TRPV3 Channel Negatively Regulates Cell Cycle Progression and Safeguards the Pluripotency of Embryonic Stem Cells

2015 ◽  
Vol 231 (2) ◽  
pp. 403-413 ◽  
Author(s):  
Iek Chi Lo ◽  
Hing Chung Chan ◽  
Zenghua Qi ◽  
Kwun Lam Ng ◽  
Chun So ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Cell Cycle Progression ◽  
Embryonic Stem ◽  
Cycle Progression

scholarly journals B-MYB Is Essential for Normal Cell Cycle Progression and Chromosomal Stability of Embryonic Stem Cells

PLoS ONE ◽  
2008 ◽  
Vol 3 (6) ◽  
pp. e2478 ◽  
Author(s):  
Kirill V. Tarasov ◽  
Yelena S. Tarasova ◽  
Wai Leong Tam ◽  
Daniel R. Riordon ◽  
Steven T. Elliott ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Normal Cell ◽  
Cell Cycle Progression ◽  
Embryonic Stem ◽  
Cycle Progression ◽  
Chromosomal Stability ◽  
Normal Cell Cycle

scholarly journals BRPF3-HUWE1-mediated regulation of MYST2 is required for differentiation and cell-cycle progression in embryonic stem cells

2020 ◽  
Vol 27 (12) ◽  
pp. 3273-3288
Author(s):  
Hye In Cho ◽  
Min Seong Kim ◽  
Jina Lee ◽  
Byong Chul Yoo ◽  
Kyung Hee Kim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Embryonic Development ◽  
Cell Cycle Progression ◽  
Histone Acetyltransferase ◽  
Embryoid Body ◽  
Embryonic Stem ◽  
Negative Regulator ◽  
Cycle Progression

AbstractBrpf-histone acetyltransferase (HAT) complexes have important roles in embryonic development and regulating differentiation in ESCs. Among Brpf family, Brpf3 is a scaffold protein of Myst2 histone acetyltransferase complex that plays crucial roles in gene regulation, DNA replication, development as well as maintaining pluripotency in embryonic stem cells (ESCs). However, its biological functions in ESCs are not elucidated. In this study, we find out that Brpf3 protein level is critical for Myst2 stability and E3 ligase Huwe1 functions as a novel negative regulator of Myst2 via ubiquitin-mediated degradation. Importantly, Brpf3 plays an antagonistic role in Huwe1-mediated degradation of Myst2, suggesting that protein–protein interaction between Brpf3 and Myst2 is required for retaining Myst2 stability. Further, Brpf3 overexpression causes the aberrant upregulation of Myst2 protein levels which in turn induces the dysregulated cell-cycle progression and also delay of early embryonic development processes such as embryoid-body formation and lineage commitment of mouse ESCs. The Brpf3 overexpression-induced phenotypes can be reverted by Huwe1 overexpression. Together, these results may provide novel insights into understanding the functions of Brpf3 in proper differentiation as well as cell-cycle progression of ESCs via regulation of Myst2 stability by obstructing Huwe1-mediated ubiquitination. In addition, we suggest that this is a useful report which sheds light on the function of an unknown gene in ESC field.

scholarly journals Direct observation of cell cycle progression in living mouse embryonic stem cells on an extracellular matrix of E-cadherin

SpringerPlus ◽  
2013 ◽  
Vol 2 (1) ◽  
pp. 585 ◽  
Author(s):  
Dragomirka Jovic ◽  
Asako Sakaue-Sawano ◽  
Takaya Abe ◽  
Chong-Su Cho ◽  
Masato Nagaoka ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Extracellular Matrix ◽  
Embryonic Stem Cells ◽  
Direct Observation ◽  
Cell Cycle Progression ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cells ◽  
Cycle Progression ◽  
Living Mouse

scholarly journals Aurkb/PP1-mediated resetting of Oct4 during the cell cycle determines the identity of embryonic stem cells

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Jihoon Shin ◽  
Tae Wan Kim ◽  
Hyunsoo Kim ◽  
Hye Ji Kim ◽  
Min Young Suh ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Cell Cycle Progression ◽  
Embryonic Stem ◽  
Aurora Kinase ◽  
Cycle Progression ◽  
Aurora Kinase B ◽  
Somatic Cell Reprogramming ◽  
M Phase

Pluripotency transcription programs by core transcription factors (CTFs) might be reset during M/G1 transition to maintain the pluripotency of embryonic stem cells (ESCs). However, little is known about how CTFs are governed during cell cycle progression. Here, we demonstrate that the regulation of Oct4 by Aurora kinase b (Aurkb)/protein phosphatase 1 (PP1) during the cell cycle is important for resetting Oct4 to pluripotency and cell cycle genes in determining the identity of ESCs. Aurkb phosphorylates Oct4(S229) during G2/M phase, leading to the dissociation of Oct4 from chromatin, whereas PP1 binds Oct4 and dephosphorylates Oct4(S229) during M/G1 transition, which resets Oct4-driven transcription for pluripotency and the cell cycle. Aurkb phosphor-mimetic and PP1 binding-deficient mutations in Oct4 alter the cell cycle, effect the loss of pluripotency in ESCs, and decrease the efficiency of somatic cell reprogramming. Our findings provide evidence that the cell cycle is linked directly to pluripotency programs in ESCs.

scholarly journals Oct-4 controls cell-cycle progression of embryonic stem cells

2010 ◽  
Vol 426 (2) ◽  
pp. 171-181 ◽  
Author(s):  
Jungwoon Lee ◽  
Yeorim Go ◽  
Inyoung Kang ◽  
Yong-Mahn Han ◽  
Jungho Kim
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Cell Cycle Progression ◽  
Es Cells ◽  
Embryonic Stem ◽  
Functional Domains ◽  
Es Cell ◽  
Down Regulation ◽  
Cycle Progression

Mouse and human ES (embryonic stem) cells display unusual proliferative properties and can produce pluripotent stem cells indefinitely. Both processes might be important for maintaining the ‘stemness’ of ES cells; however, little is known about how the cell-cycle fate is regulated in ES cells. Oct-4, a master switch of pluripotency, plays an important role in maintaining the pluripotent state of ES cells and may prevent the expression of genes activated during differentiation. Using ZHBTc4 ES cells, we have investigated the effect of Oct-4 on ES cell-cycle control, and we found that Oct-4 down-regulation in ES cells inhibits proliferation by blocking cell-cycle progression in G0/G1. Deletion analysis of the functional domains of Oct-4 indicates that the overall integrity of the Oct-4 functional domains is important for the stimulation of S-phase entry. We also show in the present study that the p21 gene is a target for Oct-4 repression. Furthermore, p21 protein levels were repressed by Oct-4 and were induced by the down-regulation of Oct-4 in ZHBTc4 ES cells. Therefore the down-regulation of p21 by Oct-4 may contribute to the maintenance of ES cell proliferation.

scholarly journals Babam2 Regulates Cell Cycle Progression and Pluripotency in Mouse Embryonic Stem Cells as Revealed by Induced DNA Damage

Biomedicines ◽  
2020 ◽  
Vol 8 (10) ◽  
pp. 397
Author(s):  
Cheuk Yiu Tenny Chung ◽  
Paulisally Hau Yi Lo ◽  
Kenneth Ka Ho Lee
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Dna Damage ◽  
Gamma Irradiation ◽  
Cellular Senescence ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Embryonic Stem ◽  
Cycle Progression ◽  
Cycle Regulation

BRISC and BRCA1-A complex member 2 (Babam2) plays an essential role in promoting cell cycle progression and preventing cellular senescence. Babam2-deficient fibroblasts show proliferation defect and premature senescence compared with their wild-type (WT) counterpart. Pluripotent mouse embryonic stem cells (mESCs) are known to have unlimited cell proliferation and self-renewal capability without entering cellular senescence. Therefore, studying the role of Babam2 in ESCs would enable us to understand the mechanism of Babam2 in cellular aging, cell cycle regulation, and pluripotency in ESCs. For this study, we generated Babam2 knockout (Babam2−/−) mESCs to investigate the function of Babam2 in mESCs. We demonstrated that the loss of Babam2 in mESCs leads to abnormal G1 phase retention in response to DNA damage induced by gamma irradiation or doxorubicin treatments. Key cell cycle regulators, CDC25A and CDK2, were found to be degraded in Babam2−/− mESCs following gamma irradiation. In addition, Babam2−/− mESCs expressed p53 strongly and significantly longer than in control mESCs, where p53 inhibited Nanog expression and G1/S cell cycle progression. The combined effects significantly reduced developmental pluripotency in Babam2−/− mESCs. In summary, Babam2 maintains cell cycle regulation and pluripotency in mESCs in response to induced DNA damage.

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