Fig. 6. Model showing the involvement of FERONIA, ADPG1, GalA₃, and WAK in the activation of defense responses following lignin modification.

The model is based on the data in the present paper and in (14). (1) Loss of function of CCR1 results in reduced lignin levels that disrupt lignin/pectin/hemicellulose interactions. (2) The altered wall structure in ccr1 results in release of wall-derived oligosaccharides such as (glucurono)xylan fragments. (3) FERONIA senses pectins or cell wall turgor to transduce the “status” of the cell wall. (4) By sensing the changes to the cell wall resulting from reduced lignin content, FERONIA activates a cytoplasmic signaling pathway that leads to transcriptional activation of a set of cell wall–degrading/modifying enzymes, including pectin lyases and ADPG1. (5 to 7) The cell wall–modifying enzymes partially degrade pectins to directly or indirectly release a range of oligosaccharides; these may come from pectin itself via the action of ADPG1 or pectin lyases or may include other wall components including (glucurono)xylans that are more accessible because of the reduced lignification of the secondary wall. (8) One or more pectic poly-/oligosaccharides are further cleaved by ADPG1 to release smaller OGs including GalA₃. (9) GalA₃ and related OGs are recognized by WAK receptor kinases. (10) WAKs transduce signals for the transcriptional activation of defense response genes such as PR1.