scholarly journals ZFP36L2 is a cell cycle-regulated CCCH protein necessary for DNA lesion-induced S-phase arrest

Biology Open ◽  
2018 ◽  
Vol 7 (3) ◽  
pp. bio031575 ◽  
Author(s):  
Aya Noguchi ◽  
Shungo Adachi ◽  
Naoto Yokota ◽  
Tomohisa Hatta ◽  
Tohru Natsume ◽  
...  
Keyword(s):  
Cell Cycle ◽  
S Phase ◽  
Dna Lesion ◽  
Phase Arrest ◽  
S Phase Arrest ◽  
A Cell

scholarly journals Cell cycle S-phase arrest drives cell extrusion

2019 ◽  
Author(s):  
Vivek K. Dwivedi ◽  
Carlos Pardo-Pastor ◽  
Rita Droste ◽  
Daniel P. Denning ◽  
Jody Rosenblatt ◽  
...  
Keyword(s):  
Cell Cycle ◽  
S Phase ◽  
C Elegans ◽  
Phase Arrest ◽  
Genome Wide ◽  
S Phase Arrest ◽  
Epithelial Cultures ◽  
A Cell ◽  
Cycle Dependent ◽  
Cell Extrusion

SUMMARYCell extrusion is a process of cell elimination in which a cell is squeezed out from its tissue of origin. Extrusion occurs in organisms as diverse as sponges, nematodes, insects, fish and mammals. Defective extrusion is linked to many epithelial disorders, including cancer. Despite broad occurrence, cell-intrinsic triggers of extrusion conserved across phyla are generally unknown. We combined genome-wide genetic screens with live-imaging studies of C. elegans embryos and mammalian epithelial cultures and found that S-phase arrest induced extrusion in both. Cells extruded from C. elegans embryos exhibited S-phase arrest, and RNAi treatments that specifically prevent S-phase entry or arrest blocked cell extrusion. Pharmacological induction of S-phase arrest was sufficient to promote cell extrusion from a canine epithelial monolayer. Thus, we have discovered an evolutionarily conserved cell-cycle-dependent trigger of cell extrusion. We suggest that S-phase-arrest induced cell extrusion plays a key role in physiology and disease.

Antimycin A as a mitochondria damage agent induces an S phase arrest of the cell cycle in HeLa cells

Life Sciences ◽  
2008 ◽  
Vol 83 (9-10) ◽  
pp. 346-355 ◽  
Author(s):  
Yong Hwan Han ◽  
Suhn Hee Kim ◽  
Sung Zoo Kim ◽  
Woo Hyun Park
Keyword(s):  
Cell Cycle ◽  
Hela Cells ◽  
S Phase ◽  
Antimycin A ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals Inhibition of tumor cell growth by adenine is mediated by apoptosis induction and cell cycle S phase arrest

Oncotarget ◽  
2017 ◽  
Vol 8 (55) ◽  
pp. 94286-94296 ◽  
Author(s):  
Ming Han ◽  
Xin Cheng ◽  
Zhiqin Gao ◽  
Rongrong Zhao ◽  
Shizhuang Zhang
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Tumor Cell ◽  
S Phase ◽  
Tumor Cell Growth ◽  
Apoptosis Induction ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals p21Cip1 and p27Kip1Regulate Cell Cycle Reentry after Hypoxic Stress but Are Not Necessary for Hypoxia-Induced Arrest

2001 ◽  
Vol 21 (4) ◽  
pp. 1196-1206 ◽  
Author(s):  
Susannah L. Green ◽  
Rachel A. Freiberg ◽  
Amato J. Giaccia
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Kinase Inhibitors ◽  
S Phase ◽  
Hypoxic Stress ◽  
Cyclin Dependent Kinase ◽  
Low Oxygen ◽  
Double Knockout ◽  
Phase Arrest ◽  
S Phase Arrest

ABSTRACT We investigated the role of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1 in cell cycle regulation during hypoxia and reoxygenation. While moderate hypoxia (1 or 0.1% oxygen) does not significantly impair bromodeoxyuridine incorporation, at very low oxygen tensions (0.01% oxygen) DNA replication is rapidly shut down in immortalized mouse embryo fibroblasts. This S-phase arrest is intact in fibroblasts lacking the cyclin kinase inhibitors p21Cip1 and p27Kip1, indicating that these molecules are not essential elements of the arrest pathway. Hypoxia-induced arrest is accompanied by dephosphorylation of pRb and inhibition of cyclin-dependent kinase 2, which results in part from inhibitory phosphorylation. Interestingly, cells lacking the retinoblastoma tumor suppressor protein also display arrest under hypoxia, suggesting that pRb is not an essential mediator of this response. Upon reoxygenation, DNA synthesis resumes by 3.5 h and reaches aerobic levels by 6 h. Cells lacking p21, however, resume DNA synthesis more rapidly upon reoxygenation than wild-type cells, suggesting that this inhibitor may play a role in preventing premature reentry into the cell cycle upon cessation of the hypoxic stress. While p27 null cells did not exhibit rapid reentry into the cell cycle, cells lacking both p21 and p27 entered S phase even more aggressively than those lacking p21 alone, revealing a possible secondary role for p27 in this response. Cdk2 activity is also restored more rapidly in the double-knockout cells when returned to normoxia. These studies reveal that restoration of DNA synthesis after hypoxic stress, but not the S phase arrest itself, is regulated by p21 and p27.

Methimazole inhibits FRTL5 thyroid cell proliferation by inducing S-phase arrest of the cell cycle.

Endocrinology ◽  
1993 ◽  
Vol 133 (5) ◽  
pp. 2403-2406 ◽  
Author(s):  
P Smerdely ◽  
V Pitsiavas ◽  
S C Boyages
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
S Phase ◽  
Thyroid Cell ◽  
Phase Arrest ◽  
S Phase Arrest

scholarly journals Cell Cycle Modulation by Marek’s Disease Virus: The Tegument Protein VP22 Triggers S-Phase Arrest and DNA Damage in Proliferating Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e100004 ◽  
Author(s):  
Laëtitia Trapp-Fragnet ◽  
Djihad Bencherit ◽  
Danièle Chabanne-Vautherot ◽  
Yves Le Vern ◽  
Sylvie Remy ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Disease Virus ◽  
S Phase ◽  
Tegument Protein ◽  
Proliferating Cells ◽  
Phase Arrest ◽  
Cell Cycle Modulation ◽  
S Phase Arrest ◽  
Protein Vp22

scholarly journals A Cds1-Mediated Checkpoint Protects the MBF Activator Rep2 from Ubiquitination by Anaphase-Promoting Complex/Cyclosome-Ste9 at S-Phase Arrest in Fission Yeast

2009 ◽  
Vol 29 (18) ◽  
pp. 4959-4970 ◽  
Author(s):  
Zhaoqing Chu ◽  
Majid Eshaghi ◽  
Suk Yean Poon ◽  
Jianhua Liu
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Transcriptional Activity ◽  
S Phase ◽  
Anaphase Promoting Complex ◽  
Cell Recovery ◽  
Cycle Progression ◽  
Phase Arrest ◽  
S Phase Arrest

ABSTRACT Transcription of the MluI cell cycle box (MCB) motif-containing genes at G1 phase is regulated by the MCB-binding factors (MBF) (also called DSC1) in Schizosaccharomyces pombe. Upon S-phase arrest, the MBF transcriptional activity is induced through the accumulation of the MBF activator Rep2. In this study, we show that the turnover of Rep2 is attributable to ubiquitin-mediated proteolysis. Levels of Rep2 oscillate during the cell cycle, with a peak at G1 phase, coincident with the MBF activity. Furthermore, we show that Rep2 ubiquitination requires the function of the E3 ligase anaphase-promoting complex/cyclosome (APC/C). Ste9 can be phosphorylated by the checkpoint kinase Cds1 in vitro, and its inhibition/phosphorylation at S-phase arrest is dependent on the function of Cds1. Our data indicate that the Cds1-dependent stabilization of Rep2 is achieved through the inhibition/phosphorylation of APC/C-Ste9 at the onset of S-phase arrest. Stabilization of Rep2 is important for stimulating transcription of the MBF-dependent genes to ensure a sufficient supply of proteins essential for cell recovery from S-phase arrest. We propose that oscillation of Rep2 plays a role in regulation of periodic transcription of the MBF-dependent genes during cell cycle progression.

scholarly journals Histone H4 acetylation during UV light induced G1and S phase arrest of the cell cycle

Cell Cycle ◽  
2008 ◽  
Vol 7 (10) ◽  
pp. 1496-1498 ◽  
Author(s):  
Miglena Koprinarova ◽  
George Russev
Keyword(s):  
Cell Cycle ◽  
Uv Light ◽  
S Phase ◽  
Histone H4 ◽  
Phase Arrest ◽  
Histone H4 Acetylation ◽  
S Phase Arrest

scholarly journals The Coordination of Centrosome Reproduction with Nuclear Events of the Cell Cycle in the Sea Urchin Zygote

1998 ◽  
Vol 140 (6) ◽  
pp. 1417-1426 ◽  
Author(s):  
Edward H. Hinchcliffe ◽  
Grizzel O. Cassels ◽  
Conly L. Rieder ◽  
Greenfield Sluder
Keyword(s):  
Cell Cycle ◽  
Sea Urchin ◽  
S Phase ◽  
Cyclin B ◽  
Cyclin Dependent Kinase ◽  
Phase Arrest ◽  
Stage Specificity ◽  
S Phase Arrest ◽  
Nuclear Events ◽  
Block Protein Synthesis

Centrosomes repeatedly reproduce in sea urchin zygotes arrested in S phase, whether cyclin-dependent kinase 1–cyclin B (Cdk1-B) activity remains at prefertilization levels or rises to mitotic values. In contrast, when zygotes are arrested in mitosis using cyclin B Δ-90, anaphase occurs at the normal time, yet centrosomes do not reproduce. Together, these results reveal the cell cycle stage specificity for centrosome reproduction and demonstrate that neither the level nor the cycling of Cdk1-B activity coordinate centrosome reproduction with nuclear events. In addition, the proteolytic events of the metaphase–anaphase transition do not control when centrosomes duplicate. When we block protein synthesis at first prophase, the zygotes divide and arrest before second S phase. Both blastomeres contain just two complete centrosomes, which indicates that the cytoplasmic conditions between mitosis and S phase support centrosome reproduction. However, the fact that these daughter centrosomes do not reproduce again under such supportive conditions suggests that they are lacking a component required for reproduction. The repeated reproduction of centrosomes during S phase arrest points to the existence of a necessary “licensing” event that restores this component to daughter centrosomes during S phase, preparing them to reproduce in the next cell cycle.

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