CLAVATA3 peptide signaling from stem cells integrates vascular organization and stem cell maintenance in Arabidopsis shoots
TL;DR
This work shows that the conserved CLAVATA3 peptide (CLV3p)-receptor stem cell signaling pathway represses vascular transcriptional programs in the shoot apical meristem, thereby preventing ectopic vascular differentiation in the stem center, and quantitatively regulates peripheral VB number.
Abstract
Terrestrial plant biomass relies on the formation of vascular bundles (VBs) comprising xylem, cambial, and phloem cells that drive secondary growth and wood formation. How VB formation and organization is coordinated with stem growth remains unclear. Here, we show that the conserved CLAVATA3 peptide (CLV3p)-receptor stem cell signaling pathway represses vascular transcriptional programs in the shoot apical meristem (SAM), thereby preventing ectopic vascular differentiation in the stem center, and quantitatively regulates peripheral VB number. Mutational analysis of conserved CLV3p residues partially uncouples its roles in vascular differentiation from stem cell maintenance. However, overexpression and mutational analysis with key phloem regulators reveals that CLV3p controls vascular and stem cell programs via a DOF (DNA-BINDING WITH ONE FINGER) and SMXL (SUPPRESSOR OF MAX2 1-LIKE) transcriptional module. Our findings identify a novel role for CLV3p signaling in shoot vascular development and establish a regulatory framework integrating stem cell signaling with vascular patterning.