Editors' ChoicePlant biology

Competing for stomata

See allHide authors and affiliations

Sci. Signal.  30 Jun 2015:
Vol. 8, Issue 383, pp. ec177
DOI: 10.1126/scisignal.aac8741

Stomata are pores on leaves that mediate gas exchange. Two guard cells surround each pore and control the size of the pore to minimize desiccation. The number and distribution of stomata are determined by a complex matrix of cell fate decisions that govern the production of pavement (epidermal) cells and guard cells (see De Vries). Receptor kinases of the ERECTA family, the coreceptor TOO MANY MOUTHS (TMM), and their peptide ligands EPF1 and EPF2 are required for even spacing of stomata in Arabidopsis thaliana. Lee et al. discovered that the peptide EPF-LIKE9 (EPFL9), which is structurally similar to EPF1 and EPF2 and also known as Stomagen, competes with EPF2 for binding to ERECTA. Whereas EPF2 inhibits the formation of stomata, overexpression of EPFL9 increased the density of stomata in a manner that was dependent on ERECTA family kinases. Genetic experiments suggested that EPFL9 antagonized EPF2 signaling through ERECTA in vivo, and in vitro binding assays and coimmunoprecipitation experiments using a transgenic Nicotiana benthamiana expression system confirmed that EPFL9 bound to ERECTA and TMM with affinities similar to those of EPF2. Application of recombinant EPF2 to Arabidopsis seedlings inhibited stomatal development, and simultaneous application of EPFL9 opposed this effect in a concentration-dependent manner. ERECTA stimulates mitogen-activated protein kinase (MAPK) signaling in response to binding EPF2. Whereas application of recombinant EPF2 to Arabidopsis seedlings stimulated phosphorylation of the MAPKs MPK3 and MPK6, application of EPFL9 did not. Thus, EPFL9 competes with EPF2 for binding to ERECTA and TMM, thereby opposing activation of the MAPK pathway and cell fate decisions driven by EPF2. Commentary by De Vries notes that this system is similar to lateral inhibition mechanisms that control fate determination in animal cells and addresses how changes in stomatal patterning might be achieved given that the two peptides bind to ERECTA with comparable affinities.

J. S. Lee, M. Hnilova, M. Maes, Y. L. Lin, A. Putarjunan, S. K. Han, J. Avila, K. U. Torii, Competitive binding of antagonistic peptides fine-tunes stomatal patterning. Nature 522, 439–443 (2015). [PubMed]

S. De Vries, Precision positioning with peptides. Nature 522, 424–425 (2015). [PubMed]