scholarly journals Hbp1 regulates the timing of neuronal differentiation during cortical development by controlling cell cycle progression

2015 ◽  
Vol 128 (14) ◽  
pp. e1.2-e1.2
Author(s):  
Naoki Watanabe ◽  
Ryoichiro Kageyama ◽  
Toshiyuki Ohtsuka
Keyword(s):  
Cell Cycle ◽  
Neuronal Differentiation ◽  
Cell Cycle Progression ◽  
Cortical Development ◽  
Cycle Progression

scholarly journals Developmental HCN channelopathy results in decreased neural progenitor proliferation and microcephaly in mice

2021 ◽  
Author(s):  
Anna Katharina Schlusche ◽  
Sabine Ulrike Vay ◽  
Niklas Kleinenkuhnen ◽  
Steffi Sandke ◽  
Rafael Campos-Martin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Membrane Potential ◽  
Cell Cycle Progression ◽  
Cortical Development ◽  
General Mechanism ◽  
Hcn Channel ◽  
Cycle Progression ◽  
Channel Function ◽  
Stem And Progenitor Cells

ABSTRACTThe development of the cerebral cortex relies on the controlled division of neural stem and progenitor cells. The requirement for precise spatiotemporal control of proliferation and cell fate places a high demand on the cell division machinery, and defective cell division can cause microcephaly and other brain malformations. Cell-extrinsic and intrinsic factors govern the capacity of cortical progenitors to produce large numbers of neurons and glia within a short developmental time window. In particular, ion channels shape the intrinsic biophysical properties of precursor cells and neurons and control their membrane potential throughout the cell cycle. We found that hyperpolarization-activated cyclic nucleotide-gated cation (HCN)-channel subunits are expressed in mouse, rat, and human neural progenitors. Loss of HCN-channel function in rat neural stem cells impaired their proliferation by affecting the cell-cycle progression, causing G1 accumulation and dysregulation of genes associated with human microcephaly. Transgene-mediated, dominant-negative loss of HCN-channel function in the embryonic mouse telencephalon resulted in pronounced microcephaly. Together, our findings suggest a novel role for HCN-channel subunits as a part of a general mechanism influencing cortical development in mammals.Significance StatementImpaired cell cycle regulation of neural stem and progenitor cells can affect cortical development and cause microcephaly. During cell cycle progression, the cellular membrane potential changes through the activity of ion channels and tends to be more depolarized in proliferating cells. HCN channels, which mediate a depolarizing current in neurons and cardiac cells, are linked to neurodevelopmental diseases, also contribute to the control of cell-cycle progression and proliferation of neuronal precursor cells. In this study, HCN-channel deficiency during embryonic and fetal brain development resulted in marked microcephaly of mice designed to be deficient in HCN-channel function in dorsal forebrain progenitors. The findings suggest that HCN-channel subunits are part of a general mechanism influencing cortical development in mammals.

Chemical fragment-based CDK4/6 inhibitors prediction and web server

RSC Advances ◽  
2016 ◽  
Vol 6 (21) ◽  
pp. 16972-16981 ◽  
Author(s):  
Ling Wang ◽  
Yecheng Li ◽  
Mengyan Xu ◽  
Xiaoqian Pang ◽  
Zhihong Liu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Neuronal Differentiation ◽  
Cell Cycle Progression ◽  
Web Server ◽  
Cycle Progression ◽  
Cyclin Dependent Kinases ◽  
Regulation Of Cell Cycle

Cyclin-dependent kinases (CDKs), a family of mammalian heterodimeric kinases, play central roles in the regulation of cell cycle progression, transcription, neuronal differentiation, and metabolism.

scholarly journals CEP120-mediated KIAA0753 recruitment onto centrioles is required for timely neuronal differentiation and germinal zone exit in the developing cerebellum

2021 ◽  
Author(s):  
Chia-Hsiang Chang ◽  
Ting-Yu Chen ◽  
I-Ling Lu ◽  
Rong-Bin Li ◽  
Jhih-Jie Tsai ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Neuronal Differentiation ◽  
Cell Cycle Progression ◽  
Joubert Syndrome ◽  
Cerebellar Development ◽  
Cycle Progression ◽  
Interacting Protein ◽  
Germinal Zone ◽  
Developing Cerebellum

Joubert syndrome (JS) is a recessive ciliopathy in which all affected individuals have congenital cerebellar vermis hypoplasia. Here, we report that CEP120, a JS-associated protein involved in centriole biogenesis and cilia assembly, regulates timely neuronal differentiation and the departure of granule neuron progenitors (GNPs) from their germinal zone during cerebellar development. Our results show that depletion of Cep120 perturbs GNP cell cycle progression, resulting in a delay of cell cycle exit in vivo. To dissect the potential mechanism, we investigated the association between CEP120 interactome and the JS database and identified KIAA0753 (a JS-associated protein) as a CEP120-interacting protein. Surprisingly, we found that CEP120 recruits KIAA0753 to centrioles, and that loss of this interaction induces accumulation of GNPs in the germinal zone and impairs neuronal differentiation. Importantly, the replenishment of wild-type CEP120 rescues the above defects, whereas expression of JS-associated CEP120 mutants, which hinder KIAA0753 recruitment, does not. Together, our data reveal a close interplay between CEP120 and KIAA0753 for the germinal zone exit and timely neuronal differentiation of GNPs during cerebellar development, and mutations in CEP120 and KIAA0753 may participate in the heterotopia and cerebellar hypoplasia observed in JS patients.

Neuronal Differentiation of Neuro 2a Cells by Inhibitors of Cell Cycle Progression, Trichostatin A and Butyrolactone I

1999 ◽  
Vol 256 (2) ◽  
pp. 372-376 ◽  
Author(s):  
Junji Inokoshi ◽  
Masako Katagiri ◽  
Shiho Arima ◽  
Haruo Tanaka ◽  
Masahiko Hayashi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Neuronal Differentiation ◽  
Cell Cycle Progression ◽  
Trichostatin A ◽  
Cycle Progression
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