ArticleeLife2023
Nuclear m6A reader YTHDC1 promotes muscle stem cell activation/proliferation by regulating mRNA splicing and nuclear export.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 74 citations in OpenAlex.
- T‑box transcription factor 15 regulated by methyltransferase‑like 3‑mediated N6‑methyladenosine modification promotes immune escape and progression of gastric cancer by activating matrix metalloproteinase 14 transcription.International journal of oncology · 2026Article
- RNA Chemical Modifications in Mammalian Skeletal Muscle Development, Homeostasis, and Disease: Regulatory Mechanisms and Chemical Biology Perspectives.Molecules (Basel, Switzerland) · 2026Review
- In vivo systematic detection of the outcomes of CRISPR-Cas9-mediated DNA repair in skeletal muscle stem cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- The YTHDC1-mInternational journal of oral science · 2026Article
- Targeted cellular micropharmacies deliver therapeutic agents to the brain.EMBO molecular medicine · 2026Article
- Emerging roles of RNA mInternational journal of oncology · 2026Review
- m6A modified circPTK2 mediates TNBC chemotherapy resistance.Translational cancer research · 2026Article
- YTHDC1-Mediated mJournal of agricultural and food chemistry · 2026Article
- RBFOX2-dependent alternative splicing of Numb regulates Notch signaling during muscle stem cell activation.Stem cell reports · 2026Article
- Recent advances in m6A RNA modification in hepatocellular carcinoma: from mechanisms to therapeutic potential.Frontiers in molecular biosciences · 2026Review
- RBM15 affects mitophagy in intracerebral hemorrhage by promoting E2F1 nuclear translocation via NXF1.Frontiers in immunology · 2026Article
- Molecular mechanisms underlying the inhibition ofMycology · 2026Article
- Review
- N6-methyladenosine: a key regulator in ocular disease mechanisms and treatment.Cell death discovery · 2025Review
- METTL3-dependent mAutophagy · 2025Article
- Unscheduled mInternational journal of molecular sciences · 2025Article
- Epitranscriptomic Regulation of Hepatitis B Virus by RNA 5-Methylcytosine: Functions, Mechanisms, and Therapeutic Potential.Viruses · 2025Review
- YTHDC1 Modulates the Osteogenic Capacity of hPDLSCs via Wnt/β-Catenin Signalling Pathway for the Treatment of Bone Defects in Osteoporosis Rats.Cell proliferation · 2025Article
- Perspectives on mitochondrial dysfunction in the regeneration of aging skeletal muscle.Cellular & molecular biology letters · 2025Review
- Crosstalk Between N6-Methyladenosine and Other Epigenetic Mechanisms in Central Nervous System Development and Disorders.Biomolecules · 2025Review
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
Abstract
Skeletal muscle stem cells (also known as satellite cells [SCs]) are essential for muscle regeneration and the regenerative activities of SCs are intrinsically governed by gene regulatory mechanisms, but the post-transcriptional regulation in SCs remains largely unknown. N(6)-methyladenosine (m6A) modification of RNAs is the most pervasive and highly conserved RNA modification in eukaryotic cells; it exerts powerful impact on almost all aspects of mRNA processing that is mainly endowed by its binding with m6A reader proteins. In this study, we investigate the previously uncharacterized regulatory roles of YTHDC1, an m6A reader in mouse SCs. Our results demonstrate that YTHDC1 is an essential regulator of SC activation and proliferation upon acute injury-induced muscle regeneration. The induction of YTHDC1 is indispensable for SC activation and proliferation; thus, inducible YTHDC1 depletion almost abolishes SC regenerative capacity. Mechanistically, transcriptome-wide profiling using LACE-seq in both SCs and mouse C2C12 myoblasts identifies m6A-mediated binding targets of YTHDC1. Next, splicing analysis defines splicing mRNA targets of m6A-YTHDC1. Furthermore, nuclear export analysis also leads to the identification of potential mRNA export targets of m6A-YTHDC1 in SCs and C2C12 myoblasts;interestingly, some mRNAs can be regulated at both splicing and export levels. Lastly, we map YTHDC1 interacting protein partners in myoblasts and unveil a myriad of factors governing mRNA splicing, nuclear export, and transcription, among which hnRNPG appears to be a bona fide interacting partner of YTHDC1. Altogether, our findings uncover YTHDC1 as an essential factor controlling SC regenerative ability through multifaceted gene regulatory mechanisms in mouse myoblast cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.