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Related Concept Videos

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Related Experiment Video

Updated: Jan 10, 2026

Lineage Tracing and Clonal Analysis in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers MADM
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ARHGAP11A maintains cortical progenitor identity through RHOA-ROCK signaling during human brain development.

Yannick Hass1, Julia Kniep2, Anne Hoffrichter1

  • 1Central Institute of Mental Health (CIMH), Heidelberg University/Medical Faculty Mannheim, J5, 68159 Mannheim, Germany; Hector Institute for Translational Brain Research (HITBR gGmbH), J5, 68159 Mannheim, Germany; German Cancer Research Center (DKFZ), INF 280, 69120 Heidelberg, Germany.

Cell Reports
|November 27, 2025
PubMed
Summary

ARHGAP11A is crucial for maintaining the integrity of the ventricular zone during mammalian brain development. Its loss disrupts progenitor cell organization and division, impacting corticogenesis.

Keywords:
ARHGAP11ACP: developmental biologyCP: neuroscienceRHOA-ROCK signalingapical progenitorscerebral organoidscleavage-plane orientationextracellular matrixhuman cortical developmentneuroepithelial architectureneurogenesis

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Genetics

Background:

  • Mammalian brain development relies on coordinated progenitor cell activities.
  • Apical progenitors (APs) in the ventricular zone (VZ) are vital for brain size and complexity.
  • The role of specific Rho GTPase-activating proteins (Rho-GAPs) in progenitor identity and VZ architecture is not fully understood.

Purpose of the Study:

  • To investigate the function of the Rho GAP ARHGAP11A in human corticogenesis using forebrain organoids.
  • To determine ARHGAP11A's role in maintaining apical progenitor identity and VZ integrity.

Main Methods:

  • Utilized human forebrain organoids for studying corticogenesis.
  • Employed CRISPR-Cas9 gene editing to create ARHGAP11A knockout organoids.
  • Investigated the RHOA-ROCK-actin pathway and used pharmacological inhibitors.

Main Results:

  • ARHGAP11A knockout led to impaired neuroepithelial organization and randomized mitotic cleavage-plane orientation.
  • Loss of ARHGAP11A caused premature apical progenitor delamination and depletion.
  • Reduced cell density and glial cell numbers were observed in ARHGAP11A-deficient organoids.
  • Pharmacological inhibition of RHOA or ROCK rescued the observed defects.

Conclusions:

  • ARHGAP11A is essential for maintaining ventricular zone integrity and apical progenitor identity in human corticogenesis.
  • ARHGAP11A regulates cytoskeletal dynamics via the RHOA-ROCK-actin axis to preserve cortical progenitor populations.
  • These findings have significant implications for understanding human brain development and related disorders.