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Published on: January 29, 2018
RhoG promotes neural progenitor cell proliferation in mouse cerebral cortex
Satoshi Fujimoto1, Manabu Negishi, Hironori Katoh
1Laboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.
Molecular Biology of the Cell
|October 9, 2009
Summary
RhoG promotes neural progenitor cell (NPC) proliferation in the developing cortex. This process requires phosphatidylinositol 3-kinase (PI3K) signaling but does not impact NPC differentiation or survival.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Neural progenitor cells (NPCs) proliferate in the ventricular zone (VZ) during early cortical development to generate neurons.
- The molecular mechanisms governing NPC proliferation remain largely unelucidated.
Purpose of the Study:
- To investigate the role of RhoG, a Rho family GTPase, in regulating neural progenitor cell proliferation during cortical development.
Main Methods:
- Utilized constitutively active RhoG expression and RNA interference (RNAi) for RhoG knockdown in NPCs.
- Assessed NPC proliferation using bromodeoxyuridine (BrdU) incorporation in vitro and Ki67-positive cell counts in vivo.
- Investigated the involvement of phosphatidylinositol 3-kinase (PI3K) and ELMO in RhoG-mediated effects.
Main Results:
- RhoG expression was detected in the VZ during early cortical development.
- Overexpression of RhoG enhanced NPC proliferation and BrdU incorporation, while RhoG knockdown suppressed these processes.
- RhoG-mediated proliferation was dependent on PI3K activity but independent of ELMO interaction.
- RhoG knockdown did not affect NPC differentiation or survival.
Conclusions:
- RhoG acts as a positive regulator of NPC proliferation in the developing cortex.
- The proliferative effect of RhoG is mediated through the PI3K signaling pathway.
- RhoG's function in proliferation is distinct from its role in differentiation and survival.

