Apical Abscission Alters Cell Polarity and Dismantles the Primary Cilium During Neurogenesis
Open accessAbstract
Developing Neurons Make the Cut: Neurons in the developing central nervous system of vertebrates derive from cells adjacent to the ventricles that then proliferate and differentiate to populate the brain. As one of these cells begins to differentiate, the cell nucleus migrates toward its new residence, away from the ventricle surface, and the cell stretches out. At some point, like any maturing adolescent, the cell has to leave home. Das and Storey (p. 200 ; see the Perspective by Tozer and Morin ) show that instead of letting go and drawing the trailing process up into the migrating cell, the cell cuts off and discards its first roots. The abscission process leaves behind the primary cilium and any signaling systems localized to the cilium.
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Quiescent cells can lose their cilium due to developmental programming or environmental insults such as mechanical stress.
“Quiescent cells can lose their cilium as a consequence of developmental programming 15–19 or in response to environmental insults such as mechanical stress 20.”
From Cellular signalling by primary cilia in development, organ function and disease (2019) · cites this paper as [15]
The Abstract and a main-text passage indexed under Abstract (page unavailable) show that apical abscission dismantles the primary cilium during neuronal differentiation. They place cilium disassembly before cell-cycle exit, however, so the paper does not establish cilium loss in already quiescent cells. The mechanical-stress clause has a separate citation and is not attributed to this source. (LLM, conf=0.88)
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Cellular signalling by primary cilia in development, organ function and disease
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- Authors
- Das, R. M., & Storey, K. G.
- Affiliations
- University of Dundee (GB)
- Corresponding author
- Storey, Kate G.
- Venue
- Science
- Published
- 2014-01-10
- Volume
- 343
- Issue
- 6167
- Pages
- 200-204
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC4066580
- OpenAlex
- W1981567186
- Cited by
- 182
- References
- 29
- Citations by year
- 2026: 4 · 2025: 15 · 2024: 14 · 2023: 11 · 2022: 22 · 2021: 16 · 2020: 20 · 2019: 13 · 2018: 21 · 2017: 10 · 2016: 17 · 2015: 6 · 2014: 13
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Discovery Research Portal (University of Dundee) (submittedVersion)
- Funders
- Wellcome Trust (083611/Z/07/Z, 083611)
- Medical Research Council (MR/K015869/1)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Kidney Cyst Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- cell polarity, neurogenesis, neural tube, Sonic hedgehog signaling, p27, N-cadherin, Neurog2, cell cycle exit, chick embryo
- MeSH terms
- Actins, Animals, Cell Division, Chick Embryo, Cilia, Myosins, Nerve Tissue Proteins, Neurons, Cadherins, Cell Polarity, Cyclin-Dependent Kinase Inhibitor p27, Mice, Basic Helix-Loop-Helix Proteins, Neural Tube, Neurogenesis, Carcinogenesis
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