Stem-cell-triggered immunity through CLV3p–FLS2 signalling

Abstract

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 enigmatic. Here we show a surprising discovery that the CLAVATA3 peptide (CLV3p), expressed and secreted from the stem cells and functioning as a key regulator of stem cell homeostasis in the Arabidopsis SAM1,2,4, can trigger immune signalling and pathogen resistance via the flagellin receptor kinase FLS25,6. CLV3p-FLS2 signalling acts independently from the stem cell signalling pathway mediated through CLV1 and CLV2 receptors 1,2,4, and is uncoupled from the FLS2-mediated growth suppression5,6. Endogenous CLV3p perception in the SAM by a pattern recognition receptor FLS2 for bacterial flagellin breaks the previously defined self and nonself discrimination in innate immunity 6,7. The dual CLV3p perceptions illustrate 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 toward immortal fate in plants and animals1,2,8.