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Significance Methylation of cytosine bases in DNA is an epigenetic modification that influences gene expression. TET (ten-eleven translocation)-family dioxygenases catalyze conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) and additional oxidized methylcytosines in DNA. Here, we show that both Tet3- and Tet1/2/3-deficient mouse ES cells showed impaired neural conversion, with skewing toward cardiac mesoderm. Genome-wide analyses showed that Tet3 mediates cell-fate decisions by inhibiting Wnt signaling. Consistent with these findings, Wnt signaling was hyperactivated in Tet1/2/3-deficient embryos, leading to aberrant differentiation of bipotent neuromesodermal progenitors into mesoderm at the expense of neuroectoderm. Our data demonstrate a key role for TET proteins in modulating Wnt signaling and establishing the proper balance between neural and mesoderm cell fate determination.

Tet proteins influence the balance between neuroectodermal and mesodermal fate choice by inhibiting Wnt signaling