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Plant and Cell Physiology Advance Access first published online on October 17, 2005
This version published online on October 20, 2005

Plant and Cell Physiology, doi:10.1093/pcp/pci217
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Plant and Cell Physiology 2005 © The Japanese Society of Plant Physiologists (JSPP); all rights reserved.
Received September 8, 2005
Accepted October 11, 2005

Regular Paper

Inhibition of Transdifferentiation into Tracheary Elements by Polar Auxin Transport Inhibitors through the Intracellular Auxin Depletion

Saiko Yoshida 1*, Hideo Kuriyama 1, and Hiroo Fukuda 1

1 Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033 Japan

* To whom correspondence should be addressed.
Saiko Yoshida, E-mail: saiko{at}biol.s.u-tokyo.ac.jp


   Abstract

Polar auxin transport is essential for the formation of continuous vascular strands in the plant body. To understand its mechanism, polar auxin transport inhibitors have often been used. However, the role of auxin in vascular differentiation at the unicellular level has remained elusive. Using a Zinnia elegans cell culture system, in which single mesophyll cells transdifferentiate into tracheary elements (TEs), we demonstrated that auxin transport inhibitors prevented TE differentiation and that high concentrations of 1-naphthalenacetic acid (NAA) and indole-3-acetic acid (IAA) overcame the repression of TE differentiation. Measurements of NAA accumulation with [3H]-labeled NAA in the presence or absence of 1-N-naphthylphthalamic acid (NPA) revealed enhanced NAA accumulation within the cell. In the NPA-treated cells, intracellular free NAA decreased, while its metabolites increased. Therefore, the polar auxin transport inhibitors may prevent auxin efflux and consequently promote NAA accumulation in Zinnia cells. The excess intracellular NAA may also activate NAA metabolism, resulting in a decrease in free NAA levels. This depletion of free NAA may prevent TE differentiation. The decreased auxin activity in NPA-treated cells was confirmed by the fact that the DR5 (a synthetic auxin-inducible promoter)-mediated expression of a reporter protein was suppressed in such cells. A gene expression analysis indicated that NPA suppressed TE differentiation at an early process of transdifferentiation into TEs. Based on these results, the interrelationship between auxin and vascular cell development at a cellular level is discussed.

Keywords: Polar auxin transport; Auxin metabolism; NAA; Tracheary element differentiation; Zinnia elegans.
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