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DEVELOPMENT AND HORMONE ACTION

Constitutive Repression and Activation of Auxin Signaling in Arabidopsis^{1,[C],[W],[OA]}

Department of Biochemistry, University of Missouri, Columbia, Missouri 65211 (H.L., G.H., T.J.G.); and Department of Horticulture, Purdue University, West Lafayette, Indiana 47907 (Y.C., A.M.)

Aux/IAA proteins are proposed to be transcriptional repressors that play a crucial role in auxin signaling by interacting with auxin response factors and repressing early/primary auxin response gene expression. In assays with transfected protoplasts, this repression was previously shown to occur when auxin concentrations in a cell are low, and derepression/activation was observed when auxin concentrations are elevated. Here we show that a stabilized version of the Arabidopsis (Arabidopsis thaliana) IAA17 repressor, when expressed constitutively or in a specific cell type in Arabidopsis plants, confers phenotypes similar to plants with decreased auxin levels. In contrast, a stabilized version of IAA17 that was converted to a transcriptional activator confers phenotypes similar to plants with increased auxin levels, when expressed under the same conditions in Arabidopsis plants. Free auxin levels were unchanged compared to control (DR5:β-glucuronidase), however, in the seedlings expressing the IAA17 repressor and activator. These results together with our previous results carried out in transfected protoplasts suggest that the hormone auxin can be bypassed to regulate auxin signaling in a cell-autonomous manner in plants.

The author responsible for the 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: Tom J. Guilfoyle (guilfoylet{at}missouri.edu).

^[C] Some figures in this article are displayed in color online but in black and white in the print edition.

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www.plantphysiol.org/cgi/doi/10.1104/pp.108.129973

^* Corresponding author; e-mail guilfoylet{at}missouri.edu.

Received September 16, 2008; accepted January 2, 2009; published January 7, 2009.

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