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The E3 ubiquitin ligase TRIM9 regulates both attractive and repulsive axonal guidance by netrin-1. TRIM9 interacts with netrin receptors DCC and UNC5C, influencing growth cone responses and neuronal development.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Netrin-1 is a guidance cue that can attract or repel axons.
  • The mechanisms by which netrin-1 elicits diverse axonal responses, beyond DCC and UNC5 receptors, are not fully understood.
  • TRIM9, an E3 ubiquitin ligase, is known to regulate attractive netrin-1 responses via DCC.

Purpose of the Study:

  • To investigate the role of TRIM9 in both attractive and repulsive axonal responses to netrin-1.
  • To determine how TRIM9 interacts with netrin receptors DCC and UNC5C.
  • To elucidate TRIM9's function in growth cone morphogenesis and neuronal development.

Main Methods:

  • Utilized microfluidic-based netrin-1 gradients and bath application to study axonal responses in murine cortical neurons.
  • Employed knockdown of UNC5C and DCC to assess their roles in netrin-1-mediated attraction and repulsion.
  • Investigated TRIM9's localization, interaction with DCC and UNC5C, and its effect on receptor surface levels and FAK activity.

Main Results:

  • Murine netrin-1 induced biphasic axonal responses (attraction at low, repulsion at high concentrations).
  • TRIM9 deletion altered both attractive and repulsive axon turning and growth cone size in response to netrin-1.
  • TRIM9 is essential for netrin-1-dependent changes in DCC and UNC5C surface levels and negatively regulates FAK activity.

Conclusions:

  • TRIM9 plays a crucial role in mediating both attractive and repulsive axonal guidance by netrin-1.
  • TRIM9 interacts with and regulates both DCC and UNC5C receptors, impacting growth cone dynamics.
  • TRIM9 is a key regulator of neuronal development by controlling netrin-1 signaling pathways.