Priming for enhanced defence responses by specific inhibition of the Arabidopsis response to coronatine

The priming agent β-aminobutyric acid (BABA) is known to enhance Arabidopsis resistance to the bacterial pathogen <i>Pseudomonas syringae</i> pv. <i>tomato</i> (<i>Pst</i>) DC3000 by potentiating salicylic acid (SA) defence signalling, notably <i>PR1</i> expression. The molecular mechanisms underlying this phenomenon remain unknown. A genome-wide microarray analysis of BABA priming during <i>Pst</i> DC3000 infection revealed direct and primed up-regulation of genes that are responsive to SA, the SA analogue benzothiadiazole and pathogens. In addition, BABA was found to inhibit the Arabidopsis response to the bacterial effector coronatine (COR). COR is known to promote bacterial virulence by inducing the jasmonic acid (JA) response to antagonize SA signalling activation. BABA specifically repressed the JA response induced by COR without affecting other plant JA responses. This repression was largely SA-independent, suggesting that it is not caused by negative cross-talk between SA and JA signalling cascades. Treatment with relatively high concentrations of purified COR counteracted BABA inhibition. Under these conditions, BABA failed to protect Arabidopsis against <i>Pst</i> DC3000. BABA did not induce priming and resistance in plants inoculated with a COR-deficient strain of <i>Pst</i> DC3000 or in the COR-insensitive mutant <i>coi1-16</i>. In addition, BABA blocked the COR-dependent re-opening of stomata during <i>Pst</i> DC3000 infection. Our data suggest that BABA primes for enhanced resistance to <i>Pst</i> DC3000 by interfering with the bacterial suppression of Arabidopsis SA-dependent defences. This study also suggests the existence of a signalling node that distinguishes COR from other JA responses.