Coronatine Induces Stomatal Reopening by Inhibiting Hormone Signaling Pathways

Abstract

Coronatine (COR), a phytotoxin, aids Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) invasion by suppressing stomatal immunity, thus promoting bacterial replication. COR also promotes disease development, increases disease resistance in non-infected plant parts, suppresses cell wall defenses, and delays the hypersensitive response. Moreover, COR inhibits stomatal closure by influencing reactive oxygen species (ROS) synthesis, by NADPH oxidases RBOHD/F, which highlights the role of NADPH oxidases in guard cell signaling. Plant resistance to Pst DC3000 is dependent on guard cell-specific mitogen-activated protein kinases (MAPKs) that function downstream of ROS in salicylic acid (SA) and abscisic acid (ABA)-mediated stomatal closure. COR inhibits the ABA signal transduction pathway in guard cells, which is linked to pathogen-associated molecular pattern (PAMP)-induced stomatal closure. Furthermore, COR uses the plant jasmonate (JA) receptor coronatine-insensitive 1 (COI1) to activate multiple NAC transcription factors, which then regulate SA metabolic genes, preventing the accumulation of SA. In this review, we highlight the negative impact of COR on ROS production, SA and ABA signaling transduction, and consequently stomatal immunity. We believe that the inhibitory effects of COR on SA and ABA-induced stomatal closure require substantially more research to fully understand the stress adaptation mechanisms of plants.