Imprinting of the MEDEA polycomb gene in the Arabidopsis endosperm

In flowering plants, two cells are fertilized in the haploid female gametop hyte. Egg and sperm nuclei fuse to form the embryo. A second sperm nucleus fuses with the central cell nucleus that replicates to generate the endospe rm, which is a tissue that supports embryo development. MEDEA (MEA) encodes an Arabidopsis SET domain Polycomb protein. Inheritance of a maternal loss -of-function mea allele results in embryo abortion and prolonged endosperm production, irrespective of the genotype of the paternal allele. Thus, only the maternal wild-type MEA allele is required for proper embryo and endosp erm development. To understand the molecular mechanism responsible for the parent-of-origin effects of mea mutations on seed development, we compared the expression of maternal and paternal MEA alleles in the progeny of cross es between two Arabidopsis ecotypes. Only the maternal MEA mRNA was detecte d in the endosperm from seeds at the torpedo stage and later. By contrast, expression of both maternal and paternal MEA alleles was observed in the em bryo from seeds at the torpedo stage and later, in seedling, leaf, stem, an d root. Thus, MEA is an imprinted gene that displays parent-of-origin-depen dent monoallelic expression specifically in the endosperm. These results su ggest that the embryo abortion observed in mutant mea seeds is due, at leas t in part, to a defect in endosperm function. Silencing of the paternal MEA allele in the endosperm and the phenotype of mutant mea seeds supports the parental conflict theory for the evolution of imprinting in plants and mam mals.