ArticleInternational journal of oral science2026
OGT mediates O-GlcNAcylation of MEIS2 and affects palatal osteogenic development.
Article in International journal of oral science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Post-translational modifications (PTMs) have been gradually elucidated in congenital malformations such as cleft palate. Among them, O-GlcNAcylation as a dynamic PTM of proteins regulates various critical biological processes including transcription, translation, and cell fate determination. In this study, a substantial decline in O-linked β-D-N-acetylglucosamine (O-GlcNAc) levels was detected within the palatine plates of all-trans retinoic acid (atRA)-induced cleft palate mice. The role of O-GlcNAc transferase (OGT), the sole enzyme responsible for catalyzing O-GlcNAcylation, was investigated in the process of palatal development. In a zebrafish model, the loss of O-GlcNAc resulted in an elevated prevalence of cleft palate and compromised palatal bone formation. Mechanistically, O-GlcNAcylation of myeloid ecotropic viral integration site 2 (MEIS2), which is mediated by OGT, was found to maintain osteogenic homeostasis by modulating its protein stability through inhibition of ubiquitination. Notably, the serine 237 residue (Ser237) was identified as a critical site for MEIS2 O-GlcNAcylation. Together, the present study uncovers the important function of MEIS2 O-GlcNAcylation in palatal bone development and establishes a novel theoretical framework for understanding the regulatory network of palatal development. This finding may provide novel avenues for the future diagnosis and prevention of cleft palate.
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