The endosperm is an ephemeral tissue surrounding the embryo that is essential for its development. Aside from the embryo nourishing function, the endosperm serves as a battlefield for epigenetic processes that have been hypothesized to reinforce transposable element silencing in the embryo. Specifically, global DNA demethylation in the central cell may serve to produce small RNAs that migrate to egg cell and embryo to induce de novo DNA methylation. The Polycomb Repressive Complex 2 (PRC2) is particularly targeted to DNA hypomethylated regions, possibly alleviating the negative effects associated with loss of DNA methylation in the endosperm. The functional requirement of the PRC2 in the endosperm can be bypassed by increasing the maternal genome dosage in the endosperm, suggesting a main functional role of the endosperm PRC2 in reducing sexual conflict. We therefore propose that the functional requirement of an endosperm PRC2 was coupled to the evolution of a sexual endosperm and mechanisms enforcing transposon silencing in the embryo. The evolutionary consequences of this scenario for genome expansion will be discussed.
Keywords: Polycomb Repressive Complex 2; endosperm; epigenetics; evolution; imprinting.