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First published online September 20, 2007; 10.1104/pp.107.104935

Plant Physiology 145:722-735 (2007)
© 2007 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

yucca6, a Dominant Mutation in Arabidopsis, Affects Auxin Accumulation and Auxin-Related Phenotypes1,[W],[OA]

Jeong Im Kim, Altanbadralt Sharkhuu, Jing Bo Jin, Pinghua Li, Jae Cheol Jeong, Dongwon Baek, Sang Yeol Lee, Joshua J. Blakeslee, Angus S. Murphy, Hans J. Bohnert, Paul M. Hasegawa, Dae-Jin Yun and Ray A. Bressan*

Center for Plant Environmental Stress Physiology (J.I.K., A.S., J.B.J., P.M.H., R.A.B.) and Department of Horticulture and Landscape Architecture (J.J.B., A.S.M.), Purdue University, West Lafayette, Indiana 47906–2010; Department of Plant Biology, University of Illinois, Urbana, Illinois 61801 (P.L., H.J.B.); and Environmental Biotechnology National Core Research Center and Division of Applied Life Science (BK21 Program), Graduate School of Gyeongsang National University, Jinju 660–701, Korea (J.C.J., D.B., S.Y.L., D.-J.Y.)

Auxin plays critical roles in many aspects of plant growth and development. Although a number of auxin biosynthetic pathways have been identified, their overlapping nature has prevented a clear elucidation of auxin biosynthesis. Recently, Arabidopsis (Arabidopsis thaliana) mutants with supernormal auxin phenotypes have been reported. These mutants exhibit hyperactivation of genes belonging to the YUCCA family, encoding putative flavin monooxygenase enzymes that result in increased endogenous auxin levels. Here, we report the discovery of fertile dominant Arabidopsis hypertall1-1D and hypertall1-2D (yucca6-1D, -2D) mutants that exhibit typical auxin overproduction phenotypic alterations, such as epinastic cotyledons, increased apical dominance, and curled leaves. However, unlike other auxin overproduction mutants, yucca6 plants do not display short or hairy root phenotypes and lack morphological changes under dark conditions. In addition, yucca6-1D and yucca6-2D have extremely tall (>1 m) inflorescences with extreme apical dominance and twisted cauline leaves. Microarray analyses revealed that expression of several indole-3-acetic acid-inducible genes, including Aux/IAA, SMALL AUXIN-UP RNA, and GH3, is severalfold higher in yucca6 mutants than in the wild type. Tryptophan (Trp) analog feeding experiments and catalytic activity assays with recombinant YUCCA6 indicate that YUCCA6 is involved in a Trp-dependent auxin biosynthesis pathway. YUCCA6:GREEN FLUORESCENT PROTEIN fusion protein indicates YUCCA6 protein exhibits a nonplastidial subcellular localization in an unidentified intracellular compartment. Taken together, our results identify YUCCA6 as a functional member of the YUCCA family with unique roles in growth and development.


1 This work was supported by the National Science Foundation (grant nos. DBI–0223905 to H.J.B and MCB–0424850 to A.S.M.), by the Biogreen 21 project of the Rural Development Administration (grant no. 20070301034030), by the Basic Science Project of the Korea Science and Engineering Foundation (KOSEF; grant no. RO1–2006–000–10123–0), by the Environmental Biotechnology National Core Research Center Project of KOSEF (grant no. R15–2003–012–01002–00), by the Brain Korea 21 Program, Ministry of Education and Human Resources Development, Korea (scholarship to J.C.J), and by Futuregene. Microscopy data was acquired in the Purdue Cancer Center Analytical Cytometry Laboratories supported by the Cancer Center NCI core grant no. NIH NCI–2P30CA23168. This work is Purdue University Agricultural Research Program Paper 2007–18193.

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: Ray A. Bressan (bressan{at}hort.purdue.edu).

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

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www.plantphysiol.org/cgi/doi/10.1104/pp.107.104935

* Corresponding author; e-mail bressan{at}hort.purdue.edu.

Received July 3, 2007; accepted September 10, 2007; published September 20, 2007.




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