Stomatal development in Arabidopsis. (A) Cell transitions and key regulatory pathways within the stomatal lineage. In the developing epidermis of photosynthetic tissues, an undifferentiated protodermal cell adopts a meristemoid mother cell (MMC, purple) identity and undergoes an asymmetric cell division (ACD), giving rise to a meristemoid (cyan). This initial step is directed by SPCH-SCRM protein heterodimers, which amplify their own expression while inducing the inhibitory secreted signals EPF2 and TMM. Signal transduction via ER family proteins and MAPKs, in turn, inhibits SPCH-SCRM, preventing neighboring cells from adopting a stomatal identity. The meristemoid reiterates ACDs, renewing itself and amplifying the surrounding stomatal-lineage ground cells (SLGCs, gray). A MUTE-SCRM module drives a meristemoid-to-guard mother cell (GMC, light green) transition, which terminates the stem cell-like state. EPF1 peptides, which signal via ERL1, TMM and the stomatal MAPK cascade, inhibit differentiation. The same pathway enforces the orientation of a secondary ACD of an SLGC, known as asymmetric spacing division. The transition from GMC to guard cell (GC, green) is specified by the FAMA-SCRM module. The MAPK cascade also promotes this step, although the upstream signal is unknown. FAMA and two paralogous MYB proteins, FLP and MYB88, restrict the GMC symmetric division by repressing cell cycle regulators such as CDKB1;1 and CYCA2. (B) The loss or gain of function of key stomatal regulators can alter epidermal cell patterning. Shown are false-colored confocal microscope images of developing Arabidopsis epidermis from wild-type plants (left), spch mutants (middle) and scrm-D mutants (right). In spch mutants [as well as in scrm scrm2 mutants, and in the case of EPF2-overexpression (OX) or constitutively active (CA) MAPK signaling], the epidermis is composed solely of pavement cells. Conversely, in scrm-Dmutants [and in the case of MUTE overexpression (OX) and dominant-negative (DN) MAPK signaling], the epidermis is entirely composed of stomata. Cyan, meristemoids; light green, GMCs; green, GCs. Images are modified from Horst et al. (2015).
Lineage-specific stem cells, signals and asymmetries during stomatal development.
by Han S. K., Torii K. U. (2016)
, Keiko U. Torii,
Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USADepartment of Biology, University of Washington, Seattle, WA 98195, USA
in Development 143: 1259-1270. [PubMed Abstract] –
http://dev.biologists.org/content/143/8/1259
A model for guard cell maintenance by epigenetic mechanisms. (A) In the mature guard cells (GCs) of wild-type plants, stomatal lineage genes are terminally turned off. In this context, FAMA physically interacts with RBR via its LxCxE motif, which might recruit a PRC2 complex that deposits H3K27me3 marks (red circles) to give rise to a repressive chromatin state. (B) When a GFP FAMA transgene or mutant FAMA lacking the LxCxE motif is introduced, stomatal lineage genes re-initiate their expression in mature GCs. In this case, RBR and the repressive complex are no longer recruited to target loci. As such, the chromatin state remains open, thereby resetting the stomatal differentiation program resulting in a stoma-in-stoma (SIS) phenotype. Confocal image in B was provided courtesy of Dr Eunkyoung Lee (University of British Columbia, Canada).
Abstract
Stomata are dispersed pores found in the epidermis of land plants that facilitate gas exchange for photosynthesis while minimizing water loss.
Stomata are formed from progenitor cells, which execute a series of differentiation events and stereotypical cell divisions. The sequential activation of master regulatory basic-helix-loop-helix (bHLH) transcription factors controls the initiation, proliferation and differentiation of stomatal cells.
Cell-cell communication mediated by secreted peptides, receptor kinases, and downstream mitogen-activated kinase cascades enforces proper stomatal patterning, and an intrinsic polarity mechanism ensures asymmetric cell divisions. As we review here, recent studies have provided insights into the intrinsic and extrinsic factors that control stomatal development. These findings have also highlighted striking similarities between plants and animals with regards to their mechanisms of specialized cell differentiation.
The integration of environmental and hormonal signals during stomatal development. During stomatal development, EPF peptides are perceived by ER family (green) and TMM (dark green) receptor complexes, which also include a receptor mediator BAK1 (gray). The actual architecture of these receptor complexes is unknown. The signal is mediated via a MAPK cascade (orange), involving YDA, MKK4/5 and MPK3/6, that inhibits SPCH-SCRM via direct phosphorylation. Signaling via the plant steroid hormone brassinosteroid (BR) is mediated by the ligand-triggered heterodimerization of BRI1 (light green) and BAK1 (gray), which activates the BSU1 phosphatase that inhibits BIN2, a downstream negative regulator of BR signaling. BIN2 inhibits not only the BR downstream TFs BZR1 and BES1, but also YDA, MKK4/5 and SPCH to modulate stomatal development. Pathogen effector signaling, via AvrPtO and HopAI1 (marine blue), probably interferes with stomatal development by suppressing the activities of BAK1 and MPK3/6, respectively. Light, auxin and CO2 induce or suppress STOMAGEN or EPF2, thereby altering the balance of positive and negative signals instructing stomatal differentiation. For example, elevated CO2 induces the expression of CRSP, a protease that cleaves the EPF2 prepeptide. Light signals perceived by phytochrome (PHY) and cryptochrome (CRY) photoreceptors probably attenuate the stomatal MAPK cascade acting via COP1.
The intrinsic and extrinsic control of polarity within the stomatal lineage. (A) In wild-type (wt) meristemoids (light cyan), BASL (orange) accumulates in the nucleus. Prior to asymmetric cell division (ACD), a fraction of BASL translocates to the cell cortex at the distal end of the cell. After the ACD, BASL stays in the nucleus of the meristemoid, which eventually expresses MUTE (cyan) and differentiates into a stomata. In the sister SLGC, BASL stays localized at the cell cortex, and this leads to high MAPK activity, loss of stomatal precursor state, and eventual differentiation to a pavement cell. In basl mutants, meristemoids occasionally produce two daughter cells of the same fate; this can be termed a symmetric cell division (SCD). Here, both daughter cells express MUTE (cyan) and hence differentiate into stomata. The confocal microscopy image shows a meristemoid preceding the ACD. BASL-GFP (orange) fusion protein is detected both in the nucleus and at the cell-cortex of the future SLGC. The confocal image was provided courtesy of Dr Juan Dong (Rutgers University, NJ, USA). (B) Extrinsic signals influence BASL dynamics. In wild-type plants, prior to an asymmetric spacing division, BASL protein (orange) switches its polar localization within the SLGC (gray), which re-acquires a meristemoid mother cell (MMC) fate. This ensures that the secondary meristemoid (cyan) forms at least one cell apart from the pre-existing stoma (one-cell spacing rule). In epf1 or tmmmutants, this polarity switch is abrogated, resulting in mis-orientation of the spacing division and, consequently, stomatal clustering.
PLANT STOMATA ENCYCLOPEDIA 
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