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Although it is well established that the Polycomb Group (PcG) complexes maintain generepression through the incorporation of H2AK121ub and H3K27me3, little is known about theeffect of these modifications on chromatin accessibility, which is fundamental to understandPcG function. Here, by integrating chromatin accessibility, histone marks and expressionanalyses in differentArabidopsisPcG mutants, we show that PcG function regulates chro-matin accessibility. Wefind that H2AK121ub is associated with a less accessible but stillpermissive chromatin at transcriptional regulation hotspots. Accessibility is further reducedby EMF1 acting in collaboration with PRC2 activity. Consequently, H2AK121ub/H3K27me3marks are linked to inaccessible although responsive chromatin. In contrast, only-H3K27me3-marked chromatin is less responsive, indicating that H2AK121ub-marked hotspots arerequired for transcriptional responses. Nevertheless, despite the loss of PcG activities leads toincreased chromatin accessibility, this is not necessarily accompanied by transcriptionalactivation, indicating that accessible chromatin is not always predictive of gene expression.