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First published online February 25, 2005; 10.1104/pp.104.053843

Plant Physiology 137:939-948 (2005)
© 2005 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

Auxin-Dependent Cell Division and Cell Elongation. 1-Naphthaleneacetic Acid and 2,4-Dichlorophenoxyacetic Acid Activate Different Pathways1

Prisca Campanoni* and Peter Nick

Istituto di Biologia e Biotecnologia Agraria, Consiglio Nazionale delle Ricerche, 20133 Milan, Italy (P.C.); and Botanisches Institut 1, Universität Karlsruhe, 76128 Karlsruhe, Germany (P.N.)

During exponential phase, the tobacco (Nicotiana tabacum) cell line cv Virginia Bright Italia-0 divides axially to produce linear cell files of distinct polarity. This axial division is controlled by exogenous auxin. We used exponential tobacco cv Virginia Bright Italia-0 cells to dissect early auxin signaling, with cell division and cell elongation as physiological markers. Experiments with 1-naphthaleneacetic acid (NAA) and 2,4-dichlorophenoxyacetic acid (2,4-D) demonstrated that these 2 auxin species affect cell division and cell elongation differentially; NAA stimulates cell elongation at concentrations that are much lower than those required to stimulate cell division. In contrast, 2,4-D promotes cell division but not cell elongation. Pertussis toxin, a blocker of heterotrimeric G-proteins, inhibits the stimulation of cell division by 2,4-D but does not affect cell elongation. Aluminum tetrafluoride, an activator of the G-proteins, can induce cell division at NAA concentrations that are not permissive for division and even in the absence of any exogenous auxin. The data are discussed in a model where the two different auxins activate two different pathways for the control of cell division and cell elongation.


1 This work was supported by the Volkswagen Foundation Nachwuchsgruppen Program and by the German Research Council (Priority Program Molecular Action of Phytohormones to P.N.).

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.104.053843.

* Corresponding author; e-mail campanoni{at}ibba.cnr.it; fax 39–(02)–23699–411.

Received September 21, 2004; returned for revision December 24, 2004; accepted January 5, 2005.




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