The nucleoporin Nup153 is the anchor for Kif1a during basal nuclear migration in brain progenitor cells.
Autor: | Falnikar A; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA. Electronic address: aditi.falnikar@gmail.com., Quintremil S; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA., Zhao HJ; Institute of Brain Science, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan., Cheng HY; Institute of Brain Science, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan., Helmer P; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA., Tsai JW; Institute of Brain Science, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan., Vallee RB; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA. Electronic address: rv2025@cumc.columbia.edu. |
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Jazyk: | angličtina |
Zdroj: | Cell reports [Cell Rep] 2024 Dec 24; Vol. 43 (12), pp. 115008. Date of Electronic Publication: 2024 Dec 11. |
DOI: | 10.1016/j.celrep.2024.115008 |
Abstrakt: | Radial glial progenitors (RGPs) are highly elongated epithelial cells that give rise to most stem cells, neurons, and glia in the vertebrate cerebral cortex. During development, the RGP nuclei exhibit a striking pattern of cell-cycle-dependent oscillatory movements known as interkinetic nuclear migration (INM), which we previously found to be mediated during G1 by the kinesin Kif1a and during G2 by cytoplasmic dynein, recruited to the nuclear envelope by the nucleoporins RanBP2 and Nup133. We now identify Nup153 as a nucleoporin anchor for Kif1a, responsible for G1-specific basal nuclear migration, providing a complete model for the mechanisms underlying this basic but mysterious behavior, with broad implications for understanding brain development. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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