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First published online April 24, 2009; 10.1104/pp.109.136671

Plant Physiology 150:748-758 (2009)
© 2009 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

Arabidopsis IAR4 Modulates Auxin Response by Regulating Auxin Homeostasis1,[OA]

Marcel Quint2, Lana S. Barkawi, Kai-Ting Fan, Jerry D. Cohen and William M. Gray*

Department of Plant Biology (M.Q., K.-T.F., W.M.G.) and Department of Horticultural Sciences (L.S.B., J.D.C.), University of Minnesota, St. Paul, Minnesota 55108

In a screen for enhancers of tir1-1 auxin resistance, we identified two novel alleles of the putative mitochondrial pyruvate dehydrogenase E1{alpha}-subunit, IAA-Alanine Resistant4 (IAR4). In addition to enhancing the auxin response defects of tir1-1, iar4 single mutants exhibit numerous auxin-related phenotypes including auxin-resistant root growth and reduced lateral root development, as well as defects in primary root growth, root hair initiation, and root hair elongation. Remarkably, all of these iar4 mutant phenotypes were rescued when endogenous indole-3-acetic acid (IAA) levels were increased by growth at high temperature or overexpression of the YUCCA1 IAA biosynthetic enzyme, suggesting that iar4 mutations may alter IAA homeostasis rather than auxin response. Consistent with this possibility, iar4 mutants exhibit increased Aux/IAA stability compared to wild type under basal conditions, but not in response to an auxin treatment. Measurements of free IAA levels detected no significant difference between iar4-3 and wild-type controls. However, we consistently observed significantly higher levels of IAA-amino acid conjugates in the iar4-3 mutant. Furthermore, using stable isotope-labeled IAA precursors, we observed a significant increase in the relative utilization of the Trp-independent IAA biosynthetic pathway in iar4-3. We therefore suggest that the auxin phenotypes of iar4 mutants are the result of altered IAA homeostasis.


1 This work was supported by the National Institutes of Health (grant no. GM067203 to W.M.G.) and a postdoctoral fellowship from the Deutsche Forschungsgemeinschaft (to M.Q.).

2 Present address: Leibniz Institute of Plant Biochemistry, Weinberg 03, 06120 Halle, Germany.

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: William Gray (grayx051{at}tc.umn.edu).

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

www.plantphysiol.org/cgi/doi/10.1104/pp.109.136671

* Corresponding author; e-mail grayx051{at}tc.umn.edu.

Received February 4, 2009; accepted April 20, 2009; published April 24, 2009.







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