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 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.

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 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 Serum Response Factor Is Required for Immediate-Early Gene Activation yet Is Dispensable for Proliferation of Embryonic Stem Cells

2001 ◽  
Vol 21 (8) ◽  
pp. 2933-2943 ◽  
Author(s):  
Gerhard Schratt ◽  
Birgit Weinhold ◽  
Ante S. Lundberg ◽  
Sebastian Schuck ◽  
Jürgen Berger ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Serum Response Factor ◽  
Es Cells ◽  
Embryonic Stem ◽  
Early Gene ◽  
Response Factor ◽  
Es Cell ◽  
Cycle Progression ◽  
Serum Response

ABSTRACT Addition of serum to mitogen-starved cells activates the cellular immediate-early gene (IEG) response. Serum response factor (SRF) contributes to such mitogen-stimulated transcriptional induction of many IEGs during the G0-G1 cell cycle transition. SRF is also believed to be essential for cell cycle progression, as impairment of SRF activity by specific antisera or antisense RNA has previously been shown to block mammalian cell proliferation. In contrast, Srf −/− mouse embryos grow and develop up to E6.0. Using the embryonic stem (ES) cell system, we demonstrate here that wild-type ES cells do not undergo complete cell cycle arrest upon serum withdrawal but that they can mount an efficient IEG response. This IEG response, however, is severely impaired in Srf −/− ES cells, providing the first genetic proof that IEG activation is dependent upon SRF. Also, Srf−/− ES cells display altered cellular morphology, reduced cortical actin expression, and an impaired plating efficiency on gelatin. Yet, despite these defects, the proliferation rates of Srf −/− ES cells are not substantially altered, demonstrating that SRF function is not required for ES cell cycle progression.

Sign in / Sign up

Export Citation Format

Share Document