Co-ordination of cell cycle and differentiation in the developing nervous system
Open accessAbstract
During embryonic development, cells must divide to produce appropriate numbers, but later must exit the cell cycle to allow differentiation. How these processes of proliferation and differentiation are co-ordinated during embryonic development has been poorly understood until recently. However, a number of studies have now given an insight into how the cell cycle machinery, including cyclins, CDKs (cyclin-dependent kinases), CDK inhibitors and other cell cycle regulators directly influence mechanisms that control cell fate and differentiation. Conversely, examples are emerging of transcriptional regulators that are better known for their role in driving the differentiated phenotype, which also play complementary roles in controlling cell cycle progression. The present review will summarise our current understanding of the mechanisms co-ordinating the cell cycle and differentiation in the developing nervous system, where these links have been, perhaps, most extensively studied.
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DYRK1A can phosphorylate and possibly regulate Cyclin D1 (G1-to-S phase transition and cell proliferation) and p27 (neuronal differentiation and cell cycle exit).
“This mechanism of action could be attributed to the ability of DYRK1A to phosphorylate and possibly regulate Cyclin D1 (G1-to-S phase transition and cell proliferation) and p27 (neuronal differentiation and cell cycle exit) (Frank and Tsai, 2009; Hindley and Philpott, 2012; Najas et al., 2015; Tejedor and Hammerle, 2011).”
From Sex-specific developmental alterations in DYRK1A expression in the brain of a Down syndrome mouse model (2024) · cites this paper as Hindley and Philpott, 2012
The Cyclins and CDKis sections (page numbers unavailable) link cyclin D1 to proliferation and p27kip1 to neuronal differentiation and cell-cycle exit. They do not say that DYRK1A phosphorylates or regulates either protein, so the proposed mechanism is not supported by this source. (LLM, conf=0.85)
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- Authors
- Hindley, C., & Philpott, A.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Philpott, Anna
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2012-05-29
- Volume
- 444
- Issue
- 3
- Pages
- 375-382
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC3365434
- OpenAlex
- W1993112528
- Cited by
- 76
- References
- 95
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 7 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 1 · 2019: 4 · 2018: 7 · 2017: 6 · 2016: 4 · 2015: 5 · 2014: 12 · 2013: 10 · 2012: 1
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Biochemical Journal (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Cancer Research UK
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cell cycle, neuronal differentiation, brain development, cyclins, cyclin-dependent kinases, cyclin-dependent kinase inhibitors, cell cycle regulators, cell fate, transcription factors, cell proliferation, neurogenesis
- MeSH terms
- Animals, Cell Cycle, Cell Differentiation, Humans, Nervous System, Embryonic Development, Neurogenesis
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