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First published online May 20, 2009; 10.1104/pp.109.138529

Plant Physiology 150:1310-1321 (2009)
© 2009 American Society of Plant Biologists

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CELL BIOLOGY AND SIGNAL TRANSDUCTION

The Tryptophan Conjugates of Jasmonic and Indole-3-Acetic Acids Are Endogenous Auxin Inhibitors1,[W],[OA]

Paul E. Staswick*

Department of Agronomy and Horticulture, University of Nebraska, Lincoln, Nebraska 68583–0915

Most conjugates of plant hormones are inactive, and some function to reduce the active hormone pool. This study characterized the activity of the tryptophan (Trp) conjugate of jasmonic acid (JA-Trp) in Arabidopsis (Arabidopsis thaliana). Unexpectedly, JA-Trp caused agravitropic root growth in seedlings, unlike JA or nine other JA-amino acid conjugates. The response was dose dependent from 1 to100 µM, was independent of the COI1 jasmonate signaling locus, and unlike the jasmonate signal JA-isoleucine, JA-Trp minimally inhibited root growth. The Trp conjugate with indole-3-acetic acid (IAA-Trp) produced a similar response, while Trp alone and conjugates with benzoic and cinnamic acids did not. JA-Trp and IAA-Trp at 25 µM nearly eliminated seedling root inhibition caused by 2 µM IAA. The TIR1 auxin receptor is required for activity because roots of tir1-1 grew only approximately 60% of wild-type length on IAA plus JA-Trp, even though tir1-1 is auxin resistant. However, neither JA-Trp nor IAA-Trp interfered with IAA-dependent interaction between TIR1 and Aux/IAA7 in cell-free assays. Trp conjugates inhibited IAA-stimulated lateral root production and DR5-β-glucuronidase gene expression. JA-deficient mutants were hypersensitive to IAA and a Trp-overaccumulating mutant was less sensitive, suggesting endogenous conjugates affect auxin sensitivity. Conjugates were present at 5.8 pmol g–1 fresh weight or less in roots, seedlings, leaves, and flowers, and the values increased approximately 10-fold in roots incubated in 25 µM Trp and IAA or JA at 2 µM. These results show that JA-Trp and IAA-Trp constitute a previously unrecognized mechanism to regulate auxin action.


1 This research is a contribution of the University of Nebraska Agricultural Research Division, supported in part by funds from the Hatch Act. Additional support was provided by the National Science Foundation (Award IOS–0744758).

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Paul E. Staswick (pstaswick1{at}unl.edu).

[W] The online version of this article contains Web-only data.

[OA] Open access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.109.138529

* E-mail pstaswick1{at}unl.edu.

Received March 11, 2009; accepted May 14, 2009; published May 20, 2009.


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