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Plant and Cell Physiology Advance Access published online on October 20, 2006
Plant and Cell Physiology, doi:10.1093/pcp/pcl023
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© The Author 2006. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Rapid paper

The ENHANCER OF SHOOT REGENERATION 2 gene in Arabidopsis regulates CUP SHAPED COTYLEDON 1 at the transcriptional level and controls cotyledon development

Yoshihisa Ikeda 1, Hiroharu Banno 2, Qi-Wen Niu 3, Stephen H. Howell 4, and Nam-Hai Chua 3 *

1 Laboratory of Plant Molecular Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10021-6399, USA; Present address: Umeå Plant Science Centre, Department of Forest Genetics and Plant Physiology, Swedish University of Agricultural Sciences, SE-901 83 Umeå Sweden.
2 Laboratory of Plant Molecular Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10021-6399, USA; Present address: Department of Environmental Biology, School of Bioscience and Biotechnology, Chubu University, 1200 Matsumoto-cho, Kasugai, Aichi 487-8501, Japan
3 Laboratory of Plant Molecular Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10021-6399, USA.
4 Plant Sciences Institute, Iowa State University, Ames, IA 50011, USA.

* To whom correspondence should be addressed.
Nam-Hai Chua, E-mail: chua{at}mail.rockefeller.edu


  Abstract

Cytokinins stimulate shoot regeneration in tissue culture but the genes required for this developmental process are not well understood. Here we show that the Arabidopsis gene, ENHANCER OF SHOOT REGENERATION2 (ESR2), encoding an AP2-domain transcriptional factor, functions in the regeneration of shoots in tissue culture. ESR2 overexpression conferred cytokinin-independent shoot regeneration from cre1/ahk4 mutant explants, suggesting that CRE1 is not required for ESR2-mediated shoot regeneration. ESR2 directly targeted CYCLIN D1;1, ARABIDOPSIS PHOSPHOTRANSMITTER 6 (AHP6), and CUP SHAPED COTYLEDON 1 (CUC1) in assays involving the translocation of ESR2-ER (estradiol receptor) fusions to the nucleus. Knock-down of ESR2 expression by RNAi reduced CUC1 expression and resulted in altered cotyledon phenotypes at a low frequency, including partially fused cotyledons and triple cotyledons. Phenotypes of induced ESR2 expression in a cuc1-1 mutant background were suppressed. Our results suggest that ESR2 plays a role in shoot regeneration through transcriptional regulation of CUC1.

Keywords: shoot regeneration; cotyledon; cytokinin; gene expression; cell cycle.
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