A fast
callose accumulation has been shown to mediate defence priming in certain plant-pathogen interactions, but the events upstream of
callose assembly following chemical priming are poorly understood, mainly because those steps comprise
sugar transfer to the
infection site. β-Amino
butyric acid (BABA)-induced resistance in Arabidopsis against Plectosphaerella cucumerina is known to be mediated by
callose priming.
Indole-3-carboxylic acid (ICOOH, also known as I3CA) mediates BABA-induced resistance in Arabidopsis against P. cucumerina. This indolic compound is found in a common fingerprint of primed metabolites following treatments with various priming stimuli. In the present study, we show that I3CA induces resistance in Arabidopsis against P. cucumerina and primes enhancement of
callose accumulation. I3CA treatment increased
abscisic acid (ABA) levels before
infection with P. cucumerina. An intact ABA synthesis pathway is needed to activate a
starch amylase (BAM1) to trigger augmented
callose deposition against P. cucumerina during I3CA-IR. To verify the relevance of the BAM1
amylase in I3CA-IR, knockdown mutants and overexpressors of the BAM1 gene were tested. The mutant bam1 was impaired to express I3CA-IR, but complemented 35S::BAM1-YFP lines in the background of bam1 restored an intact I3CA-IR and
callose priming. Therefore, a more active
starch metabolism is a committed step for I3CA-IR, inducing
callose priming in adult plants. Additionally, I3CA treatments induced expression of the
ubiquitin ligase ATL31 and
syntaxin SYP131, suggesting that vesicular trafficking is relevant for
callose priming. As a final
element in the
callose priming, an intact Powdery Mildew resistant4 (PMR4) gene is also essential to fully express I3CA-IR.