AHL-producing PGPR biopriming induces endogenous phenolic-rich accumulation associated with the suppression of Pseudomonas syringae infection in Cicer arietinum

Molecular communication plays a critical role in plant-pathogen interactions. Pseudomonas syringae (Psy) infects chickpea ( Cicer arietinum ) by utilizing quorum sensing (QS) to coordinate virulence factors. This study evaluates biopriming as a biological strategy to induce endogenous defence mechanisms. Drawing from previously published in silico evidence [ 1 ] identifying the flavonoid Quercetin as a high-affinity quorum sensing inhibitor (QSI). we evaluated whether specific rhizobacteria could induce endogenous phenolic accumulation. FEG-SEM analysis confirmed successful rhizoplane colonization and the presence of multicellular bacterial aggregates. Using exogenous Quercetin as a positive control, a 32-day pot experiment compared the efficacy of AHL (N-acyl homoserine lactone)-producing PGPR ( Ensifer meliloti and Klebsiella pneumoniae ) against the Psy pathogen. The results indicate a significant priming effect; while the Quercetin control inhibited the pathogen, biopriming with AHL-producing PGPR triggered a superior systemic biochemical defence response. Bioprimed plants challenged with Psy showed improved growth parameters, with shoot lengths reaching 52.3 cm and a 12-fold increase in Total Phenolic Content (~ 987 µg/g). The substantial increase in Phenylalanine Ammonia-Lyase (PAL) activity (271 µ g/min/g ) confirms that rhizobacterial AHL signalling directly activates the host phenylpropanoid pathway, accelerating the accumulation of protective phenolic compounds and phytoalexin precursors to suppress pathogen proliferation. This research demonstrates that AHL-producing PGPR can enhance chickpea resistance by modulating host secondary metabolism and potentially interfering with pathogen quorum sensing.