Figure 6. Proposed model for 3D growth in P. patens.

Two possible modes of PpAPB gene regulation have been proposed: (i) PpNOG1 may target PpDEK1 for proteasome-mediated degradation to relieve the repression of PpAPB gene transcription [37]; or (ii) PpNOG1 and PpDEK1 operate independently and antagonistically to degrade a repressor and activator of PpAPB transcription, respectively [40]. In either case, PpAPBs are likely to promote cytokinin biosynthesis, which in turn initiates gametophore apical cell formation. High levels of cytokinin induce PpHCT/PpNOG2 expression, which activates a CLAVATA-dependent auxin response to suppress the cytokinin response and prevent supernumerary gametophore apical cells from being formed. The correct balancing of auxin and cytokinin levels also ensures that division planes within developing gametophores are positioned correctly, a process that is dependent on microtubules, PpTPX2, and subsequently PpTON1. This can also be achieved through concerted assistance from PpCKX1 (which drives local cytokinin degradation). PpCLF and PpFIE are required to maintain the identity of gametophyte apical cells and are thus key regulators of 3D growth. The exocyst probably establishes polarity cues that both dictate apical cell fate and orient the mitotic spindle.