Functional Genomic Analysis of the <i>AUXIN/INDOLE-3-ACETIC ACID</i> Gene Family Members in <i>Arabidopsis thaliana</i>  [W]

Paul Overvoorde(Plant Gene Expression Center), Yoko Okushima(Plant Gene Expression Center), José Manuel Alonso Segura(Salk Institute for Biological Studies), April Chan(Plant Gene Expression Center), Charlie H. Chang(Plant Gene Expression Center), Joseph R. Ecker(Salk Institute for Biological Studies), Beth Hughes(Plant Gene Expression Center), Amy Liu(Plant Gene Expression Center), Courtney Onodera(Plant Gene Expression Center), Hong Quach(Plant Gene Expression Center), Alison M. Smith(Plant Gene Expression Center), Guixia Yu(Plant Gene Expression Center), Athanasios Theologis(Plant Gene Expression Center)
The Plant Cell
November 11, 2005
Cited by 406Open Access
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Abstract

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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