Fig. 1.

Model of trichome cell fate determination in Arabidopsis. GL3 physically interacts with GL1 and TTG1 separately, forming a MYB/bHLH/WD-repeat complex. Three phytohormones (GA, CK, and JA) participate in the control of trichome initiation. GA activates the expression of ZFP5, and then ZFP5 induces GIS (C2H2) expression (green arrows). In addition, ZFP8 (C2H2) and GIS2 (C2H2) are simultaneously activated by ZFP5 and CK (green arrows). The transcription of GL1 is enhanced by C2H2. JA regulates trichome formation by degrading JAZ proteins and then abolishing the interactions of JAZ proteins with bHLH and MYB factors (brown inhibitory line). The MYB/bHLH/WD-repeat complex stimulates trichome formation by activating the expression of its direct targets (SIM and RBR1 as cell cycle regulators, GL2 and TTG2 as transcription factors, and CPC, TRY, ETC1, ETC2, ETC3, and TCL1 as inhibitors). SIM and RBR1 induce trichome differentiation by repressing the expression of cell cycle-related genes, CYCD3;1 and CYCB1;2, which triggers the transition of mitosis to endoreduplication cycles. How GL2 and TTG2 regulate trichome initiation remains uncharacterized. Maybe they also control the expression of cell cycle-related genes (CYC). Inhibitors (represented by the blue rectangle) move to the neighboring cells and substitute GL1 in the complex, resulting in the loss of the activation activity of CYCD3;1 and CYCB1;2 and then leading to mitosis. Note, TTG1 acts upstream of GL3 and GL1, and can activate their transcription (purple arrows); an auto-inhibition was observed for GL3, which can bind to its own promoter (red circle); TRY and TCL1 also participate in the organ-specific control of trichome formation (brown circle). Five phases during cell cycle: M (mitosis), G1 (gap 1), S (synthesis), and G2 (gap 2), endoreduplication (E)