Plexin-B1 is a GTPase activating protein for M-Ras, remodelling dendrite morphology

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Ex Vivo Imaging of Postnatal Cerebellar Granule Cell Migration Using Confocal Macroscopy
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Published on: May 12, 2015

Yasuhiro Saito1, Izumi Oinuma, Satoshi Fujimoto

  • 1Laboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.

EMBO Reports
|May 16, 2009
PubMed

Insights

Plexin-B1 acts as a dual GTPase activating protein (GAP) for R-Ras and M-Ras. This dual function allows Plexin-B1 to regulate both axon and dendrite morphology in neurons.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Plexins are semaphorin receptors involved in axonal guidance.
  • Plexin-B1 was previously shown to act as an R-Ras GTPase activating protein (GAP), inducing growth cone collapse.
  • Ras GTPases are key regulators of cell signaling pathways.

Purpose of the Study:

  • To investigate the role of M-Ras in neuronal development.
  • To determine if Plexin-B1 exhibits GAP activity towards M-Ras.
  • To elucidate the downstream signaling pathways regulated by Plexin-B1 and M-Ras in dendrite development.

Main Methods:

  • Investigated M-Ras expression during cortical neuron development.
  • Utilized knockdown and overexpression techniques for M-Ras and R-Ras.
  • Examined the effect of semaphorin 4D (Sema4D) on M-Ras activity and dendritic morphology.
  • Assessed extracellular signal-regulated kinase (ERK) activation.

Main Results:

  • M-Ras expression increased during dendritic development.
  • M-Ras, not R-Ras, knockdown reduced dendritic outgrowth and branching.
  • Overexpression of M-Ras enhanced dendritic growth and branching.
  • Sema4D suppressed M-Ras activity and dendritic growth, effects blocked by M-Ras(Q71L).
  • M-Ras(Q71L) stimulated ERK activation, promoting dendrite growth, while Sema4D suppressed ERK.

Conclusions:

  • Plexin-B1 functions as a dual GAP for both R-Ras and M-Ras.
  • Plexin-B1 regulates axon morphology via R-Ras and dendrite morphology via M-Ras.
  • The M-Ras-ERK pathway is crucial for Sema4D-mediated regulation of dendritic development.

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