Fig. 7.

Working model for NIK1 roles in FLS2 signalling pathway and flg22-induced translational control of NIK1 signalling. (I) At the resting stage, NIK1 associates with FLS2 or BAK1 to prevent autoimmunity without pathogens invasion. (II) Upon bacterial infection, flg22 is perceived by the immune receptor FLS2, which induces the heterodimerization with BAK1, also including RLCK BIK1 and its homologues. Phosphorylation events initiates the immune signalling, and BIK1 is released from the membrane to activate downstream signal. (III) During signalling transduction, BAK1 may phosphorylate NIK1 on Thr474 residues. Phosphorylated NIK1 leads to activation of an antiviral signal through RPL10 phosphorylation and suppression of translational machinery-related gene expression. (IV) At signalling attenuation stage, phosphorylated NIK1 exhibits higher affinity to FLS2 and BAK1, and these interactions may lead to receptor complex instability or disassembly, followed by FLS2 ubiquitination and degradation