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.