Figure 3.

The Phytophthora infestans RXLR effector IPI-O and its putative host cell receptor Arabidopsis LecRK-I.9. (A) Observed changes in Arabidopsis suspension cells upon exposure to IPI-O. The CW–PM continuum (shown as green vertical bars) is disturbed (dotted vertical bars) when IPI-O has an intact RGD motif (left panel) but when RGD is mutated into RGA or RGE the continuum is not disturbed (middle panel; Senchou et al., 2004). Model depicting the membrane-associated LecRK-I.9 in interaction with a putative RGD-containing extracellular ligand (right panel). Under normal circumstances (wild-type) the CW–PM continuum is in a balanced state. (B) Observed changes in the Arabidopsis phenocopy lines 35S-ipiO1 and lecrk-I.9 (top left and right panel, respectively). Both show gain of susceptibility to Phytophthora brassicae (the gray area on the leaf depicts lesion growth) and reduced callose deposition (shown as blue dots at the cell boundaries). Arabidopsis lines expressing ipiO with a mutated RGD motif (35S-ipiO1^RGA or 35S-ipiO1^RGE) behave as the wild-type Col-0 accession (lower left and right panel, respectively); no lesion formation upon infection with P. brassicae (the brown dot represents a hypersensitive response) and efficient callose deposition (Bouwmeester et al., 2011). The model predicts that IPI-O competes with the endogenous ligand of LecRK-I.9 leading to less adhesions between CW and PM, and gain of susceptibility. A mutation in the RGD motif abolishes the competition resulting in a wild-type phenotype. In the absence of LecRK-I.9 the proper balance between endogenous ligand and receptor is disturbed and results in gain of susceptibility.