METTL3-Mediated m6A Modification is Involved in Neural Tube Defects via Modulating Wnt/β-Catenin Signaling Pathway

Abstract Neural tube defects (NTDs) remain one of the most life-threatening birth defects affecting infants. Most patients with a NTDs eventually develop lifelong disability, which cause significant morbidity and mortality and seriously reduce the quality of life. Therefore, identifiable of novel pathogenic strategies for NTDs patients is urgently required. Increasing evidence indicates that METTL3-mediated m6A modification is present in many physiopathological processes of cell apoptosis and survival. Our results demonstrate that SAM play not only a compensatory role, SAM can also lead to m6A modification changes in neural tube development and regulation. This research provides a good theoretical basis for further research on folic acid deficiency leading to NTDs, reveals the important role of SAM in the development of NTDs, and provides new clue for clinical researchers and clinical work.