Figure 2. The ROP1 signaling network that control pollen tube tip growth.

The network is composed of several pathways coordinately promoting tip-targeted exocytosis and positive and negative feedback loops, which may balance each other to maintain a certain size of the apical ROP1 cap that defines tip growth domain or may allow the oscillation of the ROP1 activity. ROP1 is locally activated in the PM to determine the site of exocytosis and activates multiple pathways leading to polar exocytosis. The RIC4 pathway promotes F-actin assembly and induces the accumulation of exocytic vesicles to the tip, and promotes positive feedback loops to increase the area of active ROP1 probably by targeting ROP1 upstream components such as RopGEFs and PRK2. Positive feedbacks coupled with diffusion rapidly generate the apical cap of active ROP1 that defines the tip growth domain. Meanwhile, ROP1 also activates the RIC3–calcium pathway. RIC3-dependent Ca²⁺ promotes tip F-actin disassembly and facilitates exocytosis. Polar exocytosis is also promoted by another likely ROP1 effector, RIP1/ICR1, which subsequently target recruits the SEC3 exocyst subunit that mediates the tethering of exocytic vesicles on the PM. Polarized exocytosis brings the REN1 RhoGAP to the apical PM, which deactivate PM-localized active ROP1. Thus the REN1-based negative-feedback globally inhibits ROP1, prevents excess ROP1 activation in the apical PM, and restricts the enlargement of the apical cap to the tip growth domain.