AI Article Synopsis
- Asymmetric cell division (ACD) during corticogenesis is not fully understood, but spindle-size asymmetry (SSA) plays a crucial role in this process and helps regulate neurogenesis.
- SSA occurs during metaphase and is maintained throughout the division, with neurons preferentially forming from the larger spindle pole.
- The regulation of SSA is influenced by the Wnt/planar cell polarity signaling pathway, specifically Wnt7a and Vangl2, with implications for proper cell cycle timing and the generation of late-born neurons.
Article Abstract
The regulation of asymmetric cell division (ACD) during corticogenesis is incompletely understood. We document that spindle-size asymmetry (SSA) between the two poles occurs during corticogenesis and parallels ACD. SSA appears at metaphase and is maintained throughout division, and we show it is necessary for proper neurogenesis. Imaging of spindle behavior and division outcome reveals that neurons preferentially arise from the larger-spindle pole. Mechanistically, SSA magnitude is controlled by Wnt7a and Vangl2, both members of the Wnt/planar cell polarity (PCP)-signaling pathway, and relayed to the cell cortex by P-ERM proteins. In vivo, Vangl2 and P-ERM downregulation promotes early cell-cycle exit and prevents the proper generation of late-born neurons. Thus, SSA is a core component of ACD that is conserved in invertebrates and vertebrates and plays a key role in the tight spatiotemporal control of self-renewal and differentiation during mammalian corticogenesis.
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| http://dx.doi.org/10.1016/j.celrep.2013.12.026 | DOI Listing |
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