Plant biology

Protect the Stem Cells

Science Signaling  24 May 2011:
Vol. 4, Issue 174, pp. ec148
DOI: 10.1126/scisignal.4174ec148

Stem cells in the shoot apical meristem (SAM) can remain infection-free even if other parts of the plant are infected. Lee et al. found that in Arabidopsis, the CLAVATA3 peptide (CLV3p), which binds to the receptors CLV1 and CLV2 to limit expansion of the SAM, also activated the pattern recognition receptor FLS2, which detects the bacterial protein flagellin. Signaling through FLS2 activates mitogen-activated protein kinases (MAPKs) and induces the recruitment of the receptor-like kinase BAK1 to FLS2. CLV3p activated MAPKs to a similar extent as flg22 (which comprises the conserved 22–amino acid portion of flagellin), an effect that was not blocked in clv1-1 or clv2-1 mutant plants but was blocked in plants with mutant alleles of fls2. Treatment with CLV3p, but not CLE40p, a peptide related to CLV3p, also induced a similar set of genes as flg22 and promoted the interaction of FLS2 and BAK1. CLV3p interacted with the same leucine-rich repeat domains in FLS2 as flg22, and binding assays suggested that CLV3p and flg22 competed for FLS2 binding. Wild-type seedlings pretreated with CLV3p showed increased general resistance to the pathogenic bacteria Pseudomonas syringae pv. tomato DC3000, whereas the SAM of clv3-2 mutant plants could be infected. RT-PCR analysis of SAM tissues indicated that CLV3p induced genes involved in innate immune signaling in a FLS2-dependent manner and suppressed WUSCHEL (which encodes a homeodomain transcription factor that determines stem cell number) in a CLV1- and CLV2-dependent manner. Thus, in addition to its ability to induce growth arrest in the SAM, CLV3p also activates pathogen defense pathways in the SAM, which the authors liken to a form of “vaccination.”

H. Lee, O.-K. Chah, J. Sheen, Stem-cell-triggered immunity through CLV3p–FLS2 signalling. Nature 473, 376–379 (2011). [PubMed]