ArticleDevelopment (Cambridge, England)2012
p57(KIP2) regulates radial glia and intermediate precursor cell cycle dynamics and lower layer neurogenesis in developing cerebral cortex.
Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 103 citations in OpenAlex.
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- IGF2 interacts with the imprinted gene Cdkn1c to promote terminal differentiation of neural stem cells.Development (Cambridge, England) · 2023Article
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- Zfp57 inactivation illustrates the role of ICR methylation in imprinted gene expression during neural differentiation of mouse ESCs.Scientific reports · 2021Article
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- Visualizing Cell Cycle Phase Organization and Control During Neural Lineage Elaboration.Cells · 2020Article
- The Role of CDKs and CDKIs in Murine Development.International journal of molecular sciences · 2020Review
- FGF2 modulates simultaneously the mode, the rate of division and the growth fraction in cultures of radial glia.Development (Cambridge, England) · 2020Article
- Role of the imprinted allele of the Cdkn1c gene in mouse neocortical development.Scientific reports · 2020Article
- Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development.Nature communications · 2020Article
- Functional Versatility of the CDK Inhibitor p57Frontiers in cell and developmental biology · 2020Review
- Epigenetic cues modulating the generation of cell-type diversity in the cerebral cortex.Journal of neurochemistry · 2019Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
During cerebral cortex development, precise control of precursor cell cycle length and cell cycle exit is required for balanced precursor pool expansion and layer-specific neurogenesis. Here, we defined the roles of cyclin-dependent kinase inhibitor (CKI) p57(KIP2), an important regulator of G1 phase, using deletion mutant mice. Mutant mice displayed macroencephaly associated with cortical hyperplasia during late embryogenesis and postnatal development. Embryonically, proliferation of radial glial cells (RGC) and intermediate precursors (IPC) was increased, expanding both populations, with greater effect on IPCs. Furthermore, cell cycle re-entry was increased during early corticogenesis, whereas cell cycle exit was augmented at middle stage. Consequently, neurogenesis was reduced early, whereas it was enhanced during later development. In agreement, the timetable of early neurogenesis, indicated by birthdating analysis, was delayed. Cell cycle dynamics analyses in mutants indicated that p57(KIP2) regulates cell cycle length in both RGCs and IPCs. By contrast, related CKI p27(KIP1) controlled IPC proliferation exclusively. Furthermore, p57(KIP2) deficiency markedly increased RGC and IPC divisions at E14.5, whereas p27(KIP1) increased IPC proliferation at E16.5. Consequently, loss of p57(KIP2) increased primarily layer 5-6 neuron production, whereas loss of p27(KIP1) increased neurons specifically in layers 2-5. In conclusion, our observations suggest that p57(KIP2) and p27(KIP1) control neuronal output for distinct cortical layers by regulating different stages of precursor proliferation, and support a model in which IPCs contribute to both lower and upper layer neuron generation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.