Molecular mechanisms of ROS burst conferred by protein phosphorylation.

• DOI: 10.3186/jjphytopath.81.1
• Publication Date: 2015-03-24T21:57:34Z
• Authors: H. YOSHIOKA; H. ADACHI; N. ISHIHAMA; T. NAKANO; Y. SHIRAISHI; N. MIYAGAWA; H. NOMURA; M. YOSHIOKA; S. ASAI
• Keywords: Respiratory burst; WRKY protein domain

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 (CDPK), or receptor-like cytoplasmic (RLCK). The pathogen-induced reactive oxygen species (ROS) burst is mainly caused by activation of an NADPH oxidase, designated as respiratory oxidase homolog (RBOH). Emerging evidence emphasizes NbRBOHB could be activated CDPK- RLCK-dependent phosphorylation in association with pattern-triggered immunity (PTI)–ROS burst. On other hand, effector-triggered (ETI)–ROS appears to regulated upregulation via MAPK–WRKY pathway, followed CDPK-mediated phosphorylation.