Plant Physiol. Journal of Pharmacology and Experimental Therapeutics
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Published on August 18, 2006; 10.1104/pp.106.085969


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Received June 29, 2006
Accepted August 2, 2006

Mutations in an Auxin Receptor Homolog AFB5 and in SGT1b Confer Resistance to Synthetic Picolinate Auxins and not to 2,4-D or IAA in Arabidopsis

Terence A. Walsh *, Roben Neal , Ann Owens Merlo , Mary Honma , Glenn R. Hicks , Karen Wolff , Wendy Matsumura , and John P. Davies

Dow AgroSciences, Discovery Research, 9330 Zionsville Road, Indianapolis, IN 46268 (T.A.W., R.N, A.O.M.); Exelixis, 170 Harbor Way, South San Francisco, CA 94083-0511 (M.H.,G.R.H.); Exelixis Plant Sciences, 16160 SW Upper Boones Ferry Road, Portland, OR 97224 (K.W., W.M., J.P.D.)

* Corresponding author; email: tawalsh{at}dow.com.

Although a wide range of structurally diverse small molecules can act as auxins, it is unclear if all of these compounds act via the same mechanisms that have been characterized for 2,4-D and indole-3-acetic acid (IAA). To address this question, we used a novel member of the picolinate class of synthetic auxins that is structurally distinct from 2,4-D to screen for Arabidopsis (Arabidopsis thaliana) mutants that show chemically-selective auxin resistance. We identified seven alleles at two distinct genetic loci that conferred significant resistance to picolinate auxins such as picloram yet had minimal cross resistance to 2,4-D or IAA. Double mutants had the same level and selectivity of resistance as single mutants. The sites of the mutations were identified by positional mapping as At4g11260 and At5g49980. At5g49980 is previously uncharacterized and encodes Auxin F-Box protein 5 (AFB5), one of five homologs of TIR1 in the Arabidopsis genome. TIR1 is the recognition component of the SCF complex associated with the ubiquitin-proteasome pathway involved in auxin signaling and has recently been shown to be a receptor for IAA and 2,4-D. At4g11260 encodes the tetratricopeptide protein SGT1b that has also been associated with SCF-mediated ubiquitination in auxin signaling and other pathways. Complementation of mutant lines with their corresponding wild type genes restored picolinate auxin sensitivity. These results show that chemical specificity in auxin signaling can be conferred by upstream components of the auxin response pathway. They also demonstrate the utility of genetic screens using structurally diverse chemistries to uncover novel pathway components.




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