top of page

The Mechanisms of Stomatal Development

In the typical dicot plant, Arabidopsis thaliana, stomata are formed via a series of stereotypical cell divisions and cell-state transitions. Stomatal progenitor cells emerge from a subset of protodermal cells as meristemoid mother cells (MMCs). An MMC undergoes an asymmetric entry division, giving rise to a meristemoid and its sister cell named a stomatal-lineage ground cell (SLGC). Meristemoids possess a stem cell-like character and reiterate asymmetric amplifying divisions, thereby maintaining the meristemoid while producing additional surrounding SLGCs. After a few rounds of asymmetric cell divisions (ACDs), meristemoids lose their stem cell-like potential and differentiate into round guard mother cells (GMCs), which divide symmetrically and terminally differentiate into paired guard cells (GCs) that surround a pore. As plant leaves expand, young SLGCs may re-establish MMC identity and undergo asymmetric spacing division to form satellite (secondary) stomata. This occurs away from the existing stoma so that the two stomata are spaced by at least one cell, a phenomenon known as the ‘one-cell spacing rule’. The rest of the cells in the epidermis differentiates into pavement cells, which protect plants from desiccation, pathogen invasion and other environmental insults.

Stomata_diagram_2019_wix-fin.jpg

Over the past decade, several key regulators of Arabidopsis stomatal development have been identified. Together these findings have revealed that the cell fate transitions within the stomatal lineage are directed by the sequential actions of three master regulatory basic-helix-loop-helix (bHLH) transcription factors (TFs) - SPEECHLESS (SPCH), MUTE and FAMA - that drive the initiation, proliferation and differentiation of stomatal precursor cells. The complete loss of function in SPCH, MUTE, and FAMA results in epidermis solely composed of pavement cells, arrested meristemods after extensive ACDs, and 'catapillar'-like tumors of GMCs with excessive symmetric divisions. These bHLHs possess activities as 'master regulators', and their ectopic overexpression confers highly-divided epidermis with excessive stomatal-lineage cells, stomata only epidermis, and epidermis covered with singular guard cells like a fish scales, respectively. These three bHLH proteins heterodimerize with two redundant partners, SCREAM (SCRM; also known as ICE1) and SCRM2 bHLH TFs, that are expressed throughout the stomatal-lineage cells and integrate the three steps of stomatal differentiation.

The proper distribution and density of stomata are enforced by cell-cell signalling . Notably, members of the EPIDERMAL PATTERNING FACTOR (EPF)/EPF-LIKE (EPFL) family of cysteine-rich secreted peptides, which are perceived by three ERECTA (ER)-family leucine-rich repeat receptor kinases (LRR-RK), ER, ER-LIKE1 (ERL1), and ERL2, and a LRR receptor-like protein, TOO MANY MOUTHS (TMM), restrict stomatal development. This involves signalling via an intracellular mitogen activated protein kinase (MAPK) cascade that includes YODA (YDA), MKK4/5, and MPK3/6. The MPK3/6 are recruited directly to the core stomatal bHLH heterodimers via SCRM, allowing direct SPCH phosphorylation and subsequent degradation, leading to inhibition of stomatal cell fate.

The identification of the above key regulators of stomatal development in recent years has moved research into new directions. The study of stomatal development has also revealed intriguing similarities between plants and animals in terms of how they generate specialized cell types, despite these two kingdoms having evolved multicellularity independently.

bottom of page