Plant Cell Advance Online Publication
Published on November 11, 2005; 10.1105/tpc.105.036723
Received August 3, 2005
Returned for revision September 26, 2005
Accepted October 13, 2005
Functional Genomic Analysis of the AUXIN/INDOLE-3-ACETIC ACID Gene Family Members in Arabidopsis thaliana
Paul J. Overvoorde 1, Yoko Okushima 1, Jose M. Alonso 2, April Chan 1, Charlie Chang 1, Joseph R Ecker 2, Beth Hughes 1, Amy Liu 1, Courtney Onodera 1, Hong Quach 1, Alison Smith 1, Guixia Yu 1, and Athanasios Theologis 1*
1 Plant Gene Expression Center, Albany, California 94710
2 Salk Institute for Biological Studies, La Jolla, California 92037
* To whom correspondence should be addressed. E-mail: theo{at}nature.berkeley.edu.
Auxin regulates various aspects of plant growth and development. The AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA) genes encode short-lived transcriptional repressors that are targeted by the TRANSPORT INHIBITOR RESPONSE1/AUXIN RECEPTOR F-BOX proteins. The Aux/IAA proteins regulate auxin-mediated gene expression by interacting with members of the AUXIN RESPONSE FACTOR protein family. Aux/IAA function is poorly understood; herein, we report the identification and characterization of insertion mutants in 12 of the 29 Aux/IAA family members. The mutants show no visible developmental defects compared with the wild type. Double or triple mutants of closely related Aux/IAA genes, such as iaa8-1 iaa9-1 or iaa5-1 iaa6-1 iaa19-1, also exhibit wild-type phenotypes. Global gene expression analysis reveals that the molecular phenotypes of auxin-treated and untreated light-grown seedlings are unaffected in the iaa17-6 and iaa5-1 iaa6-1 iaa19-1 mutants. By contrast, similar analysis with the gain-of-function axr3-1/iaa17-1 mutant seedlings reveals dramatic changes in basal and auxin-induced gene expression compared with the wild type. Expression of several type-A ARABIDOPSIS RESPONSE REGULATOR genes and a number of genes involved in cell wall biosynthesis and degradation is repressed in axr3-1/iaa17-1. The data suggest extensive functional redundancy among Aux/IAA gene family members and that enhanced stability of the AXR3/IAA17 protein severely alters the molecular phenotype, resulting in developmental defects.
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