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Abstract Many craniofacial disorders linked to mutations in enhancer-associated chromatin modifiers, including Kabuki syndrome (KS), present with skeletal abnormalities. KS is a craniofacial developmental disorder characterized by mutations in KMT2D, a histone H3 lysine 4 (H3K4) methyltransferase. The cellular origins and molecular pathways leading to KMT2D-dependent skeletal deficits in KS are not well characterized.
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