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DEVELOPMENT AND HORMONE ACTION

Involvement of Phytosulfokine in the Attenuation of Stress Response during the Transdifferentiation of Zinnia Mesophyll Cells into Tracheary Elements^1,[W],[OA]

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

Phytosulfokine (PSK) is a sulfated peptide hormone required for the proliferation and differentiation of plant cells. Here, we characterize the physiological roles of PSK in transdifferentiation of isolated mesophyll cells of zinnia (Zinnia elegans ‘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 24 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 a transient to a continuous pattern. On the contrary, administration of PSK significantly reduces the 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 down-regulated and 42 genes up-regulated in the presence of PSK. The large majority of down-regulated genes show significant similarity to various families of stress-related proteins, including chitinases, phenylpropanoid biosynthesis enzymes, 1-aminocyclopropane-1-carboxylic acid synthase, and receptor-like protein kinases. These results suggest the involvement of PSK in the attenuation of stress response and healing of wound-activated cells during the early stage of TE differentiation.

² Present address; Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University, Tsushimanaka 3–1–1, Okayama 700–8530, Japan.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Hiroyasu Motose (motose{at}bio.c.u-tokyo.ac.jp).

^[W] The online version of this article contains Web-only data.

^[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.109.135954

^* Corresponding author; e-mail motose{at}bio.c.u-tokyo.ac.jp.

Received January 26, 2009; accepted February 25, 2009; published March 6, 2009.