‐9‐arabinoside (BAPA) to induce resistance against the bacterial pathogen Pseudomonas syringae in Arabidopsis thaliana . Treatment with either t Z or BAPA significantly reduced bacterial growth after a later infection. This chemically induced resistance (IR) required the CK receptor AHK3, highlighting its critical role in mediating resistance by t Z and BAPA. This is remarkable as these compounds show either high or no affinity for this CK receptor, respectively. Surprisingly, t Z, but not BAPA, induced the expression of CK response genes, including ARR5 , suggesting divergent mechanisms of action. Resistance caused by both compounds was abolished in the npr1 mutant, underpinning the functional relevance of the salicylic acid (SA) signalling pathway. Transcriptomic analysis showed that both BAPA and t Z triggered the expression of distinct sets of genes associated with SA and reactive oxygen species (ROS) but not with jasmonic acid (JA) signalling. BAPA and, to a lesser extent, also t Z activated pattern‐triggered immunity (PTI) signalling genes, including genes responsible for PTI signal amplification ( PREPIP2 ) and pathogen‐associated molecular pattern (PAMP) signalling ( PH1 , IDL6 ). This supported the hypothesis that the PTI pathway mediates the protective effect. Similarities and differences of chemically triggered IR by t Z and BAPA, as well as their potential for application, are discussed.
