ThePolycombgroup protein MEDEA and the DNA methyltransferase MET1 interact to repress autonomous endosperm development in Arabidopsis

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In flowering plants, double fertilization of the female gametes, the egg and the central cell, initiates seed development to give rise to a diploid embryo and the triploid endosperm. In the absence of fertilization, the FERTILIZATION-INDEPENDENT SEEDPolycombRepressive Complex 2 (FIS-PRC2) represses this developmental process by histone methylation of certain target genes. TheFERTILIZATION-INDEPENDENT SEED (FIS)class genesMEDEA(MEA) andFERTILIZATION-INDEPENDENT ENDOSPERM(FIE) encode two of the core components of this complex. In addition, DNA methylation establishes and maintains the repression of gene activity, for instance via DNA METHYLTRANSFERASE1 (MET1), which maintains methylation of symmetric CpG residues. Here, we demonstrate that Arabidopsis MET1 interacts with MEAin vitroand in a yeast two-hybrid assay, similar to the previously identified interaction of the mammalian homologues DNMT1 and EZH2. MET1 and MEA share overlapping expression patterns in reproductive tissues before and after fertilization, a prerequisite for an interactionin vivo. Importantly, a much higher percentage of central cells initiate endosperm development in the absence of fertilization inmea-1MEA; met1-3/MET1as compared tomea-1MEAmutant plants. In addition, DNA methylation at thePHERES1andMEAloci, imprinted target genes of the FIS-PRC2, was affected in themea-1mutant compared with 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 FIS-PRC2 core component MEA. This concerted action is relevant for the repression of seed development in the absence of fertilization.

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