Stem-cell-triggered immunity through CLV3p–FLS2 signalling

Abstract
The plant stem cells in the shoot apical meristem provide a self-renewable reservoir for leaf, stem and flower organogenesis and are generally protected against stresses and disease. The molecular basis of this immunity has now been discovered. The CLV3 peptide (CLV3p) signal — which is secreted by stem cells in the Arabidopsis shoot apical meristem and which normally controls stem-cell homeostasis through CLV1 and CLV2 receptors — also triggers innate immune signalling through the bacterial flagellin peptide receptor kinase FLS2. The CLV3p–FLS2 signalling acts independently from the stem-cell signalling pathway. These findings suggest co-evolution in peptide–receptor signalling for development and immunity. Stem cells in the shoot apical meristem (SAM) of plants are the self-renewable reservoir for leaf, stem and flower organogenesis1,2. In nature, disease-free plants can be regenerated from SAM despite infections elsewhere, which underlies a horticultural practice for decades3. However, the molecular basis of the SAM immunity remains unclear. Here we show that the CLAVATA3 peptide (CLV3p), expressed and secreted from stem cells and functioning as a key regulator of stem-cell homeostasis in the SAM of Arabidopsis1,2,4, can trigger immune signalling and pathogen resistance via the flagellin receptor kinase FLS2 (refs 5, 6). CLV3p–FLS2 signalling acts independently from the stem-cell signalling pathway mediated through CLV1 and CLV2 receptors1,2,4, and is uncoupled from FLS2-mediated growth suppression5,6. Endogenous CLV3p perception in the SAM by a pattern recognition receptor for bacterial flagellin, FLS2, breaks the previously defined self and non-self discrimination in innate immunity6,7. The dual perception of CLV3p illustrates co-evolution of plant peptide and receptor kinase signalling for both development and immunity. The enhanced immunity in SAM or germ lines may represent a common strategy towards immortal fate in plants and animals1,2,8.