Fig. 7.

Regulatory network of terminal division of stomatal development. When the meristemoid (M) acquires a GMC fate, CDKA;1 activity is required for G₁ to S transition in the cell cycle. In the loss-of-function cdka;1 mutant or dominant-negative CDKA;1.N146 transgenic lines, an undivided GMC still could acquire a GC fate, resulting in SGCs with 2C ploidy. CDKB1 and CYCA2 are required for the G₂ to M transition phase. In the cdkb1;1 1;2 double mutant or dominant-negative CDKB1;1.N161 lines, the undivided GMCs differentiate into SGCs with 4C ploidy. Mutants of cyca2;234 also produce SGCs with 4C ploidy. CDKA;1, CDKB1;1, and CYCA2 transcription can all be negatively regulated by FLP/MYB88 transcriptional factors through cis-regulatory elements. Expression of CDKA;1 could partially rescue GMC division defects. Overexpression of CYCA2 or CYCD3 also reduces the number of SGCs in CDKB1;1.N161. In flp myb88 and fama mutants, high activity of CDKA;1 and CDKB1 causes excessive GMC divisions. RBR1 is essential to prevent GC subdivision, but the regulatory network of CDK–cyclin–RBR1 and the feedback loop in terminal division remain unclear. (This figure is available in colour at JXB online.)