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The Lin28/let-7 axis is critical for myelination in the peripheral nervous system

Author

Listed:
  • Deniz Gökbuget

    (Institute of Molecular Health Sciences, ETH Zurich)

  • Jorge A. Pereira

    (Institute of Molecular Health Sciences, ETH Zurich)

  • Sven Bachofner

    (Institute of Molecular Health Sciences, ETH Zurich)

  • Antonin Marchais

    (Institute of Agricultural Sciences, ETH Zurich)

  • Constance Ciaudo

    (Institute of Molecular Health Sciences, ETH Zurich)

  • Markus Stoffel

    (Institute of Molecular Health Sciences, ETH Zurich)

  • Johannes H. Schulte

    (Children's Hospital Essen)

  • Ueli Suter

    (Institute of Molecular Health Sciences, ETH Zurich)

Abstract

MicroRNAs (miRNAs) are crucial regulators of myelination in the peripheral nervous system (PNS). However, the miRNAs species involved and the underlying mechanisms are largely unknown. We found that let-7 miRNAs are highly abundant during PNS myelination and that their levels are inversely correlated to the expression of lin28 homolog B (Lin28B), an antagonist of let-7 accumulation. Sustained expression of Lin28B and consequently reduced levels of let-7 miRNAs results in a failure of Schwann cell myelination in transgenic mouse models and in cell culture. Subsequent analyses revealed that let-7 miRNAs promote expression of the myelination-driving master transcription factor Krox20 (also known as Egr2) through suppression of myelination inhibitory Notch signalling. We conclude that the Lin28B/let-7 axis acts as a critical driver of PNS myelination, in particular by regulating myelination onset, identifying this pathway also as a potential therapeutic target in demyelinating diseases.

Suggested Citation

  • Deniz Gökbuget & Jorge A. Pereira & Sven Bachofner & Antonin Marchais & Constance Ciaudo & Markus Stoffel & Johannes H. Schulte & Ueli Suter, 2015. "The Lin28/let-7 axis is critical for myelination in the peripheral nervous system," Nature Communications, Nature, vol. 6(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9584
    DOI: 10.1038/ncomms9584
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