Phosphorylation-dependent differential regulation of plant growth, cell death, and innate immunity by the regulatory receptor-like kinase BAK1

• Published in: PLoS genetics 2011-04, Vol.7 (4), p.e1002046-e1002046
• Main Authors: Schwessinger, Benjamin, Roux, Milena, Kadota, Yasuhiro, Ntoukakis, Vardis, Sklenar, Jan, Jones, Alexandra, Zipfel, Cyril
• Format: Article
• Language: English
• Subjects: Alleles; Apoptosis; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - immunology; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Biology; Cell Death; Charitable foundations; Cloning, Molecular; Enzymes; Gene Expression Regulation, Plant; Genes; Genetic aspects; Hypocotyl - growth & development; Immunity, Innate; Kinases; Ligands; Medical research; Natural immunity; Phosphorylation; Phosphotransferases; Physiological aspects; Plants, Genetically Modified - genetics; Plants, Genetically Modified - growth & development; Plants, Genetically Modified - immunology; Plants, Genetically Modified - metabolism; Point Mutation; Protein Kinases - genetics; Protein Kinases - metabolism; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism; Proteins; Reactive Oxygen Species - metabolism; Receptors, Pattern Recognition - genetics; Receptors, Pattern Recognition - metabolism; Recombinant Fusion Proteins - metabolism; Regulation; Signal Transduction; Steroids - metabolism; Studies
• ISSN: 1553-7404; 1553-7390; 1553-7404
• DOI: 10.1371/journal.pgen.1002046

Plants rely heavily on receptor-like kinases (RLKs) for perception and integration of external and internal stimuli. The Arabidopsis regulatory leucine-rich repeat RLK (LRR-RLK) BAK1 is involved in steroid hormone responses, innate immunity, and cell death control. Here, we describe the differential regulation of three different BAK1-dependent signaling pathways by a novel allele of BAK1, bak1-5. Innate immune signaling mediated by the BAK1-dependent RKs FLS2 and EFR is severely compromised in bak1-5 mutant plants. However, bak1-5 mutants are not impaired in BR signaling or cell death control. We also show that, in contrast to the RD kinase BRI1, the non-RD kinases FLS2 and EFR have very low kinase activity, and we show that neither was able to trans-phosphorylate BAK1 in vitro. Furthermore, kinase activity for all partners is completely dispensable for the ligand-induced heteromerization of FLS2 or EFR with BAK1 in planta, revealing another pathway specific mechanistic difference. The specific suppression of FLS2- and EFR-dependent signaling in bak1-5 is not due to a differential interaction of BAK1-5 with the respective ligand-binding RK but requires BAK1-5 kinase activity. Overall our results demonstrate a phosphorylation-dependent differential control of plant growth, innate immunity, and cell death by the regulatory RLK BAK1, which may reveal key differences in the molecular mechanisms underlying the regulation of ligand-binding RD and non-RD RKs.