Nature 522, 439–443 (2015)

Credit: NATURE

Stomata are microscopic pores on the plant epidermis that mediate gas exchange while minimizing water loss. Genetic studies have identified a peptide from the epidermal pattern factor family, EPF2, that represses stomatal development and an EPF-like peptide, STOMAGEN, that promotes stomatal development. EPF2 is secreted from the stomatal lineage cells and interacts with the ERECTA (ER) family of leucine-rich repeat receptor kinases (ER, ERL1 and ERL2) and the co-receptor TOO MANY MOUTHS (TMM), which are expressed in the surrounding cells. This activation of these receptors was thought to prevent the ectopic formation of stomata. STOMAGEN is secreted by cells underlying the epidermis, but the mechanism by which STOMAGEN promotes stomatal development was still unclear. One possibility was that STOMAGEN and EPF2 might compete for access to the ER family of receptors. To test this model, Lee et al. performed a series of genetic experiments and found that overexpression of STOMAGEN, which normally increases stomatal number, retained activity unless all ER receptors were mutated, suggesting that STOMAGEN required the ER receptors for activity. Consistent with this, co-immunoprecipitation experiments revealed that STOMAGEN directly interacts with all ER receptors and TMM. The authors used a quartz crystal microbalance (QCM) biosensor platform to examine STOMAGEN and EPF2 binding to ER and TMM and found that both peptides bound to each receptor with similar affinity. The authors confirmed the theory that STOMAGEN and EPF2 might compete for access to ER by showing that increasing the amounts of STOMAGEN relative to EPF2 blocked EPF2-ER binding and reduced EPF2-mediated inhibition of stomatal development. These findings should inspire further studies to determine whether changes in ligand concentration or receptor sensitivity dictate stomatal formation during plant development.