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Published on April 24, 2009; 10.1104/pp.109.138099

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Received March 4, 2009
Accepted April 20, 2009

BIN2 Functions Redundantly with Other Arabidopsis GSK3-Like Kinases to Regulate Brassinosteroid Signaling

Zhenyan Yan , Jun Zhao , Peng Peng , Ray K. Chihara , and Jianming Li *

Department of Molecular, Cellular, & Developmental Biology, University of Michigan, Ann Arbor, MI 48109-1048

* Corresponding author; email: jian{at}umich.edu.

Glycogen synthase kinase 3 (GSK3) is a highly conserved serine/threonine kinase involved in a variety of developmental signaling processes. The Arabidopsis genome encodes 10 GSK3-like kinases that are clustered into 4 groups. Forward genetic screens have so far uncovered 8 mutants, all of which carry gain-of-function mutations in BRASSINOSTEROID-INSENSITIVE 2 (BIN2), one of the three members in group II. Genetic and biochemical studies have implicated a negative regulatory role for BIN2 in brassinosteroid (BR) signaling. Here we report identification of 8 EMS-mutagenized loss-of-function bin2 alleles and one T-DNA insertional mutation each for BIN2 and its two closest homologs, BIN2-Like 1 (BIL1) and BIN2-Like 2 (BIL2). Our genetic, biochemical, and physiological assays revealed that despite functional redundancy, BIN2 plays a dominant role among the three group II members in regulating BR signaling. Surprisingly, the bin2bil1bil2 triple T-DNA insertional mutant still responds to BR and accumulates more phosphorylated form of a BIN2 substrate than the wild-type plant. Using a specific GSK3 inhibitor LiCl, we have provided strong circumstantial evidence for involvement of other Arabidopsis GSK3-like kinases in BR signaling. Interestingly, LiCl treatment was able to suppress the gain-of-function bin2-1 mutation but had a much weaker effect on a strong BR receptor mutant, suggesting the presence of a BIN2-independent regulatory step downstream of BR receptor activation.






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