Being sessile in soil, plants are continuously confronted with threats from their enemies in habitats, including bacteria, fungi, viruses, and insects. During the co-evolutionary arms race with pathogens, plants have developed sophisticated defence machinery to cope with such dangers. Consequently, a comprehensive understanding towards the mechanisms employed by plants may be crucial for improving crop yield and realizing sustainable development in an efficient manner.
Plasma membrane-located Receptor-Like Kinases (RLKs) can perceive conserved microbial signatures and further transduce these dangerous signals across the plant membrane to trigger downstream responses in hosts. Among these RLKs, FERONIA (FER) is the most well-studied member in the Catharanthus roseus RLK 1 (CrRLK1L) family. In addition to its function of plant growth and development, FER has received extensive research interests owing to its emerging roles in regulating the interaction between plants and pathogens.
Catharanthus roseus from Kew on Flikr.FER regulates pathogen perception in multiple species, in different ways.
Pathogens always employ versatile strategies to facilitate their infection and plants have evolved many strategies to detect pathogens before they become a problem. FER has been connected with pathogen perception systems in plants e.g., responding to the well-known bacterial chemical: flagellin. FER is involved in the ligand-induced immune complex formation and promotes the association of FLS2/EFR to its co-receptor BAK1, while RALF23, the ligand of FER, inhibits this process, implying that FER functions as a scaffold, regulating formation of the immune receptor complex (see title figure).
Moreover, FER is also involved in the signalling events in response to fungal invasion. Homozygous fer mutants have higher resistance to Golovinomyces orontii. In contrast, Fusarium oxysporum secretes F-RALF, which binds to FER and blocks AHA2-mediated H+ efflux and elevates the extracellular pH of roots, thus facilitating F. oxysporum infection.
These results suggest differential roles of FER in the battles with pathogens of different lifestyles. Given that endocytic trafficking may contribute to basal resistance, by modulating the abundance of immunity-related RLKs at cell surface, flg22 treatment stimulates lateral diffusion and concomitant endocytosis of FER from the plasma membrane, resembling the stimulated internalization of FLS2. Further elucidation for the intracellular trafficking route of FER and posttranslational modifications on FER during this process may expand our insights into its function.
Interestingly, FER also enriches Pseudomonas fluorescens in the rhizosphere microbiome by modulating reactive oxygen species, while adjusting specialized root microbiome to alleviate phosphate starvation.
This review mainly summarizes advances in understanding the roles of FER in plant-microbe interactions. When mysteries encompassing FER functions are successively unravelled in the near future, we may eventually uncover the veil for this busy goddess.
Zhikun Duan, Wei Liu, Kaiwen Li, Wenwen Duan, Shengwei Zhu, Jingjing Xing, Tong Chen, Xiaomin Luo published this review in Molecular Plant Pathology:
TITLE IMAGE: Various functions of FER in controlling the ligand-induced immune response. The bacterial flagellin (flg22) and elongation factor Tu (elf18) trigger the formation of FLS2-BAK1 and EFR-BAK1 immune complex, further activating downstream immune responses, such as Ca2+ oscillations, NADPH oxidase-induced oxidative burst, and mitogen-activated protein kinase cascades. FER destabilizes the FLS2–BAK1 and EFR–BAK1 immune complex by interacting with RALF23-LLGs, thereby modulating the plant immune response. FER also interacts with RIPK and phosphorylates it, thus regulating the activity of AHA2 and affecting the pH. F-RALF and M-RALFs peptides secreted by Fusarium oxysporium or nematodes can also bind FER and hijack the FER-RALF pathway. In Valsa canker resistance, FER interacts with a hypersensitive reaction (HR)-induced protein HIR1 and disrupts HIR self-interaction. The FER–HIR complex compromises resistance by altering the salicylic acid (SA) level, suppressing polyphenol accumulation and blocking the HIR1-mediated HR. ET, ethylene; JA, jasmonic acid; PCD, programmed cell death; ROS, reactive oxygen species; SA, salicylic acid; TF, transcription factor. All images used with permission of the author.
