A regulatory network promotes apoplastic alkalinization to prime plant immunity in tissues distal to site of infection

 Highlights

• Bacteria trigger extracellular alkalinization to prime defenses in uninfected tissues

• CPKs phosphorylate and inhibit plasma membrane proton pumps to induce alkalinization

• Alkaline pH sensitizes perception and production of the phytocytokines Peps and SCOOPs

• Phytocytokines and alkalinization jointly propagate to promote cell-cell communication

Summary

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.

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https://www.sciencedirect.com/science/article/pii/S0092867426001145