Signaling to stomatal initiation and cell division

Abstract

Stomata are two-celled valves that control epidermal pores whose opening and spacing optimizes shoot-atmosphere gas exchange. Arabidopsis stomatal formation involves at least one asymmetric division and one symmetric division. Stomatal formation and patterning are regulated by the frequency and placement of asymmetric divisions. This model system has already led to significant advances in developmental biology, such as the regulation of cell fate, division, differentiation, and patterning. Over the last 30 years, stomatal development has been found to be controlled by numerous intrinsic genetic and environmental factors. This mini review focuses on the signaling involved in stomatal initiation and in divisions in the cell lineage.

Keywords: cell division; cell fate; development; signaling; stomata.

FIGURE 1

Overview of stomatal development. The stomatal lineage initiates from meristemoid mother cells (MMCs). MMC undergoes asymmetric entry divisions and produces a meristemoid (M) as well as a larger sister cell (termed a stomatal lineage ground cell, SLGC). Meristemoids can undergo asymmetric amplifying divisions before differentiating into a guard mother cell (GMC). SLGCs can differentiate into a pavement cells or reacquire a MMC fate and initiate asymmetric spacing divisions that produce “satellite meristemoids.” Stomatal complexes form after at least one unequal division of a stem cell, and then by a single equal division of a GMC. SPCH, MUTE, FAMA, and FLP/MYB88 are transcription factors that regulate key fate transitions during stomatal development. SCRM and SCRM2 heterodimerize with SPCH, MUTE, and FAMA to promote stomatal–lineage transitions. AGO1 is involved in an AGL16-mediated microRNA post-transcriptional regulatory pathway that blocks asymmetric spacing divisions in SLGCs. ABA might be involved in stomatal initiation and differentiation by repressing SPCH and MUTE. RBR activity is predominantly regulated by CDKA;1. RBR participates in the regulation of asymmetric as well as symmetric divisions.

FIGURE 2

The stomatal signaling pathway. EPF1, EPF2, and STOMAGEN/EPFL9 signals are received by TMM–ERf leading to transduction and the YODA–MKK–MPK cascade. Light regulates stomatal production via COP1 which is upstream of YODA. In stems or hypocotyls TMM dampens CHALf peptide binding with the ERf receptor. BR signals received by BRI1–BAK1 inhibit BIN2 activity. BIN2 suppresses SPCH by directly phosphorylating or indirectly thorough YODA or MKK4/5.