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Hypothetical model. Our results show that, during NCC specification, miR-203 is highly expressed and prevents the initial accumulation of SNAIL2 and PHF12. Prior to NCC delamination, the accumulation of SNAIL2 causes epigenetic silencing of miR-203, mediated by DNMT3B. This silencing enables rapid concomitant upregulation of both Snail2 and Phf12, resulting in Cad6b repression at the beginning of the NCC epithelial-to-mesenchymal transition.
