Chemical Genetics Reveal the Novel Transmembrane Protein BIL4, Which Mediates Plant Cell Elongation in Brassinosteroid Signaling

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  • YAMAGAMI Ayumi
    Plant Chemical Biology Research Unit, RIKEN Advanced Science Institute Department of Biology, Ochanomizu University
  • NAKAZAWA Miki
    Plant Function Genomics Research Team, Plant Functional Genomics Research Group, RIKEN Plant Science Center
  • MATSUI Minami
    Plant Function Genomics Research Team, Plant Functional Genomics Research Group, RIKEN Plant Science Center
  • TUJIMOTO Masafumi
    Laboratory of Cellular Biochemistry, RIKEN Advanced Science Institute
  • SAKUTA Masaaki
    Department of Biology, Ochanomizu University
  • ASAMI Tadao
    Laboratory of Cellular Biochemistry, RIKEN Advanced Science Institute Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • NAKANO Takeshi
    Plant Chemical Biology Research Unit, RIKEN Advanced Science Institute PRESTO, JST (Japan Science and Technology Agency)

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説明

Steroid hormones are conserved between animals and plants as signaling molecules to control growth and development. Plant steroid hormones, brassinosteroids (BRs), appear to play an important role in plant cell elongation. BRs bind to leucine-rich repeat kinase BRASSINOSTEROID-INSENSITIVE 1 (BRI1) localized to the plasma membrane, activate transcription factors in collaboration with cytosolic kinases and phosphatases, and regulate BR-responsive gene expression, but the details regarding the BR signaling pathway from perception to nuclear events remain unknown. In this study we used chemical genetics to identify an evolutionarily conserved transmembrane protein, Brz-insensitive-long hypocotyls 4 (BIL4), and demonstrated its role as a critical component of plant cell elongation occurring upon BR signaling. A dominant mutation, bil4-1D, showed cell elongation in the presence of the BR-specific inhibitor Brz. Brz suppresses expression of the BIL4 gene in wild-type plants, and overexpression of BIL4 in bil4-1D suppresses the BR deficiency caused by Brz. Our results indicate that BIL4 mediates cell elongation on BR signaling.

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