{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang F"],"funding":["National Institute of Neurological Disorders and Stroke","Dr. Miriam and Sheldon G. Adelson Medical Research Foundation","NHGRI NIH HHS","NINDS NIH HHS","National Institutes of Health"],"pagination":["144-156.e8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11698649"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["32(1)"],"pubmed_abstract":["Quiescence acquisition of proliferating neural stem cells (NSCs) is required to establish the adult NSC pool. The underlying molecular mechanisms are not well understood. Here, we showed that conditional deletion of the m<sup>6</sup>A reader Ythdf2, which promotes mRNA decay, in proliferating NSCs in the early postnatal mouse hippocampus elevated quiescence acquisition in a cell-autonomous fashion with decreased neurogenesis. Multimodal profiling of m<sup>6</sup>A modification, YTHDF2 binding, and mRNA decay in hippocampal NSCs identified shared targets in multiple transforming growth factor β (TGF-β)-signaling-pathway components, including TGF-β ligands, maturation factors, receptors, transcription regulators, and signaling regulators. Functionally, Ythdf2 deletion led to TGF-β-signaling "],"journal":["Cell stem cell"],"pubmed_title":["m&lt;sup&gt;6&lt;/sup&gt;A/YTHDF2-mediated mRNA decay targets TGF-β signaling to suppress the quiescence acquisition of early postnatal mouse hippocampal NSCs."],"pmcid":["PMC11698649"],"funding_grant_id":["R35 NS097370","R35 NS116843","R35NS116843","R35NS097370","R35 NS137480","RM1HG008935","RM1 HG008935"],"pubmed_authors":["Zhang F","He C","Fu Y","Kawaguchi R","Zhao T","Song H","Sun Y","Jimenez-Cyrus D","Wang Q","Zhang Z","Ming GL","Shen Y","Geschwind DH"],"additional_accession":[]},"is_claimable":false,"name":"m&lt;sup&gt;6&lt;/sup&gt;A/YTHDF2-mediated mRNA decay targets TGF-β signaling to suppress the quiescence acquisition of early postnatal mouse hippocampal NSCs.","description":"Quiescence acquisition of proliferating neural stem cells (NSCs) is required to establish the adult NSC pool. The underlying molecular mechanisms are not well understood. Here, we showed that conditional deletion of the m<sup>6</sup>A reader Ythdf2, which promotes mRNA decay, in proliferating NSCs in the early postnatal mouse hippocampus elevated quiescence acquisition in a cell-autonomous fashion with decreased neurogenesis. Multimodal profiling of m<sup>6</sup>A modification, YTHDF2 binding, and mRNA decay in hippocampal NSCs identified shared targets in multiple transforming growth factor β (TGF-β)-signaling-pathway components, including TGF-β ligands, maturation factors, receptors, transcription regulators, and signaling regulators. Functionally, Ythdf2 deletion led to TGF-β-signaling ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-06T08:56:28.105Z","creation":"2026-05-28T03:12:06.736Z"},"accession":"S-EPMC11698649","cross_references":{"pubmed":["39476834"],"doi":["10.1016/j.stem.2024.10.002"]}}