Antagonistic peptides and stomatal patterning

 

Competitive binding of antagonistic peptides fine-tunes stomatal patterning

by Lee J. S., Hnilova M., Maes M.Lin Y.-C. L.Putarjunan A.Han S.-K.Avila J.,Torii K. U. (2015)

in Nature 522,439–443(25 June 2015) doi:10.1038/nature14561

nature14561-f2
Figure 2: STOMAGEN overexpression on stomatal development in tmm hypocotyl epidermis with combinatorial loss-of-function in ER-family genes. – a–h, Representative confocal microscopy images of hypocotyl epidermis from 10-day-old light-grown transgenic Est::STOMAGEN (oestradiol-induced STOMAGEN) seedlings of tmm (a, b); tmm er (c, d); tmm erl1 erl2 (e, f); and tmm er erl1 erl2… – http://www.nature.com/nature/journal/v522/n7557/carousel/nature14561-f2.jpg

Abstract

During development, cells interpret complex and often conflicting signals to make optimal decisions. Plant stomata, the cellular interface between a plant and the atmosphere, develop according to positional cues, which include a family of secreted peptides called epidermal patterning factors (EPFs). How these signalling peptides orchestrate pattern formation at a molecular level remains unclear.

Here we report in Arabidopsis that Stomagen (also called EPF-LIKE9) peptide, which promotes stomatal development, requires ERECTA (ER)-family receptor kinases and interferes with the inhibition of stomatal development by the EPIDERMAL PATTERNING FACTOR 2 (EPF2)–ER module.

Both EPF2 and Stomagen directly bind to ER and its co-receptor TOO MANY MOUTHS. Stomagen peptide competitively replaced EPF2 binding to ER. Furthermore, application of EPF2, but not Stomagen, elicited rapid phosphorylation of downstream signalling components in vivo.

Our findings demonstrate how a plant receptor agonist and antagonist define inhibitory and inductive cues to fine-tune tissue patterning on the plant epidermis.

Antagonistic peptides fine-tunes stomatal patterning

Photo credit: Nature

Figure 2: STOMAGEN overexpression on stomatal development intmm hypocotyl epidermis with combinatorial loss-of-function in ER-family genes.

Competitive binding of antagonistic peptides fine-tunes stomatal patterning

Lee J. S., Hnilova M., Maes M., Lin Y.-C L., Putarjunan A., Han S.-K., Avila J., Torii K.  (2015)

in Nature 522,439–443(25 June 2015)

http://www.nature.com/nature/journal/v522/n7557/full/nature14561.html

DOI: 10.1038/nature14561

Abstract

During development, cells interpret complex and often conflicting signals to make optimal decisions. Plant stomata, the cellular interface between a plant and the atmosphere, develop according to positional cues, which include a family of secreted peptides called epidermal patterning factors (EPFs). How these signalling peptides orchestrate pattern formation at a molecular level remains unclear.

Here we report in Arabidopsis that Stomagen (also called EPF-LIKE9) peptide, which promotes stomatal development, requires ERECTA (ER)-family receptor kinases and interferes with the inhibition of stomatal development by the EPIDERMAL PATTERNING FACTOR 2 (EPF2)–ER module. Both EPF2 and Stomagen directly bind to ER and its co-receptor TOO MANY MOUTHS. Stomagen peptide competitively replaced EPF2 binding to ER. Furthermore, application of EPF2, but not Stomagen, elicited rapid phosphorylation of downstream signalling components in vivo.

Our findings demonstrate how a plant receptor agonist and antagonist define inhibitory and inductive cues to fine-tune tissue patterning on the plant epidermis.