The need for Eed

Genomic imprinting, the process that causes genes to be expressed in a parental origin-specific manner, is a useful model for studying the epigenetic control of genome function in mammals. Parallels between the mechanisms of X inactivation and autosomal imprinting have been proposed(1). On page 502 of this issue, Jesse Mager and colleagues(2) address whether Eed, required for X inactivation, is also required for imprinting on autosomes. Their results offer further insight into the similarities and differences between X inactivation and autosomal imprinting. The finding that a few silent imprinted alleles are activated in mice with mutations in Eed allows us to assess regulatory mechanisms at those loci from a different perspective.