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Emerging largely evidence suggests that Receptor for Activated C\u2010kinase 7 (RACK7), an epigenetic reader protein, may play a role in brain development and neural developmental disease, but in vivo explorations are still lacking. Here, a <jats:italic>Rack7<\/jats:italic> conditional knock\u2010out mouse model is established and shows that <jats:italic>Rack7<\/jats:italic>\u2010deficient mice exhibit overt developmental defects associated with aberrant astrocyte development. Mechanistically, it is found that RACK7 interacts with the histone H3 lysine 27 (H3K27) methyltransferase, i.e., the Polycomb Repressive Complex 2 (PRC2)\u00a0complex, to establish the genomic locations of Suppressor of Zeste 12 homolog (SUZ12) and H3K27 methylation. Deletion of <jats:italic>Rack7<\/jats:italic> in astrocytes leads to a remarkable decrease of H3K27me3 chromatin localization genome\u2010wide. 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