During embryogenesis, Polycomb group (PcG) complexes deposit silencing histone modifications and target homeotic genes, which regulate the patterning of other transcription factors. This transcriptional network further maintains cell fate. However, genome-wide identification of histone modifications has suggested that PcG complexes might regulate genes other than those encoding transcription factors. In Arabidopsis, we show that PcG activity directly targets the actin regulator formin ARABIDOPSIS FORMIN HOMOLOGUE 5 (AtFH5). PcG activity silences the paternal allele of AtFH5, restricting its expression to the maternal allele. AtFH5 thus appears to be a new, maternally expressed imprinted gene. We further demonstrate that AtFH5 is responsible for morphological defects caused by the loss of PcG activity in the seed.