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DEVELOPMENT AND HORMONE ACTION

Interaction of Auxin and ERECTA in Elaborating Arabidopsis Inflorescence Architecture Revealed by the Activation Tagging of a New Member of the YUCCA Family Putative Flavin Monooxygenases¹

Department of Biology, University of Washington, Seattle, Washington 98195–5325 (C.W., S.M.B., E.J.H., K.U.T.); Department of Biological Sciences, University of Tokyo, Hongo, Tokyo 113–0033, Japan (S.S.); and Department of Biological Sciences, Tokyo Metropolitan University, Hachioji, Tokyo 192–0397, Japan (T.K.)

The aboveground body of higher plants has a modular structure of repeating units, or phytomers. As such, the position, size, and shape of the individual phytomer dictate the plant architecture. The Arabidopsis (Arabidopsis thaliana) ERECTA (ER) gene regulates the inflorescence architecture by affecting elongation of the internode and pedicels, as well as the shape of lateral organs. A large-scale activation-tagging genetic screen was conducted in Arabidopsis to identify novel genes and pathways that interact with the ER locus. A dominant mutant, super1-D, was isolated as a nearly complete suppressor of a partial loss-of-function allele er-103. We found that SUPER1 encodes YUCCA5, a novel member of the YUCCA family of flavin monooxygenases. The activation tagging of YUCCA5 conferred increased levels of free indole acetic acid, increased auxin response, and mild phenotypic characteristics of auxin overproducers, such as elongated hypocotyls, epinastic cotyledons, and narrow leaves. Both genetic and cellular analyses indicate that auxin and the ER pathway regulate cell division and cell expansion in a largely independent but overlapping manner during elaboration of inflorescence architecture.

² These authors contributed equally to the paper.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.105.063495.

^* Corresponding author; e-mail ktorii{at}u.washington.edu; fax 206–685–1728.

Received March 30, 2005; returned for revision June 14, 2005; accepted June 14, 2005.

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