DNA methylation plays an essential role in plant growth and development, however, its specific influence on maize kernel development remains uncertain. In this study, we investigated the gene responsible for the maize kernel mutant smk313 and identified it as the DNA methyltransferase ZmMET1. The smk313 mutants displayed a distinct small kernel phenotype and exhibited developmental abnormalities in the basal endosperm transfer layer (BETL), the endosperm adjacent to the scutellum cell (EAS), and the starchy endosperm cells (SEs). Compared with that of the wild-type (WT), we found that the mutants had lower CG methylation density across the whole genome through whole genome methylation sequencing (WGBS), and there were many accessible chromatin regions (ACRs) through assay for targeting accessible chromatin with high-throughout sequencing (ATAC-seq). Combining these findings with the transcriptome analysis revealed a cascade of effects caused by the loss of ZmMET1 function. This deficiency leads to alterations in genomic methylation and chromatin accessibility, which in turn influences the expression of genes related to starch and protein synthesis, as well as material transport processes. These alterations were consistent with the delayed development and dysplasia observed in EAS and BETLs of smk313 kernels. Consequently, our investigation emphasizes the vital role of ZmMET1 in maize seed development.