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. 2021 Jun 16;14:687581. doi: 10.3389/fnmol.2021.687581

FIGURE 6.

FIGURE 6

Schematic synopsis of how BAF complex may drive radial neuronal migration. (A) Schema showing the normal course of radial neuronal migration in the developing wild-type cortex. The parent cortical neural progenitor that generates majority of excitatory neurons is the radial glia cell (RGC). It is typically anchored at the ventricular surface by adhesion proteins (AdP) and extends a long slender fiber that traverses the marginal zone (MZ) to be anchored at the pial surface. The fiber acts as scaffold that supports the radially migrating neurons. After the RGC gives rise to a newborn neuron in the ventricular zone (VZ), the young postmitotic neuron usually attaches to the parent glial fiber and quickly migrates into the border between the subventricular (SVZ) and intermediate zones (IZ), where it acquires a multipolar neuronal (MN) identity and briefly stops migrating to receive spatiotemporal molecular cues for further oriented migration. The MN then switches to bipolar neuron (BP) and re-attaches to the glial fiber to migrate into the cortical plate (CP). In the CP, the migrating neuron detaches from the glial fiber to undergo somal translocation leading to its correct layer placement and ensures proper cortical lamination. The optimal activity of WNT signaling in the cortical germinal zone is indicated by a light shade of red and critical for neuronal migration. (B) Schema showing that loss of BAF complex in neural progenitors causes loss of adhesion proteins, glial fiber, disturbance of MN-to-BN transition, and increase in WNT signaling activity (indicated with a deep shade of red). These alterations result in accumulation of nascent neurons and MNs, leading to abnormal radial migration and cortical laminar malformation. Red cross denotes deletion or loss. (C) Picture showing outcome of rescue experiment following inhibition of the increased WNT signaling in the BAF complex mutant (dcKO_hGFAP-Cre) cortex. WNT inhibition (WNTi) with the chemical ICG001 led to substantial preservation of neuronal polarization, glial fibers, and cell adhesion leading to partial rescue of radial neuronal migration and cortical lamination.