Mature dry seeds have a particular mechanism that allows them to survive with loss of >90% of water content called desiccation tolerance (DT). The seed-DT is tightly regulated, being acquired during seed development and lost shortly after germination. The timing of loss of DT after germinated can be extended by exogenous stimuli e.g., a mild osmotic stress (re-induction of the DT to germinated seeds). The molecular processes involved in DT acquisition/loss and re-induction have been well studied at the transcriptomic level, which resulted in identification of DT-associated gene networks. However, our understanding of molecular mechanisms that switch-on/off the genetic networks of seed-DT remains fragmentary, especially from epigenetic aspects. Here, we identified DT-core genes (a cluster of genes specifically associated with DT re-induction) in root tissues of germinated Medicago by RNA-Seq, followed by analyses to determine the chromatin status of the loci of these DT-core genes. ATAC-Seq revealed that the chromatin state of genomic regions containing the DT-core genes is clearly linked to their expression levels and phenotypes; more opened chromatin with higher gene expressions in desiccation tolerant-tissue stimulated by a mild osmotic stress, conversely more closed chromatin with lower expressions in desiccation sensitive-tissues especially at a later stage of post-germination. Additionally, ChIP-Seq for histone repressive marks detected a prominent signal of H3K27me3 on the DT core-gene sequences at the later stage tissue with condensed chromatin, suggesting that silencing of DT in post-germination developmental programs will be mainly due to the H3K27me3 marks by the action of the PRC2 complex.