Fig. 2.

Overview of CWI signaling components, their interactions and coordination between CWI and PTI signaling. Mechanical distortion of the CW induces CWI responses through THE1 and leads to production of elicitor peptides PEP1 and PEP3, which can suppress CWI responses and growth via PEPR1/2 (represented here by PEPR1) [198]. In parallel to mechanical distortion, the action of THE1 can be regulated by RALF34, which binds to THE1 at high apoplastic pH, leading to further alkalinisation of the apoplast [233]. THE1 activates CWI responses via MCA1 and FEI2 and NIA1 NIA2-dependent processes, which repress growth actively [198]. RALF1 and RALF23 induce alkalinization of the apoplast in a FER-dependent manner [247, 250]. Both of them also affect hormone signaling pathways through FER: RALF23 by inhibiting the de-stabilizing effect of FER on the transcription factor MYC2, a master regulator of JA signaling; RALF1 by activating ABI2, a repressor of ABA signaling [247–249]. In addition, RALF23 has been shown to inhibit FER’s scaffold activity for pattern-recognition receptors (PRR) and their co-receptor BAK1, thus reducing sensitivity of the plant to respective PAMPs [232]. In addition to being involved in chemical signaling through PAMPs, RALFs and phytohormones, FER is capable of sensing physical signals from the CW, possibly through LRX proteins linking FER to CW [234]. Brown bars represents the cell wall (CW), grey bars represent the plasma membrane (PM). The white space in between the CW and PM represents the CW–PM interphase, where solutes can diffuse freely and changes in the mechanical forces are being sensed. Abbreviations are explained in main text