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First published online April 30, 2007
doi: 10.1242/10.1242/dev.001891
1 National Research Laboratory of Plant Developmental Genetics, Department of
Biological Sciences, Seoul National University, Seoul, 151-742, Korea.
2 Global Research Laboratory for Flowering at SNU and UW, Seoul, 151-742,
Korea.
3 Environmental Biotechnology National Core Research Center, Gyeongsang National
University, Jinju 660-701, Korea.
4 Plant Metabolism Research Center, Kyung Hee University, Suwon 449-701,
Korea.
* Author for correspondence (e-mail: ilhalee{at}snu.ac.kr)
Accepted 13 March 2007
The SWR1 complex (SWR1C) in yeast catalyzes the replacement of nucleosomal H2A with the H2AZ variant, which ensures full activation of underlying genes. We compared the phenotype of mutants in the homologs of SWR1C components in Arabidopsis thaliana. Mutations in Arabidopsis SWC6 (AtSWC6), SUPPRESSOR OF FRIGIDA 3 (SUF3) and PHOTOPERIOD-INDEPENDENT EARLY FLOWERING 1 (PIE1), homologs of SWC6, ARP6 and SWR1, respectively, caused similar developmental defects, including leaf serration, weak apical dominance, flowers with extra petals and early flowering by reduction in expression of FLOWERING LOCUS C (FLC), a strong floral repressor. Chromatin immunoprecipitation assays showed that AtSWC6 and SUF3 bind to the proximal region of the FLC promoter, and protoplast transfection assays showed that AtSWC6 colocalizes with SUF3. Protein interaction analyses suggested the formation of a complex between PIE1, SUF3, AtSWC6 and AtSWC2. In addition, H2AZ, a substrate of SWR1C, interacts with both PIE1 and AtSWC2. Finally, knockdown of the H2AZ genes by RNA interference or artificial microRNA caused a phenotype similar to that of atswc6 or suf3. Our results strongly support the presence of an SWR1C-like complex in Arabidopsis that ensures proper development, including floral repression through full activation of FLC.
Key words: Flowering, Chromatin remodeling, SWR1 complex, FLC, AtARP6
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