Plant GSK3 proteins regulate xylem cell differentiation downstream of TDIF–TDR signalling

Yuki Kondo (), Tasuku Ito, Hirofumi Nakagami, Yuki Hirakawa, Masato Saito, Takayuki Tamaki, Ken Shirasu and Hiroo Fukuda ()
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Yuki Kondo: Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
Tasuku Ito: Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
Hirofumi Nakagami: RIKEN Center for Sustainable Resource Science, 7-22 Suehiro-cho, Tsurumi-ku, Kanagawa, Yokohama, Japan
Yuki Hirakawa: Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
Masato Saito: Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
Takayuki Tamaki: Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
Ken Shirasu: RIKEN Center for Sustainable Resource Science, 7-22 Suehiro-cho, Tsurumi-ku, Kanagawa, Yokohama, Japan
Hiroo Fukuda: Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: Abstract During plant radial growth typically seen in trees, procambial and cambial cells act as meristematic cells in the vascular system to self-proliferate and differentiate into xylem cells. These two processes are regulated by a signalling pathway composed of a peptide ligand and its receptor; tracheary element differentiation inhibitory factor (TDIF) and TDIF RECEPTOR (TDR). Here we show that glycogen synthase kinase 3 proteins (GSK3s) are crucial downstream components of the TDIF signalling pathway suppressing xylem differentiation from procambial cells. TDR interacts with GSK3s at the plasma membrane and activates GSK3s in a TDIF-dependent fashion. Consistently, a specific inhibitor of plant GSK3s strongly induces xylem cell differentiation through BRI1-EMS SUPPRESSOR 1 (BES1), a well-known target transcription factor of GSK3s. Our findings provide insight into the regulation of cell fate determination in meristem maintenance.

Date: 2014
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DOI: 10.1038/ncomms4504

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