Abstract
In flowering plants, double fertilization of the female gametes, the egg and central cell, initiates seed development to give rise to a diploid embryo and the triploid endosperm. In the absence of fertilization, the MEA-FIE Polycomb Repressive Complex 2 (PRC2) represses this developmental process by histone methylation of certain target genes. The imprinted gene MEDEA (MEA), as well as the FERTILIZATION-INDEPENDENT ENDOSPERM (FIE) gene, encode two of the core components of this complex. In addition, DNA methylation establishes and maintains the repression of gene activity, for instance via the DNA METHYLTRANSFERASE 1 (MET1), which maintains methylation of symmetric CpG residues. Here, we demonstrate that Arabidopsis MET1 interacts with MEA in vitro and in a yeast two-hybrid assay similar to the interaction of the mammalian homologues DNMT1 and EZH2 that was previously identified. MET1 and MEA share overlapping expression patterns in reproductive tissues before and after fertilization, a precondition to allow interaction in vivo. Importantly, a much higher percentage of central cells initiate endosperm development in the absence of fertilization in mea-1/MEA; met1-3/MET1 as compared to mea-1/MEA mutant plants. In addition, DNA methylation at the PHERES1 and MEA loci, imprinted MEA-FIE PRC2 target genes, was affected in mutant mea-1 as compared to wild-type embryos. In conclusion, our data suggest a mechanistic link between two major epigenetic pathways involved in histone and DNA methylation in plants by physical interaction of MET1 with the MEA-FIE PRC2 core component MEA, relevant for the repression of seed development in the absence of fertilization. © 2012 The Authors. The Plant Journal © 2012 Blackwell Publishing Ltd.
Schmidt, Anja