A regulatory network promotes apoplastic alkalinization to prime plant immunity in tissues distal to site of infection
Hongze Wang, Xiuming Li, Keran Zhai, Jack Rhodes, Tian Sang, Jiwen Zhao, Yong Gao, Shengwei Ma, Beibei Song, Qing Pan, Meijuan Hu, Peiyong Xin, JinFang CHU, Pengcheng Wang, Cyril Zipfel, Jian-Min Zhou
Abstract
Immune activation in plants triggers extracellular alkalinization, presumably by inhibiting plasma membrane H + -ATPases. The precise role and underlying mechanisms of this process remain poorly understood. Here, we show that Pseudomonas syringae bacteria induce apoplastic alkalinization not only at the site of infection but also in neighboring distal tissues to prime defenses and disease resistance in Arabidopsis . We show that several calcium-dependent protein kinases phosphorylate Ser899 of two major autoinhibited H + -ATPases to dampen their activity, leading to alkalinization. The distal alkalinization is accompanied by the transcriptional activation of phytocytokines, including plant elicitor peptides, serine-rich endogenous peptides, and their receptors. We show that these phytocytokines promote distal alkalinization and disease resistance, whereas the apoplastic alkalinization sensitizes the phytocytokine perception that further induces phytocytokine genes. Our study suggests that apoplastic alkalinization and phytocytokine gene expression mutually potentiate and act as a combined signal that propagates in local-distal communication and disease resistance priming.