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First published online November 11, 2005; 10.1105/tpc.105.036723

The Plant Cell 17:3282-3300 (2005)
© 2005 American Society of Plant Biologists

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

Paul J. Overvoordea,1,2, Yoko Okushimaa,1,3, José M. Alonsob,4, April Chana, Charlie Changa, Joseph R. Eckerb, Beth Hughesa, Amy Liua, Courtney Onoderaa, Hong Quacha, Alison Smitha, Guixia Yua and Athanasios Theologisa,5

a Plant Gene Expression Center, Albany, California 94710
b Salk Institute for Biological Studies, La Jolla, California 92037

5 To whom correspondence should be addressed. E-mail theo{at}nature.berkeley.edu; fax 510-559-5678.

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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