Figure 12.

A current model for TOPP4 controlling interdigitated PC growth. In wild-type (WT) PCs, PIN kinase and TOPP4 phosphatase regulate PIN1 polarity in the lobes and indentations of PCs. The PIN1 polarity determines auxin flow and establishes auxin gradients in two adjacent PCs. This extracellular auxin in turn activates ROP GTPase signaling through the ABP1-TMK complex to control PC morphogenesis. By contrast, in topp4-1 PCs, dephosphorylation of PIN1 is diminished, causing PIN1 to localize to indentation or nonlobing regions. Thus, the nonpolarity PIN1 reduces auxin accumulation in lobes and neighboring indentations of two adjacent PCs, disturbing the ROP GTPase signaling and causing the PC interdigitation defect (Pietra and Grebe, 2010; Chen and Yang, 2014). +P indicates phosphorylated status, and −P indicates dephosphorylated status. PM, Plasma membrane.