Stomatal Patterning

Email a friend
Contact the editor about this article
How to cite

Stomatal Patterning

Martin Bringmann, Stanford University, Stanford, California, USA
Dominique C Bergmann, Stanford University, Stanford, California, USA

Published online: September 2013

DOI: 10.1002/9780470015902.a0020125.pub2

Full Article on Wiley Online Library

Abstract
Images
References

Abstract

Stomatal development is a model for understanding the integration of multiple inputs into a simple cell fate choice. Intense research during the past decade has revealed mechanisms that govern stomatal development including inter‐ and intracellular signalling, transcriptional regulation, cell polarisation and asymmetric cell divisions. Recent discoveries in Arabidopsis include conserved families of transcription factors that drive differentiation and morphogenesis in the stomatal lineage. Specific proteins and pathways that mediate the transduction of signals, and thereby contribute to fate decisions such as secreted protein ligands, receptor kinases, mitogen activated protein kinase kinases and light and hormones have also recently been described. Studies in Arabidopsis and maize revealed novel proteins polarised within dividing stomatal lineage precursors. Together, these discoveries set the foundation to untangle mechanisms that lead to pattern and cell fate acquisition in plant systems.

Key Concepts:

Stomata are cellular pores that regulate gas exchange in plant leaves.
Stomatal density and distribution is modulated by the environment and responds to changes in light, CO₂ and humidity.
Stomatal development provides a framework for the understanding of cell fate, cell–cell signalling and cell polarity in plants.
Progression through the stages of stomatal development in Arabidopsis requires a balance of fate promoting transcription factors, and fate and division repressing cell–cell signalling.
Based on genetic studies, plants and animals display considerable conservation in the molecules and mechanisms used for developmental fates, but plant‐specific modules are used to generate physically asymmetric cell divisions that characterise early stomatal development.

Keywords: stomata; guard cells; receptor‐like kinases; MAP kinases; cell signalling; development; asymmetric cell division; bHLH transcription factors; cell polarity

Article Title:	Stomatal Patterning
* Name:
* E-mail:
* Note:

	Figure 1. Stomatal distribution and development in leaves. (a) Environmental factors such as light intensity, humidity and CO₂ abundance influence stomatal density in leaves. (b) Micrograph of the abaxial Arabidopsis leaf epidermis. Arrowheads indicate pairs of guard cells (GCs) forming stomatal pores. According to the ‘one‐cell spacing rule’, stomata are always separated by at least one pavement cell (P). (c) SPCH, MUTE and FAMA are fate determinants that, with their heterodimerisation partners ICE1/SCRM2, drive stomatal development from undifferentiated protodermal cells (top, white) to meristemoid mother cells (MMC, red), to guard mother cells (GMC, yellow) to pairs of GCs (green).
	Figure 2. Diversity of stomatal pattern. (a) Scanning electron micrograph (SEM) image of pine needle, white arrow points to one of many stomata arranged in long files. (b–c) Resin impression of a leaf of a monocot, the ‘spider plant’. (b) Bottom of leaf, white arrow points to one stoma within a highly regular array of stomata positioned between the leaf veins and (c) top of the same leaf lacking any stomata. (d–e) SEM of the top (d) and bottom (e) of a California poppy (dicot) leaf, white arrows point to stomata present on both surfaces. (f) Impression of a developing Arabidopsis leaf epidermis. Arrows in inset (at higher magnification) show stomata obeying the one‐cell spacing rule.
	Figure 3. Signalling cascades integrate inter‐ and intracellular signals to promote certain fate decisions. The secreted peptides EPF1/2 and STOMAGEN bind to membrane bound receptors TOO MANY MOUTHS (TMM, pink) and receptor kinases from the ERECTA family (ERf, blue, green and turquoise). The three members of ER family can potentially interact with each other in several ways; here, one example of different heterodimers is shown. TMM can bind to ERf complexes and regulate their function. On activation, ERf receptors lead to the phosphorylation of the MAPKKK YODA which in turn phosphorylates MKK4/5 which phosphorylates MPK3/6. This cascade inhibits SPCH action and therefore limits meristemoid production. The GSK3β kinase BRASSINOSTEROID INSENSITIVE 2 (BIN2) inhibits YDA, MKK4 and SPCH, a counterintuitive regulation because the MAPKs act oppositely of SPCH, however, such forms of regulation have been seen as fine tuning regulatory responses. The RING E3 ubiquitin ligase CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) integrates light signals and inhibits meristemoid production, presumably through interaction with YODA.