SPEECHLESS and MUTE Mediate Feedback Regulation of Signal Transduction during Stomatal Development

Stomatal density, spacing, and patterning greatly influence the efficiency of gas exchange, photosynthesis, and water economy. They are regulated by a complex of extracellular and intracellular factors through the signaling pathways. After binding the extracellular epidermal patterning factor 1 (EPF1) and 2 (EPF2) as ligands, the receptor-ligand complexes activate by phosphorylation through the MAP-kinase cascades, regulating basic helix-loop-helix (bHLH) transcription factors SPEECHLESS (SPCH), MUTE, and FAMA. In this review, we summarize the molecular mechanisms and signal transduction pathways running within the transition of the protodermal cell into a pair of guard cells with a space (aperture) between them, called a stoma, comprising asymmetric and symmetric cell divisions and draw several functional models. The feedback mechanisms involving the bHLH factors SPCH and MUTE are not fully recognized yet. We show the feedback mechanisms driven by SPCH and MUTE in the regulation of EPF2 and the ERECTA family. Intersections of the molecular mechanisms for fate determination of stomatal lineage cells with the role of core cell cycle-related genes and stabilization of SPCH and MUTE are also reported.

Automated summary

Stomatal density, spacing, and patterning play a crucial role in gas exchange efficiency, photosynthesis, and water economy, regulated by a complex of extracellular and intracellular factors through signaling pathways. The activation of receptor-ligand complexes via MAP-kinase cascades regulates bHLH transcription factors and epidermal patterning factors, influencing stomatal transition and guard cell formation. The feedback mechanisms involving bHLH factors and the regulation of EPF2 and the ERECTA family are not fully understood yet, requiring further investigation.