Molecular analysis reveals TET1 as an epigenetic nexus in developing embryos, highlighting mechanisms that drive folic acid resistance.
The etiology of neural tube defects (NTDs) involves complex gene-environmental interactions. Folic acid (FA) prevents NTDs, but the mechanisms remain poorly understood and at least 30% of human NTDs resist the beneficial effects of FA supplementation. Here, we identify the DNA demethylase TET1 as a nexus of folate-dependent one-carbon metabolism and genetic risk factors post-neural tube closure. We determine that cranial NTDs in
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Veer et al. (2024) studied this question.
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