Abstract
Summary
In plant development, key receptor kinases are often active in disparate cell types, with each requiring vastly different signalling outputs. The ERECTA (ER) receptor kinase and its homologs ERL1 and ERL2 exemplify this pleiotropy. In Arabidopsis , they influence stomatal patterning, shoot meristem function, ovule morphogenesis, xylem fiber differentiation, and cell division in the vascular cambium 1–6 . Such diverse expression and functionality raises the question of how ER signalling can specify such distinct cell behaviours. One mechanism is via cell-type specific interactions with co-receptors, ligands, or other proteins that modulate signalling. However, little is known about ER interactors in the vascular cambium, a bifacial stem cell niche that generates phloem and xylem ( Figure 1A ). Combinatorial mutations between ER, ERL1 and ERL2 and receptor kinases of a second family, PXY, PXL1 , and PXL2 , show severe cambial defects 5,7 , but the mechanism underpinning these phenotypes is not known. Here we discovered that PXY proteins form protein complexes with ER and ERL2. PXY signalling can be manipulated by altering levels of its cognate ligand, TDIF. In genetic analysis, plant lines in which TDIF levels were altered had dramatic phenotypic changes that required the presence of ER or ERL2. Our results demonstrate that PXY signalling mediated cambium regulation depends on ER signalling and explains ER function in the cambium. Because the cambium produces xylem, which constitutes the wood in vascular plants, our findings position PXY-ER complexes at the centre of the accumulation of this versatile biomaterial and essential carbon sink.
