Chromatin modification and remodelling are the basis for epigenetic regulation of gene expression. LEAFY COTYLEDON 1 (LEC1), LEAFY COTYLEDON 2 (LEC2), ABSCISIC ACID-INSENSITIVE 3 (ABI3) and FUSCA3 (FUS3) are key regulators of embryo development and are repressed after seed maturation. The chromatin remodelling CHD3 protein PICKLE (PKL) is involved in the epigenetic silencing of the genes. However, the chromatin mechanism that establishes the active state of these genes during early embryo development is not clear. We show that the Arabidopsis CHD1-related gene, CHR5, is activated during embryo development. Mutation of the gene reduced expression of LEC1, ABI3 and FUS3 in developing embryo and accumulation of seed storage proteins. Analysis of double mutants revealed an antagonistic function between CHR5 and PKL in embryo gene expression and seed storage protein accumulation, which likely acted on the promoter region of the genes. CHR5 was shown to be associated with the promoters of ABI3 and FUS3 and to be required to reduce nucleosome occupancy near the transcriptional start site. The results suggest that CHR5 is involved in establishing the active state of embryo regulatory genes by reducing nucleosomal barrier, which may be exploited to enhance seed protein production.