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Sci. STKE, 9 May 2006
Vol. 2006, Issue 334, p. tw155
[DOI: 10.1126/stke.3342006tw155]

EDITORS' CHOICE

PLANT HORMONES Departing from the Wnt Model

Brassinosteroids (BRs), plant steroid hormones involved in growth and development, signal through a cell surface receptor (BRI1) and a glycogen synthase kinase-3 (GSK-3)-type kinase (BIN2) to activate the BES1 and BRZ1 transcription factors. This scheme resembles that of the canonical Wnt pathway, and current models of BR signaling have proposed that BIN2 regulation of BES1 and BRZ1 echoes GSK-3 regulation of β-catenin in Wnt signaling. Thus, the cytoplasmic phosphorylation of BES1 and BRZ1 by BIN2 would lead to their destruction in the absence of BR, whereas BR signaling would promote their stabilization and translocation to the nucleus. Vert and Chory found that, although Arabidopsis expressing a BIN2 loss-of-function allele had an essentially normal phenotype, plants lacking the three group II GSK3-type kinases showed increased abundance of dephosphorylated BES1 and a phenotype consistent with constitutive BR signaling. Experiments involving fusion proteins consisting of wild-type BIN2 or a gain-of-function mutant (bin2) tagged with green fluorescent protein (BIN2-GFP or bin2-GFP, respectively) showed that BIN2-GFP was present in the nucleus as well as the cytoplasm and that bin2-GFP was mostly in the nucleus. Moreover, plants expressing a bin2 fusion protein containing a heterologous nuclear export signal showed a less extreme phenotype than those expressing bin2 alone. Although treatment with a BR promoted BES1 dephosphorylation, treatment with a BR or with a BR inhibitor affected neither BES1 abundance nor localization of BES1-GFP (which was constitutively nuclear). Rather, phosphorylation by BIN1 inhibited BES1's ability to bind DNA and its transcriptional activity. This suggests an alternative model for BR signaling that involves regulation of BES1's DNA-binding activity rather than its abundance or localization.

G. Vert, J. Chory, Downstream nuclear events in brassinosteroid signalling. Nature 441, 96-100 (2006). [PubMed]

Citation: Departing from the Wnt Model. Sci. STKE 2006, tw155 (2006).


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