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

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, Shreya Chand, Edsel A. Pena, Alma L. Burlingame, Clifford J. Woolf, Mike Fainzilber, Arthur W. English and Jeffery L. Twiss ()
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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

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-05647-x

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