Figure 7.

model illustrating how RFO1 functions at the plasma membrane.

(A) Pectin secreted to the cell wall is heavily methyl- and acetyl-esterified. RFO1 acts as a sensor of the methyl-esterification level of pectins.

(B) When the ratio of mPectin/dmPectin increases at the cell wall, as observed in plants overexpressing PMEI (PMEIox) or during EGCG treatment, RFO1 increases its dwell time at the PM and triggers BR signaling to cause reduced plant growth. RFO1 may be part of the BRI1-BAK1 complex in this signaling process (dashed double arrow).

(C) When the ratio of mPectin/dmPectin is low, as observed during F. oxysporum (Fo) infection or exogenous dmPectin treatment, RFO1 might release signaling partner(s), such as WAK2 (dashed), to increase MAPK activation and downstream expression of defense-related genes. In the absence of RFO1, those potential signaling partners (i.e., WAK2) are constitutively free of RFO1-mediated repression, leading to increased basal levels of MAPK phosphorylation. RFO1 sensing of mPectin/dmPectin ratio is required to upregulate the MAPK signaling cascade and thereby activate defense responses. BAK1 liberation from BRI1 after F. oxysporum infection is required for plant defense against this pathogen and might enable direct or indirect association of BAK1 with RFO1 (dashed double arrow).