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Published on April 24, 2009; 10.1104/pp.109.136671

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Received February 4, 2009
Accepted April 20, 2009

Arabidopsis IAR4 modulates auxin response by regulating auxin homeostasis

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

Department of Plant Biology and Department of Horticultural Sciences, University of Minnesota-Twin Cities, St. Paul, MN 55108

* Corresponding author; email: grayx051{at}tc.umn.edu.

In a screen for enhancers of tir1-1 auxin resistance, we identified two novel alleles of the putative mitochondrial pyruvate dehydrogenase E1{alpha} subunit, 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 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 tryptophan-independent IAA biosynthetic pathway in iar4-3. We therefore suggest that the auxin phenotypes of iar4 mutants are the result of altered IAA homeostasis.






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