scholarly journals Inhibition of transcription blocks cell cycle progression of NIH3T3 fibroblasts specifically in G1

1993 ◽  
Vol 105 (1) ◽  
pp. 113-122 ◽  
Author(s):  
S. Adolph ◽  
S. Brusselbach ◽  
R. Muller
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Cell Cycle Progression ◽  
Video Recording ◽  
Cycle Progression ◽  
Nih3t3 Cells ◽  
Restriction Point ◽  
Alpha Amanitin

We have analysed the role of RNA polymerase II-dependent transcription in cell cycle progression. Time-lapse video recording and cytogenetic analysis were used to determine the sensitivity of NIH3T3 cells to the RNA polymerase II inhibitor alpha-amanitin at different stages of the cell cycle. Our results show that alpha-amanitin blocks cells specifically in G1, irrespective of the concentration within the range of 3 to 30 micrograms/ml. This indicates that transcription in G1 is required to overcome a restriction point located in this phase of the cell cycle. In agreement with this conclusion is the requirement for an uninhibited protein synthesis during G1 progression. In addition, the insensitivity of S-phase cells to RNA polymerase II inhibition suggests that the transcription of genes thought to be normally induced during S/G2 is not required for the completion of an ongoing cell cycle. S/G2 progression was however clearly dependent on protein synthesis. This suggests that cells exposed to alpha-amanitin are able to complete their cell cycle because sufficiently high levels of mRNA are present in S/G2 due to basal level transcription, or are left from preceding cell cycles. It is therefore unlikely that transcriptional regulation in S or G2 plays a crucial role in the control of cell cycle progression in NIH3T3 cells.

scholarly journals Human Transcription Factor hTAFII150 (CIF150) Is Involved in Transcriptional Regulation of Cell Cycle Progression

1999 ◽  
Vol 19 (8) ◽  
pp. 5548-5556 ◽  
Author(s):  
Jay Martin ◽  
Robert Halenbeck ◽  
Jörg Kaufmann
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Cell Cycle Progression ◽  
Core Promoter ◽  
Cyclin B1 ◽  
Cycle Progression ◽  
Mammalian Cell Lines ◽  
Human Transcription Factor

ABSTRACT Here we present evidence that CIF150 (hTAFII150), the human homolog of Drosophila TAFII150, plays an important and selective role in establishing gene expression patterns necessary for progression through the cell cycle. Gel filtration experiments demonstrate that CIF150 (hTAFII150) seems to be less tightly associated with human transcription factor IID than hTAFII130 is associated with hTAFII250. The transient functional knockout of CIF150 (hTAFII150) protein led to cell cycle arrest at the G2/M transition in mammalian cell lines. PCR display analysis with the RNA derived from CIF150-depleted cells indicated that CIF150 (hTAFII150) is required for the transcription of only a subset of RNA polymerase II genes. CIF150 (hTAFII150) directly stimulated cyclin B1 and cyclin A transcription in cotransfection assays and in vitro assays, suggesting that the expression of these genes is dependent on CIF150 (hTAFII150) function. We defined a CIF150 (hTAFII150) consensus binding site and demonstrated that a CIF150-responsive cis element is present in the cyclin B1 core promoter. These results suggest that one function of CIF150 (hTAFII150) is to select specific RNA polymerase II core promoter elements involved in cell cycle progression.

scholarly journals POLR2A Promotes the Proliferation of Gastric Cancer Cells by Advancing the Overall Cell Cycle Progression

2021 ◽  
Vol 12 ◽  
Author(s):  
Qiuyu Jiang ◽  
Jinyuan Zhang ◽  
Fang Li ◽  
Xiaoping Ma ◽  
Fei Wu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Cancer Progression ◽  
Cell Cycle Progression ◽  
Gastric Cancer Cells ◽  
Cycle Progression

RNA polymerase II subunit A (POLR2A) is the largest subunit encoding RNA polymerase II and closely related to cancer progression. However, the biological role and underlying molecular mechanism of POLR2A in gastric cancer (GC) are still unclear. Our study demonstrated that POLR2A was highly expressed in GC tissue and promoted the proliferation of GC in vitro and in vivo. We also found that POLR2A participated in the transcriptional regulation of cyclins and cyclin-dependent kinases (CDKs) at each stage and promoted their expression, indicated POLR2A’s overall promotion of cell cycle progression. Moreover, POLR2A inhibited GC cell apoptosis and promoted GC cell migration. Our results indicate that POLR2A play an oncogene role in GC, which may be an important factor involved in the occurrence and development of GC.

scholarly journals TheSaccharomyces cerevisiaeRuvB-like Protein, Tih2p, Is Required for Cell Cycle Progression and RNA Polymerase II-directed Transcription

2000 ◽  
Vol 275 (29) ◽  
pp. 22409-22417 ◽  
Author(s):  
Chun Ren Lim ◽  
Yukio Kimata ◽  
Hidezumi Ohdate ◽  
Tetsuro Kokubo ◽  
Noriko Kikuchi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals The Human RNA Polymerase II-Associated Factor 1 (hPaf1): A New Regulator of Cell-Cycle Progression

PLoS ONE ◽  
2009 ◽  
Vol 4 (9) ◽  
pp. e7077 ◽  
Author(s):  
Nicolas Moniaux ◽  
Christophe Nemos ◽  
Shonali Deb ◽  
Bing Zhu ◽  
Irena Dornreiter ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Associated Factor

scholarly journals Mutagenesis of ARS2 Domains To Assess Possible Roles in Cell Cycle Progression and MicroRNA and Replication-Dependent Histone mRNA Biogenesis

2015 ◽  
Vol 35 (21) ◽  
pp. 3753-3767 ◽  
Author(s):  
Connor O'Sullivan ◽  
Jennifer Christie ◽  
Marcus Pienaar ◽  
Jake Gambling ◽  
Philip E. B. Nickerson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rna Polymerase Ii ◽  
Cell Cycle Progression ◽  
Rna Recognition Motif ◽  
Rna Recognition ◽  
Histone Mrna ◽  
Cycle Progression ◽  
Transcript Processing ◽  
C Terminus ◽  
Domain Of Unknown Function

ARS2 is a regulator of RNA polymerase II transcript processing through its role in the maturation of distinct nuclear cap-binding complex (CBC)-controlled RNA families. In this study, we examined ARS2 domain function in transcript processing. Structural modeling based on the plant ARS2 orthologue, SERRATE, revealed 2 previously uncharacterized domains in mammalian ARS2: an N-terminal domain of unknown function (DUF3546), which is also present in SERRATE, and an RNA recognition motif (RRM) that is present in metazoan ARS2 but not in plants. Both the DUF3546 and zinc finger domain (ZnF) were required for association with microRNA and replication-dependent histone mRNA. Mutations in the ZnF disrupted interaction with FLASH, a key component in histone pre-mRNA processing. Mutations targeting the Mid domain implicated it in DROSHA interaction and microRNA biogenesis. The unstructured C terminus was required for interaction with the CBC protein CBP20, while the RRM was required for cell cycle progression and for binding to FLASH. Together, our results support a bridging model in which ARS2 plays a central role in RNA recognition and processing through multiple protein and RNA interactions.

Regulatory effect of thromboxane A2 on proliferation of vascular smooth muscle cells from rats

1992 ◽  
Vol 263 (5) ◽  
pp. H1331-H1338 ◽  
Author(s):  
T. Nagata ◽  
Y. Uehara ◽  
A. Numabe ◽  
T. Ishimitsu ◽  
N. Hirawa ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cell Cycle Progression ◽  
Thromboxane A2 ◽  
Cycle Progression ◽  
M Phase ◽  
Rapid Transition

We investigated the regulatory effects of the vasoconstrictor thromboxane A2 on the proliferation of vascular smooth muscle cells (VSMC) from Wistar-Kyoto rats using 9,11-epithio-11,12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2. STA2 dose dependently increased incorporation of [3H]thymidine into DNA in randomly cycling VSMC and significantly shortened the doubling time. Cell cycle analysis revealed that the increased cell cycle progression was primarily due to a rapid transition from the DNA synthetic (S) to the G2/mitotic (M) phase. Moreover, STA2 enhanced protein synthesis in VSMC during the G2/M phase, whereas the protein synthesis was unaffected in the G0/G1 period. In fact, STA2 prompted the cells in G2/M phase to synthesize actin, a major cytoskeleton protein. Conversely, inhibition of protein synthesis by puromycin retarded the transition from S to G2/M. In addition, depolymerization of the actin molecules by cytochalasin D offset the quick progression to the G2/M phase by STA2. These data indicate that thromboxane A2 stimulates the cell cycle progression in VSMC primarily through a rapid transition from S to G2/M. This enhanced progression is attributable partly to a rapid buildup of the cytoskeleton proteins during the G2/M period.

scholarly journals Dephosphorylation of eIF2α is essential for protein synthesis increase and cell cycle progression after sea urchin fertilization

2012 ◽  
Vol 365 (1) ◽  
pp. 303-309 ◽  
Author(s):  
Vlad Costache ◽  
Stefania Bilotto ◽  
Laurent Laguerre ◽  
Robert Bellé ◽  
Bertrand Cosson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Sea Urchin ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals Regulation of CDK7–Carboxyl-Terminal Domain Kinase Activity by the Tumor Suppressor p16INK4A Contributes to Cell Cycle Regulation

2000 ◽  
Vol 20 (20) ◽  
pp. 7726-7734 ◽  
Author(s):  
Eiji Nishiwaki ◽  
Saralinda L. Turner ◽  
Susanna Harju ◽  
Shiro Miyazaki ◽  
Masahide Kashiwagi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Rna Polymerase Ii ◽  
Cell Cycle Progression ◽  
Kinase Activity ◽  
Alternative Pathway ◽  
Cycle Progression ◽  
Terminal Domain ◽  
Carboxyl Terminal Domain ◽  
Carboxyl Terminal

ABSTRACT The eukaryotic cell cycle is regulated by cyclin-dependent kinases (CDKs). CDK4 and CDK6, which are activated by D-type cyclins during the G1 phase of the cell cycle, are thought to be responsible for phosphorylation of the retinoblastoma gene product (pRb). The tumor suppressor p16INK4A inhibits phosphorylation of pRb by CDK4 and CDK6 and can thereby block cell cycle progression at the G1/S boundary. Phosphorylation of the carboxyl-terminal domain (CTD) of the large subunit of RNA polymerase II by general transcription factor TFIIH is believed to be an important regulatory event in transcription. TFIIH contains a CDK7 kinase subunit and phosphorylates the CTD. We have previously shown that p16INK4A inhibits phosphorylation of the CTD by TFIIH. Here we report that the ability of p16INK4A to inhibit CDK7-CTD kinase contributes to the capacity to induce cell cycle arrest. These results suggest that p16INK4A may regulate cell cycle progression by inhibiting not only CDK4-pRb kinase activity but also by modulating CDK7-CTD kinase activity. Regulation of CDK7-CTD kinase activity by p16INK4A thus may represent an alternative pathway for controlling cell cycle progression.

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