期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2016
卷号：113
期号：51
页码：E8326-E8334
DOI：10.1073/pnas.1609626113
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：SignificanceReceptor-like kinase FERONIA (FER) is a versatile regulator of cell growth under both normal and stress environments. FER binds its peptide ligand, rapid alkalinization factor 1 (RALF1), and triggers downstream events to inhibit cell growth in primary roots. However, the mechanism of RALF1 reception by FER is still largely unknown. In this study, we identified a receptor-like cytoplasmic kinase (RPM1-induced protein kinase, RIPK) that directly interacts with and is phosphorylated by FER in a RALF1 peptide-dependent manner. The defects of fer-4 mutant in RALF1 response and root hair development are mimicked by ripk loss-of-function but partially compensated by RIPK overexpression. These and other data suggest that formation of the FER-RIPK complex serves as a crucial step in the RALF1 signaling pathway. A number of hormones work together to control plant cell growth. Rapid Alkalinization Factor 1 (RALF1), a plant-derived small regulatory peptide, inhibits cell elongation through suppression of rhizosphere acidification in plants. Although a receptor-like kinase, FERONIA (FER), has been shown to act as a receptor for RALF1, the signaling mechanism remains unknown. In this study, we identified a receptor-like cytoplasmic kinase (RPM1-induced protein kinase, RIPK), a plasma membrane-associated member of the RLCK-VII subfamily, that is recruited to the receptor complex through interacting with FER in response to RALF1. RALF1 triggers the phosphorylation of both FER and RIPK in a mutually dependent manner. Genetic analysis of the fer-4 and ripk mutants reveals RIPK, as well as FER, to be required for RALF1 response in roots. The RALF1-FER-RIPK interactions may thus represent a mechanism for peptide signaling in plants.
