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TPX2 regulates neuronal morphology through kinesin-5 interaction

Olga I Kahn1, Ngoc Ha1, Michelle A Baird2

  • 1Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, Pennsylvania.

Cytoskeleton (Hoboken, N.J.)
|August 11, 2015
PubMed

Insights

Targeting protein for Xklp2 (TPX2) regulates kinesin-5 in neurons. Depleting TPX2 accelerates neuronal process outgrowth, similar to kinesin-5 inhibition, highlighting TPX2

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Targeting protein for Xklp2 (TPX2) is a key mitotic spindle assembly factor in mammalian cells.
  • TPX2 interacts with and regulates the mitotic motor protein kinesin-5 (Eg5/Kif11).
  • Kinesin-5 inhibition in neurons accelerates axon growth and thins dendrites.

Purpose of the Study:

  • To investigate the role of TPX2 in neuronal process outgrowth.
  • To determine if TPX2's interaction with kinesin-5 is critical for its function in neurons.

Main Methods:

  • Depletion of TPX2 in cultured neurons using RNA interference.
  • Assessment of neuronal process outgrowth rates.
  • Rescue experiments with wild-type TPX2 and a TPX2 mutant lacking the kinesin-5-interacting domain.

Main Results:

  • Depletion of TPX2 significantly speeds up neuronal process outgrowth.
  • This phenotype is rescued by re-expressing TPX2.
  • Re-expression of a TPX2 mutant lacking the kinesin-5-interacting domain does not rescue the phenotype.

Conclusions:

  • TPX2 levels and distribution regulate kinesin-5 activity in neurons.
  • The interaction domain between TPX2 and kinesin-5 is essential for TPX2's function in neurite outgrowth.
  • TPX2 plays a crucial role in determining the timing and location of kinesin-5 action during neuronal development.
Keywords:
Eg5TPX2kif11microtubulemolecular motorneuron

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