Fig. 1.

Key factors involved in fate determination and leaf epidermal patterning during development. (A) Three trajectories describe the three distinct cell types of the leaf epidermis. The development and size of the shoot apical meristem (SAM) is controlled by the CLAVATA3 (CLV3)-WUSCHEL (WUS)-mediated negative feedback loop. The transcription factor (TF) genes ARABIDOPSIS THALIANA MERISTEM LAYER1 (ATML1) and PROTODERMAL FACTOR2 (PDF2) are expressed in the outermost layer (L1, blue) in the SAM to establish epidermal cell identity. Cells in the L1 layer called protoderms give rise to trichome-initiating cells (yellow), meristemoid mother cells (light blue), and pavement cells (grey). During trichome development, the major TF, GLABRA2 (GL2), drives cells to become polyploid trichome cells; the differentiation state is maintained by endoreduplication. To form a stomate, the master TF, SPEECHLESS (SPCH), initiates asymmetric cell division in a meristemoid mother cell to generate a small meristemoid (green) and a stomatal lineage ground cell (SLGC, white). MUTE then replaces SPCH and commits the cell to becoming a guard mother cell. Subsequently, FAMA in the guard mother cell drives symmetric cell division, resulting in a pair of guard cells. An SLGC can either undergo differentiation to become a pavement cell or divide asymmetrically again to produce another stomate (labelled by a dashed line). To date, no cell-type-specific driving factors have been associated with pavement cell formation. However, pavement cell maturation is often coupled with endoreduplication. (B) The cell–cell communication between trichome and non-trichrome cells relies on TRIPTYCHON (TRY). Before trichome initiation, GL1, GL3, and TRANSPARENT TESTA GLABRA1 (TTG1) form a stable MBW complex to activate GL2 transcription. GL2 accumulation promotes trichome cell fate. Besides GL2, the MBW complex also activates TRY expression in trichome cells. TRY tends to move to the neighbouring non-trichome cell to replace GL1 and disrupt the formation of the MBW complex, thus repressing GL2 and inhibiting the trichome cell fate. (C) Stomatal patterning follows the one-cell-spacing rule, meaning that two stomata never directly contact each other, and this signalling is mediated through peptide-mediated inhibitory signals and polarity establishment during stomatal development. SPCH drives the accumulation of a signalling peptide, EPIDERMAL PATTERNING FACTOR2 (EPF2), in meristemoids. The secreted peptides then bind to members of the receptor-like kinase ERECTA family and the receptor-like protein TMM on the surface of neighbouring cells. The binding triggers a MAPK cascade that phosphorylates and inhibits SPCH activity, thus preventing stomatal fate in these neighbouring cells. The interplay of chemical transduction and the polarity complex consisting of BASL, BREVIS RADIX-LIKE2 (BRXL2), and POLAR is required for asymmetric cell division and serves as a scaffold for recruiting and exerting inhibitory signalling in non-stomatal lineage cells. (D) Pavement cell formation is controlled biochemically by auxin. The high auxin concentration at the lobe initiation site induces the asymmetric accumulation of RHO-RELATED PROTEIN FROM PLANTS (ROP)-ROP-INTERACTIVE CRIB MOTIF-CONTAINING PROTEIN (RIC) in the two pavement cells. For the lobing cell (left), the recruitment of ROP2 and RIC4 helps the formation of actin filaments (F-actin) and further results in the protrusion of the cell. For the indented cell (right), ROP6 and RIC1 stabilise microtubule organisation under parallel direction and further pull the cell, forming an indentation.