Figure 2.

Stomatal Development in Arabidopsis.

(A) Schematic diagram of stomatal development. The cell states of stomatal precursors are driven by three paralogous bHLH transcription factors, which likely dimerize with SCRM and SCRM2 as a mechanism for coordinated action. Initial specification of the stomatal cell lineage, in which a protodermal cell becomes a meristemoid mother cell (MMC), is controlled by SPCH. Protodermal cells not entering the stomatal lineage differentiate into pavement cells. The MMC divides asymmetrically to form a meristemoid (M) and SLGC and may reiterate similar divisions several times. MUTE controls the cell-state transition from M to GMC, and FAMA is required for correct division of the GMC into GCs forming a functional stoma. It is proposed that a MAP kinase signaling cascade following putative ligands EPF1 and EPF2 (EPF1 expressed in GMC, light green, and EPF2 expressed in MMC, blue, and M, cyan) perceived by TMM and the ER family of RLKs acts to suppress stomatal identity in cells adjacent to developing stomata; new meristemoids can differentiate at least one cell away, as shown near GMC. An image of wild-type epidermis is shown at the top right.

(B) Epidermal phenotypes of stomatal differentiation mutants. Shown are the rosette leaf epidermis of (from left) scrm scrm2, mute, fama, and scrm-D. scrm scrm2 produces epidermis solely composed of pavement cells, a phenotype identical to that of spch as well as gain-of-function mutants in stomatal cell–cell signaling genes. mute and fama produce epidermis with arrested stomatal precursor cells similar to scrm scrm2/+ and scrm, respectively. scrm-D produces epidermis solely composed of stomata, a phenotype similar to loss of function in stomatal signaling genes. Images are reproduced from Kanaoka et al. (2008).