Cep120 and TACCs Control Interkinetic Nuclear Migration and the Neural Progenitor Pool

• Published in: Neuron (Cambridge, Mass.) Vol. 56; no. 1; pp. 79 - 93
• Main Authors: Xie, Zhigang, Moy, Lily Y., Sanada, Kamon, Zhou, Ying, Buchman, Joshua J., Tsai, Li-Huei
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 04-10-2007; Elsevier Limited
• Subjects: Animals; Cell cycle; Cell Cycle Proteins - genetics; Cell Cycle Proteins - physiology; Cell Division - physiology; Cell Movement - physiology; Cell Nucleus - metabolism; CELLBIO; DEVBIO; Electroporation - methods; Embryo, Mammalian; Embryos; Female; In Vitro Techniques; Kinases; Mice; Microtubule-Associated Proteins - genetics; Microtubule-Associated Proteins - physiology; Migration; MOLNEURO; Neocortex - cytology; Neocortex - embryology; Neocortex - physiology; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; Neurogenesis; Neurons - physiology; Plasmids; Pregnancy; Protein Transport; Proteins; RNA, Small Interfering - genetics; RNA, Small Interfering - metabolism; Stem Cells - cytology; Stem Cells - physiology; Studies; Time Factors; Transfection - methods; CELLBIO; DEVBIO; MOLNEURO
• ISSN: 0896-6273; 1097-4199
• DOI: 10.1016/j.neuron.2007.08.026

Centrosome- and microtubule-associated proteins have been shown to be important for maintaining the neural progenitor pool during neocortical development by regulating the mitotic spindle. It remains unclear whether these proteins may control neurogenesis by regulating other microtubule-dependent processes such as nuclear migration. Here, we identify Cep120, a centrosomal protein preferentially expressed in neural progenitors during neocortical development. We demonstrate that silencing Cep120 in the developing neocortex impairs both interkinetic nuclear migration (INM), a characteristic pattern of nuclear movement in neural progenitors, and neural progenitor self-renewal. Furthermore, we show that Cep120 interacts with transforming acidic coiled-coil proteins (TACCs) and that silencing TACCs also causes defects in INM and neural progenitor self-renewal. Our data suggest a critical role for Cep120 and TACCs in both INM and neurogenesis. We propose that sustaining INM may be a mechanism by which microtubule-regulating proteins maintain the neural progenitor pool during neocortical development.