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Oligodendrocyte differentiation alters tRNA modifications and codon optimality-mediated mRNA decay

Author

Listed:
  • Sophie Martin

    (Johns Hopkins University School of Medicine)

  • Kevin C. Allan

    (Case Western Reserve University School of Medicine)

  • Otis Pinkard

    (Case Western Reserve University School of Medicine)

  • Thomas Sweet

    (Case Western Reserve University School of Medicine)

  • Paul J. Tesar

    (Case Western Reserve University School of Medicine)

  • Jeff Coller

    (Johns Hopkins University School of Medicine
    Johns Hopkins University School of Medicine)

Abstract

Oligodendrocytes are specialized cells that confer neuronal myelination in the central nervous system. Leukodystrophies associated with oligodendrocyte deficits and hypomyelination are known to result when a number of tRNA metabolism genes are mutated. Thus, for unknown reasons, oligodendrocytes may be hypersensitive to perturbations in tRNA biology. In this study, we survey the tRNA transcriptome in the murine oligodendrocyte cell lineage and find that specific tRNAs are hypomodified in oligodendrocytes within or near the anticodon compared to oligodendrocyte progenitor cells (OPCs). This hypomodified state may be the result of differential expression of key modification enzymes during oligodendrocyte differentiation. Moreover, we observe a concomitant relationship between tRNA hypomodification and tRNA decoding potential; observing oligodendrocyte specific alterations in codon optimality-mediated mRNA decay and ribosome transit. Our results reveal that oligodendrocytes naturally maintain a delicate, hypersensitized tRNA/mRNA axis. We suggest this axis is a potential mediator of pathology in leukodystrophies and white matter disease when further insult to tRNA metabolism is introduced.

Suggested Citation

  • Sophie Martin & Kevin C. Allan & Otis Pinkard & Thomas Sweet & Paul J. Tesar & Jeff Coller, 2022. "Oligodendrocyte differentiation alters tRNA modifications and codon optimality-mediated mRNA decay," Nature Communications, Nature, vol. 13(1), pages 1-21, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-32766-3
    DOI: 10.1038/s41467-022-32766-3
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    References listed on IDEAS

    as
    1. J. Blaze & A. Navickas & H. L. Phillips & S. Heissel & A. Plaza-Jennings & S. Miglani & H. Asgharian & M. Foo & C. D. Katanski & C. P. Watkins & Z. T. Pennington & B. Javidfar & S. Espeso-Gil & B. Ros, 2021. "Neuronal Nsun2 deficiency produces tRNA epitranscriptomic alterations and proteomic shifts impacting synaptic signaling and behavior," Nature Communications, Nature, vol. 12(1), pages 1-16, December.
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