Fig. 1

Model of FER signaling pathways. The FER signaling pathway could be modulated by a 4-layers mechanism. Firstly, the extracellular ligands (RALFs, pectin and PCP-Bs) and ligand combinations (LRXs) could trigger relatively specific FER signal activation. PCP-Bs compete with RALF23/33 to deactivate FER regulated polytubey block and pollen-pistil recognition. RALF4/19 and pectin activate FER mediated pollen tube rupture and salt stress response, respectively. RALF22/23 prefer to interact with cell wall-associated LRXs at acidic pH, and RALF22/23-LRXs complex could be disassociated under salt stress or alkaline conditions to release RALF22/23 and activate FER signaling pathway. Secondly, the diverse co-receptors(ANJ/HERK1, LRE and LLGs) provide diverse perception and responses mode for FER. FER forms a complex with ANJ/HERK1 to sense PCP-Bs and RALF23/33 signals. The FER-RALF4/19-LRE complex was formed upon recognizing RALF4/19 ligands. Moreover, FER form complexes with LLGs to sense pectin and RALFs. The third FER signaling modification layer was compromised of downstream components of FER. NTA, YUC, MYC2, ROP6, PIN2 and PHOT1 are downstream components for FER, which mediate FER regulated pollen tube rupture, IAA biosynthesis, JA response, PC morphogenesis, polar auxin transport and phototropic cell growth, respectively. The FER downstream GEF1/4/10-ROP11-ABI2 pathway was also revealed to regulate ABA response. MRI and RIPK are two RLCKs downstream of FER and RIPK directly interact with TOR to regulate FER related nitrogen starvation response. However, more RLCKs downstream of FER and more pathways downstream of the RLCKs remain to be discovered. Moreover, FER interacts with FLS2 to facilate the formation of FLS2-flg22-BAK1 complex and thus activate FLS2-BIK1-BSU1-MAPKs mediated immunity responses