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Repeat-element RNAs integrate a neuronal growth circuit.

Eitan Erez Zahavi1, Indrek Koppel2, Riki Kawaguchi3

  • 1Departments of Biomolecular Sciences and Molecular Neuroscience, Weizmann Institute of Science, Rehovot, Israel.

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Newly identified growth-inducing B2-SINEs (GI-SINEs) promote axonal growth after neuronal injury. These transposable elements link gene transcription to local RNA translation, crucial for neuronal regeneration.

Keywords:
RNA localizationShort Interspersed Nuclear Elementsaxon growthaxonal transportlocal translationnerve injuryneuronal length sensingnon-coding RNA

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Neuronal growth and regeneration depend on local mRNA translation within axons.
  • Understanding the molecular mechanisms regulating axonal repair is critical for treating neurological injuries.

Purpose of the Study:

  • To investigate changes in RNA polyadenylation following sensory neuron injury.
  • To identify novel elements involved in regulating axonal regeneration.

Main Methods:

  • Analysis of RNA polyadenylation in injured sensory neurons.
  • Induction and expression of B2-SINE repeat elements (GI-SINEs).
  • Assessment of axonal growth in various neuronal models (sensory, retinal, corticospinal).
  • Investigation of GI-SINE interactions with ribosomal proteins and nucleolin.
  • Use of antisense oligonucleotides to disrupt GI-SINE function.

Main Results:

  • Upregulation of specific polyadenylated B2-SINE repeat elements (GI-SINEs) in injured sensory neurons.
  • GI-SINEs are induced from AP-1 promoter-associated loci.
  • Exogenous GI-SINE expression promotes axonal growth in multiple neuronal types.
  • GI-SINEs interact with ribosomal proteins and nucleolin to modulate cytoplasmic translation.
  • Antisense inhibition of GI-SINEs impairs sensory neuron outgrowth and nucleolin-ribosome interactions.

Conclusions:

  • A specific subfamily of transposable elements, GI-SINEs, plays an integral role in neuronal regeneration.
  • GI-SINEs bridge AP-1 transcription factors with localized RNA translation machinery in neurons.
  • These findings reveal a novel regulatory circuit for axonal growth and repair.