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CELL BIOLOGY AND SIGNAL TRANSDUCTION

Binding of Arabinogalactan Proteins by Yariv Phenylglycoside Triggers Wound-Like Responses in Arabidopsis Cell Cultures^1,[w]

Department of Botany and Plant Sciences, University of California, Riverside, California 92521

Arabinogalactan-proteins (AGPs) are cell wall proteoglycans and are widely distributed in the plant kingdom. Classical AGPs and some nonclassical AGPs are predicted to have a glycosylphosphatidylinositol lipid anchor and have been suggested to be involved in cell-cell signaling. Yariv phenylglycoside is a synthetic probe that specifically binds to plant AGPs and has been used to study AGP functions. We treated Arabidopsis suspension cell cultures with Yariv phenylglycoside and observed decreased cell viability, increased cell wall apposition and cytoplasmic vesiculation, and induction of callose deposition. The induction of cell wall apposition and callose synthesis led us to hypothesize that Yariv binding of plant surface AGPs triggers wound-like responses. To study the effect of Yariv binding to plant surface AGPs and to further understand AGP functions, an Arabidopsis whole genome array was used to monitor the transcriptional modifications after Yariv treatment. By comparing the genes that are induced by Yariv treatment with genes whose expressions have been previously shown to be induced by other conditions, we conclude that the gene expression profile induced by Yariv phenylglycoside treatment is most similar to that of wound induction. It remains uncertain whether the Yariv phenylglycoside cross-linking of cell surface AGPs induces these genes through a specific AGP-based signaling mechanism or through a general mechanical perturbation of the cell surface.

^[w] The online version of this article contains Web-only data.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.104.039370.

^* Corresponding author; e-mail eugene.nothnagel{at}ucr.edu; fax 909–787–4437.

Received January 16, 2004; returned for revision March 29, 2004; accepted April 3, 2004.

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