BZR1 Is a Transcriptional Repressor with Dual Roles in Brassinosteroid Homeostasis and Growth Responses

American Association for the Advancement of Science (AAAS) - Tập 307 Số 5715 - Trang 1634-1638 - 2005
Jun‐Xian He1,2, Joshua M. Gendron1,2, Yu Sun1,2, Srinivas S. L. Gampala1,2, Nathan Gendron1,2, Catherine Qing Sun1,2, Zhiyong Wang1,2
1Department of Biological Sciences, Stanford University, Stanford, CA 94305 USA
2Department of Plant Biology, Carnegie Institution, Stanford, CA 94305, USA

Tóm tắt

Brassinosteroid (BR) homeostasis and signaling are crucial for normal growth and development of plants. BR signaling through cell-surface receptor kinases and intracellular components leads to dephosphorylation and accumulation of the nuclear protein BZR1. How BR signaling regulates gene expression, however, remains unknown. Here we show that BZR1 is a transcriptional repressor that has a previously unknown DNA binding domain and binds directly to the promoters of feedback-regulated BR biosynthetic genes. Microarray analyses identified additional potential targets of BZR1 and illustrated, together with physiological studies, that BZR1 coordinates BR homeostasis and signaling by playing dual roles in regulating BR biosynthesis and downstream growth responses.

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Molecular interaction data have been deposited in the Biomolecular Interaction Network Database (BIND) with accession codes 197445 and 197446. We thank M. Szekeres for providing the CDP- GUS constructs; T. J. Guilfoyle for the UAS- GUS VP16-LexA and IAA17 a 1-Gal4 constructs; V. Walbot for the 35S- Luciferase vector; W. Frommer for the BY2 cells; B-H. Hou and T. Hamman for assistance with microarray analysis; Y. Yang and N. Marinova for technical assistance; Y. Lou for assistance with promoter cis-element analysis; and W. Briggs D. Bergmann D. Ehrhardt Z. He A. Grossman and C. Somerville for helpful comments on the manuscript. This work was supported by grants from NIH (R01 GM66258-01) the U.S. Department of Energy (DE-FG02-04ER15525) and the Carnegie Institution of Washington (Z.-Y.W.) and by a training grant from NIH (5T32GM007276) (J.M.G.).