Schwann cell articles within Nature Communications

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  • Article
    | Open Access

    Schwannomas are mainly caused by NF2 tumour suppressor inactivation, but they display intratumoural heterogeneity. Here the authors show that this heterogeneity is caused by the loss of polarity and acquisition of different programmes of ErbB ligand production in NF2-mutant Schwann cells.

    • Christine Chiasson-MacKenzie
    • , Jeremie Vitte
    •  & Andrea I. McClatchey
  • Article
    | Open Access

    The mechanism of CGRP-evoked peripheral pain is unclear. Here, the authors show that the CGRP-mediated neuronal/Schwann cell pathway mediates allodynia associated with neurogenic inflammation, contributing to the algesic action of CGRP in mice.

    • Francesco De Logu
    • , Romina Nassini
    •  & Pierangelo Geppetti
  • Article
    | Open Access

    Prohibitin 2 can localize to the axon-Schwann-cell interface and is required for myelin formation. Here, the authors show that deletion of prohibitin 1 in Schwann cells instead triggers severe myelin loss likely caused by mitochondrial dysfunction, and not rescued by inhibition of the ensuing integrated stress response.

    • Gustavo Della-Flora Nunes
    • , Emma R. Wilson
    •  & M. Laura Feltri
  • Article
    | Open Access

    Schwann cells (SCs) can acquire a repair phenotype following nerve injury. Here, the authors show that stromal SCs in ganglioneuromas express nerve-repair genes. Importantly, neuroblastoma cells respond to repair-related SCs increasing neuronal differentiation and reducing proliferation via EGFL8.

    • Tamara Weiss
    • , Sabine Taschner-Mandl
    •  & Inge M. Ambros
  • Comment
    | Open Access

    Myelinating Schwann cells control the diameter of the axons they ensheath by an unknown mechanism. In a recent article in Nature Communications, Eichel and colleagues identify the tetraspan protein CMTM6 as a regulator of axonal caliber.

    • Nimrod Elazar
    •  & Elior Peles
  • Article
    | Open Access

    The molecular mechanisms regulating remyelination are unclear. Here, the authors show that promoting deacetylation of eEF1A1 prevents the translocation of Sox10 outside the nucleus, contributing to maintaining the expression of Sox10 target genes and increasing remyelination efficiency.

    • Mert Duman
    • , Adrien Vaquié
    •  & Claire Jacob
  • Article
    | Open Access

    The peripheral nervous system has been implicated in wound healing. Here, Parfejevs and colleagues report that cutaneous wounding in mice induces the de-differentiation and proliferation of Schwann cells, which disseminate into the wound bed, secrete soluble factors, and promote wound healing.

    • Vadims Parfejevs
    • , Julien Debbache
    •  & Lukas Sommer
  • Article |

    Specific Schwann cell-axon interactions control the initiation of myelination in the peripheral nervous system. Here the authors show that the tumour suppressor protein Lkb1 is asymmetrically localized to the Schwann cell-axon interface and co-localizes with the polarity protein Par-3 to establish the initiation of myelination.

    • Yun-An A. Shen
    • , Yan Chen
    •  & Q. Richard Lu
  • Article |

    Myelination of peripheral axons by Schwann cells is essential for proper transmission of nerve signals but the underlying mechanisms are not completely understood. Here the authors show that metabolic changes are required to ensure Schwann cell differentiation and proper myelination, and involve the tumour suppressor Lkb1 in regulating this process.

    • Shabnam Pooya
    • , Xiaona Liu
    •  & Biplab Dasgupta