在植物的茎端分生组织（SAM）的干细胞是叶、茎和花等器官形成的自我再生的源头。在自然界中，尽管局部感染，无病植物可从SAM更新，这正是几十年来园艺实践的基础所在。然而SAM免疫性的分子基础仍不清楚。
美国科学家Horim Lee等发现，在拟南芥SAM中，CLAVATA3肽（CLV3p）从茎干细胞表达分泌，其表现的茎干细胞动态平衡关键调节功能可通过鞭毛蛋白受体激酶（FLS2）触发免疫信号和病原体抗性。CLV3p–FLS2信号独立于由CLV1 和CLV2受体介导的茎干细胞通路，并从FLS2 介导的生长抑制中解耦。内源的CLV3p在SAM中的感应是通过细菌鞭毛蛋白FLS2的模式识别受体执行，打破了先天免疫中预先定义的自我与非自我识别。CLV3p的双重识别感应阐明了植物肽与受体激酶信号在发展与免疫中的共进化。在SAM或者生殖系统增强免疫力可能代表了植物与动物永续发展的一个共适的策略。（生物谷Bioon.com）
生物谷推荐原文出处：
Nature (2011) Published online 17 April 2011 doi:10.1038/nature09958
Stem-cell-triggered immunity through CLV3p–FLS2 signalling
Horim Lee,1 Ok-Kyong Chah1 & Jen Sheen1
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.
