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- Title
Receptor-like cytoplasmic kinases of different subfamilies differentially regulate SOBIR1/BAK1-mediated immune responses in Nicotiana benthamiana.
- Authors
Huang, Wen R. H.; Braam, Ciska; Kretschmer, Carola; Villanueva, Sergio Landeo; Liu, Huan; Ferik, Filiz; van der Burgh, Aranka M.; Boeren, Sjef; Wu, Jinbin; Zhang, Lisha; Nürnberger, Thorsten; Wang, Yulu; Seidl, Michael F.; Evangelisti, Edouard; Stuttmann, Johannes; Joosten, Matthieu H. A. J.
- Abstract
Cell-surface receptors form the front line of plant immunity. The leucine-rich repeat (LRR)-receptor-like kinases SOBIR1 and BAK1 are required for the functionality of the tomato LRR-receptor-like protein Cf-4, which detects the secreted effector Avr4 of the pathogenic fungus Fulvia fulva. Here, we show that the kinase domains of SOBIR1 and BAK1 directly phosphorylate each other and that residues Thr522 and Tyr469 of the kinase domain of Nicotiana benthamiana SOBIR1 are required for its kinase activity and for interacting with signalling partners, respectively. By knocking out multiple genes belonging to different receptor-like cytoplasmic kinase (RLCK)-VII subfamilies in N. benthamiana:Cf-4, we show that members of RLCK-VII-6, −7, and −8 differentially regulate the Avr4/Cf-4-triggered biphasic burst of reactive oxygen species. In addition, members of RLCK-VII-7 play an essential role in resistance against the oomycete pathogen Phytophthora palmivora. Our study provides molecular evidence for the specific roles of RLCKs downstream of SOBIR1/BAK1-containing immune complexes. Cell-surface receptors form the front line of plant immunity. Here, the authors show that the RLP co-receptors SOBIR1 and BAK1 directly phosphorylate each other, leading to activation of the immune receptor complex in which RLCKs are differentially required for production of reactive oxygen species that play a role in resistance against Phytophthora palmivora.
- Subjects
RECEPTOR-like kinases; REACTIVE oxygen species; NICOTIANA benthamiana; DISEASE resistance of plants; IMMUNE complexes
- Publication
Nature Communications, 2024, Vol 15, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-024-48313-1