1. NCAM regulates temporal specification of neural progenitor cells via profilin2 during corticogenesis
- Author
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Yu-Fang Ma, Melitta Schachner, Hua Min Qin, Rui Huang, Xue-Song Liang, Xiaoyan Lan, Shao Li, Vladimir Sytnyk, Guang-Yin Xu, Quan-Hong Ma, Yue Gao, Shen Li, Johannes Boltze, and De-Juan Yuan
- Subjects
Cellular differentiation ,Neurogenesis ,Mice, Transgenic ,Biology ,Article ,03 medical and health sciences ,Mice ,Profilins ,0302 clinical medicine ,Neural Stem Cells ,medicine ,otorhinolaryngologic diseases ,Animals ,Actin ,Cells, Cultured ,Research Articles ,030304 developmental biology ,Cell Proliferation ,Cerebral Cortex ,Mice, Knockout ,Neurons ,0303 health sciences ,Cell Differentiation ,Cell Biology ,QP ,Neural stem cell ,CD56 Antigen ,Cortex (botany) ,Cell biology ,Mice, Inbred C57BL ,Corticogenesis ,stomatognathic diseases ,medicine.anatomical_structure ,nervous system ,Cerebral cortex ,Neural cell adhesion molecule ,Neuroglia ,030217 neurology & neurosurgery - Abstract
The role of NCAM in corticogenesis is incompletely understood. The authors demonstrate that NCAM controls NPC proliferation and fate decision through profilin2-dependent regulation of actin polymerization. This finding sheds new light on NCAM’s functions in neurodevelopmental and mental disorders., The development of cerebral cortex requires spatially and temporally orchestrated proliferation, migration, and differentiation of neural progenitor cells (NPCs). The molecular mechanisms underlying cortical development are, however, not fully understood. The neural cell adhesion molecule (NCAM) has been suggested to play a role in corticogenesis. Here we show that NCAM is dynamically expressed in the developing cortex. NCAM expression in NPCs is highest in the neurogenic period and declines during the gliogenic period. In mice bearing an NPC-specific NCAM deletion, proliferation of NPCs is reduced, and production of cortical neurons is delayed, while formation of cortical glia is advanced. Mechanistically, NCAM enhances actin polymerization in NPCs by interacting with actin-associated protein profilin2. NCAM-dependent regulation of NPCs is blocked by mutations in the profilin2 binding site. Thus, NCAM plays an essential role in NPC proliferation and fate decision during cortical development by regulating profilin2-dependent actin polymerization.
- Published
- 2020