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Basic Science and Pathogenesis.

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Ras homolog abundant in the striatum (Rhes) protein promotes tunneling nanotubes (TNTs) formation and transfer of disease proteins like Tau and mutant huntingtin (mHTT). Targeting Rhes offers a potential therapy for neurodegenerative diseases.

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Area of Science:

  • Cell Biology
  • Neuroscience
  • Molecular Biology

Background:

  • Tunneling nanotubes (TNTs) are F-actin-based cell connections facilitating intercellular cargo transfer.
  • Proteins implicated in neurodegenerative diseases, such as Tau and mutant huntingtin (mHTT), are transported via TNTs.
  • The molecular mechanisms of TNT formation, particularly in the brain, are not fully understood.

Purpose of the Study:

  • To investigate the role of Ras homolog abundant in the striatum (Rhes) in TNT formation and cargo transfer.
  • To identify novel regulators of Rhes-mediated TNTs.
  • To explore the therapeutic potential of targeting Rhes for neurodegenerative diseases.

Main Methods:

  • Utilized cell culture models, co-immunoprecipitation, high-resolution microscopy, and mass spectrometry.
  • Employed pharmacological and knockout approaches to study the impact of SLC4A7.
  • Investigated Rhes-mediated TNT formation and mHTT/Tau transfer in neuronal and microglial cells, as well as in the brain.

Main Results:

  • Rhes was found to induce TNT-like protrusions and mediate the transfer of mHTT in neuronal cells and the brain.
  • Solute carrier family four member 7 (SLC4A7), a pH regulator, was identified as a novel binding partner and regulator of Rhes in TNT formation.
  • Loss of SLC4A7 inhibited TNT formation and mHTT dissemination, while Rhes also enhanced TNT formation in microglia.

Conclusions:

  • Rhes is critical for TNT production and the spread of Tau and mHTT in the brain via neurons and microglia.
  • Targeting Rhes presents a promising therapeutic strategy for Huntington's disease and tauopathies.