Seed dormancy is a crucial developmental transition that affects the adaption and survival of plants. Arabidopsis DELAY OF GERMINATION 1 (DOG1) is known as a master regulator of seed dormancy. However, although several upstream factors of DOG1 have been reported, the exact regulation of DOG1 is not fully understood. Histone acetylation is an important regulatory layer, controlled by histone acetyltransferases and histone deacetylases. Histone acetylation strongly correlates with transcriptionally active chromatin, whereas heterochromatin is generally characterized by hypoacetylated histones. Here we describe that loss of function of two plant-specific histone deacetylases, HD2A and HD2B, resulted in enhanced seed dormancy in Arabidopsis. Interestingly, the silencing ofHD2AandHD2Bcaused hyperacetylation of theDOG1locus and promoted the expression ofDOG1during seed maturation and imbibition. Knockout ofDOG1could rescue the seed dormancy and partly rescue the disturbed development phenotype ofhd2ahd2b. Transcriptomic analysis of thehd2ahd2bline shows that many genes involved in seed development were impaired. Moreover, we demonstrated that HSI2 and HSL1 interact with HD2A and HD2B. In sum, these results suggest that HSI2 and HSL1 might recruit HD2A and HD2B toDOG1to negatively regulateDOG1expression and to reduce seed dormancy, consequently, affecting seed development during seed maturation and promoting seed germination during imbibition.