The CLAVATA signaling pathway mediating stem cell fate in shoot meristems requires Ca2+ as a secondary cytosolic messenger

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CLAVATA1 (CLV1) is a receptor protein expressed in the shoot apical meristem (SAM) that translates perception of a non-cell-autonomous CLAVATA3 (CLV3) peptide signal into altered stem cell fate. CLV3 reduces expression ofWUSCHEL(WUS) andFANTASTIC FOUR 2(FAF2) in the SAM. Expression ofWUSandFAF2leads to maintenance of undifferentiated stem cells in the SAM. CLV3 binding to CLV1 inhibits expression of these genes and controls stem cell fate in the SAM through an unidentified signaling pathway. Cytosolic Ca2+ elevations, cyclic nucleotide (cGMP)-activated Ca2+ channels, and cGMP have been linked to signaling downstream of receptors similar to CLV1. Hence, we hypothesized that cytosolic Ca2+ elevation mediates the CLV3 ligand/CLV1 receptor signaling that controls meristem stem cell fate. CLV3 application to Arabidopsis seedlings results in elevation of cytosolic Ca2+ and cGMP. CLV3 control ofWUSwas prevented in a genotype lacking a functional cGMP-activated Ca2+ channel. In wild-type plants, CLV3 inhibition ofWUSandFAF2expression was impaired by treatment with either a Ca2+ channel blocker or a guanylyl cyclase inhibitor. When CLV3-dependent repression ofWUSis blocked, altered control of stem cell fate leads to an increase in SAM size; we observed a larger SAM size in seedlings treated with the Ca2+ channel blocker. These results suggest that the CLV3 ligand/CLV1 receptor system initiates a signaling cascade that elevates cytosolic Ca2+, and that this cytosolic secondary messenger is involved in the signal transduction cascade linking CLV3/CLV1 to control of gene expression and stem cell fate in the SAM.

Significance Statement

In the shoot apical meristem, stem cell fate is controlled by the CLAVATA3 ligand binding to the CLAVATA1 receptor kinase, subsequently affecting the activity of transcription factors such as WUSCHEL. However, the signal transduction cascade from the plasma membrane-localized receptor and the downstream transcription factors is not fully defined. Here we show that CLV3 application elevates cytosolic Ca2+; thus implicating cytosolic Ca2+ as a key secondary messenger in the signal transduction cascade.

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