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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 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.

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Figure 1: CLV3p and flg22 activate similar downstream responses through FLS2.
Figure 2: CLV3p and flg22 share similar perception through FLS2.
Figure 3: CLV3p-mediated SAM arrest and immune signalling are uncoupled from flg22-triggered growth suppression.
Figure 4: CLV3p–FLS2 signalling enhances innate immunity for SAM protection.

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Acknowledgements

We thank T. Laux for the pWUS::GUS line, Y. Matsubayashi for the purified Ara-CLV3 peptide and advice, A. Collmer for the GFP-labelled P. syringae pv. tomato DC3000, L. Shan and P. He for constructs, G. Tena, F. Ausubel, J. Bush, J. Plotnikova and ABRC for mutant seeds and bacterial strains, and Y. Xiong, M. McCormack, Y. Niu, M. Ramon and J. Li for critically reading of the manuscript. Funding was provided by the NSF, NIH and the MGH CCIB fund to J.S.

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H.L. and J.S. initiated the project and designed the experiments; H.L. carried out the experiments and prepared the data with assistance from O.-K.C.; H.L and J.S. wrote the manuscript.

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Correspondence to Horim Lee or Jen Sheen.

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The authors declare no competing financial interests.

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Lee, H., Chah, OK. & Sheen, J. Stem-cell-triggered immunity through CLV3p–FLS2 signalling. Nature 473, 376–379 (2011). https://doi.org/10.1038/nature09958

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