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YODA-Mediated Growth Regulation in Brassinosteroid Signaling Tae-Woo Kim1, Zhi-Yong Wang2, and Tae-Wuk Kim1* 1 Department of Life Science, College of Natural Science, Hanyang University, Seoul 133-791, Korea 2 Department of Plant Biology, Carnegie Institution for Science, Stanford, CA 94305, USA A MAP kinase pathway initiated by YODA MAP kinase kinase kinase (MAP3K) tightly controls stomatal development of Arabidopsis leaf. Loss-of-function mutant of YODA shows extreme stomatal cluster while gain-of-function mutation of YODA (CA-YODA) abolishes stomatal formation. Recent study indicates that brassinosteroid (BR) regulates stomatal development by a GSK3-like kinase BIN2-mediated inhibition of YODA MAP3K. Although homozygous CA-YODA mutant displays severe growth defects including dwarfism, which are most likely due to deficiency of photosynthesis, heterozygote CA-YODA mutant shows promoted stem elongation. This led us to investigate the possibility that YODA MAP3K may regulate cell growth, which is linked to BR signaling. Genetic studies using CA-YODA and YODA overexpression plants showed that activation of YODA strongly suppressed the growth defects of bri1-5 and bin2-1 mutant. Phosphorylation status of BR-responsive transcription factor BZR1 was not altered in CA-YODA mutant. However, we found that MKK4 MAP2K interacted with BZR1 in vivo, suggesting that MKK4 MAP2K phosphorylated by YODA MAP3K might directly regulate BZR1. Our results suggest that BZR1-mediated cell growth is affected by YODA-MKK4 module. *E-mail: [email protected]
