During seed development, plants detect the paternal genome dose through gene expression from the paternally derived genome in the endosperm. To achieve this, the homologous genes in the maternally derived genome are silenced by polycomb repressive complex 2 (PRC2), and loss of PRC2 function or excess paternal genome dose both lead to seed abortion through the so-called ‘triploid block’. PRC2 requires the activity of accessory proteins of the VERNALIZATION INSENSITIVE 3-LIKE (VEL) family, of which the atypical VEL3 protein is required for endosperm development. Here, we characterize the function of the remaining family members, using CRISPR-Cas9 to generate multiple mutants in Arabidopsis. Loss-of-function analyses establish VEL3 as the sole regulator of primary seed dormancy depth, whereas VEL1 and VRN5 act redundantly alongside VEL3 to prevent seed abortion but without affecting dormancy. VEL2 and VIN3 exhibited no detectable influence on seed abortion or dormancy. Comparative RNA-seq of mature endosperm revealed that both vel3-1 and vel1-2 vrn5-9 mutants upregulate programmed cell-death genes, whereas vel3-1 uniquely deregulates chromatin remodellers and metabolic repressors, consistent with heterochromatin relaxation at germination loci and elevated metabolic activity. Our results establish that the role of VEL3 in seed dormancy is independent of PRC2, as they suggest the involvement of novel members of central cell and endosperm PRC2 complexes in regulating the maternally derived genome in the endosperm.