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Published on March 6, 2009; 10.1104/pp.109.135954

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Received January 26, 2009
Accepted February 25, 2009

Involvement of Phytosulfokine in the Attenuation of Stress Response during the Transdifferentiation of Zinnia Mesophyll Cells into Tracheary Elements

Hiroyasu Motose *, Kuninori Iwamoto , Satoshi Endo , Taku Demura , Youji Sakagami , Yoshikatsu Matsubayashi , Kevin L. Moore , and Hiroo Fukuda

Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153-8902, Japan (H. M.); Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan (K. I., S. E., H. F.); Plant Science Center, RIKEN, Suehiro 1-7-22, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan (T. D.); Graduate School of Bio-agricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan (Y. S., Y. M); Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation and the Departments of Cell Biology and Medicine, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73104, USA (K. L. M.)

* Corresponding author; email: motose{at}bio.c.u-tokyo.ac.jp.

Phytosulfokine (PSK) is a sulfated peptide hormone required for the proliferation and differentiation of plant cells. Here, we characterize physiological roles of PSK in transdifferentiation of isolated mesophyll cells of zinnia (Zinnia elegans L. cv Canary Bird) into tracheary elements (TEs). Transcripts for a zinnia PSK precursor gene, ZePSK1, show two-peaks of expression during TE differentiation; the first accumulation is transiently induced in response to wounding at the 24th h of culture, and the second accumulation is induced in the final stage of TE differentiation and is dependent on endogenous brassinosteroids. Chlorate, a potent inhibitor of peptide sulfation, is successfully applied as an inhibitor of PSK action. Chlorate significantly suppresses TE differentiation. The chlorate-induced suppression of TE differentiation is overcome by exogenously applied PSK. In the presence of chlorate, expression of stress-related genes for proteinase inhibitors and a pathogenesis-related protein is enhanced and changed from transient to continuous pattern. On the contrary, administration of PSK significantly reduces accumulation of transcripts for the stress-related genes. Even in the absence of auxin and cytokinin, addition of PSK suppresses stress-related gene expression. Microarray analysis reveals 66 genes downregulated and 42 genes upregulated under the presence of PSK. The large majority of downregulated genes show significant similarity to various families of stress-related proteins, including chitinases, phenylpropanoid-biosynthesis enzymes, ACC synthase, and receptor-like protein kinases. These results implicate involvement of PSK in the attenuation of stress response and healing of wound-activated cells during the early stage of TE differentiation.






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