Molecular mechanisms of ROS burst conferred by protein phosphorylation.

Abstract

Recent research has illustrated that signaling networks, after the plant host perceives diverse pathogen-derived signals, facilitate defense responses through mitogen-activated protein kinase (MAPK) cascades, calcium-dependent protein kinase (CDPK), or receptor-like cytoplasmic kinase (RLCK). The pathogen-induced reactive oxygen species (ROS) burst is mainly caused by activation of an NADPH oxidase, designated as the respiratory burst oxidase homolog (RBOH). Emerging evidence emphasizes that NbRBOHB could be activated by CDPK- or RLCK-dependent phosphorylation in association with the pattern-triggered immunity (PTI)–ROS burst. On the other hand, the effector-triggered immunity (ETI)–ROS burst appears to be regulated by upregulation of NbRBOHB via the MAPK–WRKY pathway, followed by the activation of NbRBOHB through CDPK-mediated phosphorylation.