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March 13, 2026Journal of Clinical InvestigationOpen Access

Methyltransferase complex subunit METTL3 maintains genome stability of erythroid cells via MTHFD1-mediated nucleotide biosynthesis

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Authors

LZLinlin ZhangHZHuizhi ZhaoSWShihui Wang

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Overview

Erythroid cell genome stability is maintained through METTL3's role in MTHFD1-mediated nucleotide biosynthesis, suggesting potential implications for anemia.

Key Points

  • To examine the role of METTL3 in maintaining genome stability through nucleotide biosynthesis during erythropoiesis.
  • Utilized EpoR-Cre mouse model for Mettl3 deletion
  • Performed m6A sequencing and RNA-seq analysis
  • Conducted biochemical assays to identify Mthfd1 as a target gene
  • Analyzed phenotypic changes in human erythroid cells upon METTL3 inhibition
  • Mettl3 deletion resulted in microcytic/hypochromic anemia and defective erythropoiesis
  • Disruption of nucleotide biosynthesis was linked to DNA damage and apoptosis in CFU-E cells
  • Decreased Mthfd1 expression and shortage of nucleotides dTMP and IMP were observed in erythroid cells
  • Inhibition of METTL3 in human cells mirrored the effects seen in mice, indicating conserved functionality

Cite This Study

Zhang et al. (2026) studied this question.

synapsesocial.com/papers/69b3acd302a1e69014ccedbchttps://doi.org/10.1172/jci196578
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Essential role of METTL3 in mitochondrial function and epigenetic regulation during preimplantation development in mice2026
  2. 2METTL3 Uncouples Chromatin Accessibility from Transcription during Retinal Development2025
  3. 3METTL3 uncouples chromatin accessibility from transcription during retinal development2025 · 1 citations
  4. 4Stage-specific requirement for METTL3-dependent m6A epitranscriptomic regulation during myogenesis2025
  5. 5Targeting METTL3 disrupts oncogenic transcriptional programs and activates immune and apoptotic pathways in Acute Myeloid Leukemia2025