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Axonal G3BP1 stress granule protein limits axonal mRNA translation and nerve regeneration

Author

Listed:
  • Pabitra K. Sahoo

    (University of South Carolina)

  • Seung Joon Lee

    (University of South Carolina)

  • Poonam B. Jaiswal

    (Emory University College of Medicine)

  • Stefanie Alber

    (Weizmann Institute of Science)

  • Amar N. Kar

    (University of South Carolina)

  • Sharmina Miller-Randolph

    (University of South Carolina)

  • Elizabeth E. Taylor

    (University of South Carolina)

  • Terika Smith

    (University of South Carolina)

  • Bhagat Singh

    (FM Kirby Neurobiology Center and Boston Children’s Hospital and Harvard Medical School)

  • Tammy Szu-Yu Ho

    (FM Kirby Neurobiology Center and Boston Children’s Hospital and Harvard Medical School)

  • Anatoly Urisman

    (University of California San Francisco)

  • Shreya Chand

    (University of California San Francisco)

  • Edsel A. Pena

    (University of South Carolina)

  • Alma L. Burlingame

    (University of California San Francisco)

  • Clifford J. Woolf

    (FM Kirby Neurobiology Center and Boston Children’s Hospital and Harvard Medical School)

  • Mike Fainzilber

    (Weizmann Institute of Science)

  • Arthur W. English

    (Emory University College of Medicine)

  • Jeffery L. Twiss

    (University of South Carolina)

Abstract

Critical functions of intra-axonally synthesized proteins are thought to depend on regulated recruitment of mRNA from storage depots in axons. Here we show that axotomy of mammalian neurons induces translation of stored axonal mRNAs via regulation of the stress granule protein G3BP1, to support regeneration of peripheral nerves. G3BP1 aggregates within peripheral nerve axons in stress granule-like structures that decrease during regeneration, with a commensurate increase in phosphorylated G3BP1. Colocalization of G3BP1 with axonal mRNAs is also correlated with the growth state of the neuron. Disrupting G3BP functions by overexpressing a dominant-negative protein activates intra-axonal mRNA translation, increases axon growth in cultured neurons, disassembles axonal stress granule-like structures, and accelerates rat nerve regeneration in vivo.

Suggested Citation

  • Pabitra K. Sahoo & Seung Joon Lee & Poonam B. Jaiswal & Stefanie Alber & Amar N. Kar & Sharmina Miller-Randolph & Elizabeth E. Taylor & Terika Smith & Bhagat Singh & Tammy Szu-Yu Ho & Anatoly Urisman , 2018. "Axonal G3BP1 stress granule protein limits axonal mRNA translation and nerve regeneration," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-05647-x
    DOI: 10.1038/s41467-018-05647-x
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    Cited by:

    1. Topaz Altman & Ariel Ionescu & Amjad Ibraheem & Dominik Priesmann & Tal Gradus-Pery & Luba Farberov & Gayster Alexandra & Natalia Shelestovich & Ruxandra Dafinca & Noam Shomron & Florence Rage & Kevin, 2021. "Axonal TDP-43 condensates drive neuromuscular junction disruption through inhibition of local synthesis of nuclear encoded mitochondrial proteins," Nature Communications, Nature, vol. 12(1), pages 1-17, December.
    2. Lance T. Denes & Chase P. Kelley & Eric T. Wang, 2021. "Microtubule-based transport is essential to distribute RNA and nascent protein in skeletal muscle," Nature Communications, Nature, vol. 12(1), pages 1-19, December.

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