Regulation of imprinting in angiosperms and placental mammals. The four panels show the regulation of MEGs and PEGs in angiosperms (a and b) and placental mammals (c and d). (a) In both the female and male gametophyte, DME actively removes methylation from the central cell and vegetative cell, respectively. Paternal alleles of MEGs are then re-methylated via RdDM, and methylation status can be reinforced via METHYLTRANSFERASE1 (MET1), resulting in repressed expression. Conversely, maternal copies of MEGs are hypomethylated and expressed. (b) PEGs can be expressed through multiple mechanisms: 1) DNA methylation via MET1 or RdDM may prevent deposition of tri-methylate lysine 27 on histone H3 (H3K27me3) by FIS-PRC2, allowing for expression. 2) Paternal alleles of PEGs are neither methylated nor the target of H3K27me3 deposition, allowing expression. Or 3) H3K27me3 marks are removed, allowing expression. The maternal alleles of PEGs are silenced via FIS-PRC2 deposition. (c) MEGs expression in mammals is achieved by the suppression of the paternal allele either through DNA methylation via DNA methyltransferase 3a/b (DNMT3) at imprinting control regions (ICRs) or the binding of Polycomb repressive complex (PRC). (d) PEGs expression in mammals is achieved by the suppression of the maternal alleles through DNA methylation at ICRs via DNMT3a/b, PRC, or the histone methyltransferase G9a. In all cases, a blunted arrow indicates that expression is inhibited, while a pointed arrow denotes that expression occurs (indicated by the black waves).