A cell surface O-glycosylated peptide, AGP21, acts on the brassinosteroid pathway and modulates root hair cell fate

Root hairs (RHs) develop from specialized epidermal cells called trichoblasts, whereas epi-dermal cells that lack RHs are known as atrichoblasts. The mechanism controlling root epi-dermal cell fate is only partially understood. Root epidermis cell fate is regulated by a tran-scription factor complex that promotes the expression of the homeodomain protein GLA-BRA 2 (GL2), which blocks RH development by inhibiting ROOT HAIR DEFECTIVE 6 (RHD6). Suppression of GL2 expression activates RHD6, a series of downstream TFs including ROOT HAIR DEFECTIVE 6 LIKE-4 (RSL4 [1] and their target genes, and causes epidermal cells to de-velop into RHs. Brassinosteroids (BRs) influence root epidermis cell fate. In the absence of BRs, phosphorylated BIN2 (a Type-II GSK3-like kinase) inhibits a protein complex that directly downregulates GL2 [2]. Here, we demonstrate that the genetic and pharmacological pertur-bation of the arabinogalactan protein (AGP) AGP21 in Arabidopsis thaliana, triggers aberrant RH development, similar to that observed in plants with defective BR signaling. We reveal that an O-glycosylated AGP21 peptide, which is positively regulated by BZR1, a transcription factor activated by BR signaling, affects RH cell fate by altering GL2 expression in a BIN2-dependent manner. These results indicate that perturbation of a cell surface AGP disrupts BR perception and inhibits the downstream effect of BIN2 on the RH repressor GL2 in root epi-dermal cells. In addition, AGP21 also acts in a BR-independent, AGP-dependent mode that together with BIN2 signalling cascade controls RH cell fate.