Spontaneous [Ca2+]i oscillations in G1/S phase-synchronized cells

2009 ◽  
Vol 58 (5) ◽  
pp. 321-329 ◽  
Author(s):  
A. D. Russa ◽  
C. Maesawa ◽  
Y.-i. Satoh
Keyword(s):  
S Phase ◽  
Synchronized Cells

scholarly journals Maximal binding levels of an H1 histone gene-specific factor in S-phase correlate with maximal H1 gene transcription.

1988 ◽  
Vol 8 (10) ◽  
pp. 4576-4578 ◽  
Author(s):  
S Dalton ◽  
J R Wells
Keyword(s):  
Cell Cycle ◽  
Nucleic Acids ◽  
Gene Transcription ◽  
S Phase ◽  
Histone Gene ◽  
Specific Factor ◽  
Synchronized Cells ◽  
Phase Regulation ◽  
G2 Phase ◽  
Binding Component

Levels of trans-acting factor (H1-SF) binding to the histone H1 gene-specific motif (5'-AAACACA-3' [L. S. Coles and J. R. E. Wells, Nucleic Acids Res. 13:585-594, 1985]) increase 12-fold from G1 to S-phase in synchronized cells and decrease again in G2 phase of the cell cycle. Since the H1 element is required for S-phase expression of H1 genes (S. Dalton and J. R. E. Wells, EMBO J. 7:49-56, 1988), it is likely that the increased levels of H1-SF binding component play an important role in S-phase regulation of H1 gene transcription.

Interferon inhibition of DNA synthesis and cell division

1972 ◽  
Vol 18 (2) ◽  
pp. 145-151 ◽  
Author(s):  
M. V. O'Shaughnessy ◽  
S. H. S. Lee ◽  
K. R. Rozee
Keyword(s):  
Cell Division ◽  
Antiviral Activity ◽  
Dna Synthesis ◽  
S Phase ◽  
Cell Suspensions ◽  
Depression Effect ◽  
Growth Depression ◽  
Synchronized Cells ◽  
Inhibition Of Dna Synthesis ◽  
New Protein

Using monodispersed cell suspensions, interferon preparations were shown to have both a lethal and a growth-depression effect in the same concentration range as that required for antiviral activity. In addition, synchronized cells treated with interferon respond by delaying their normal uptake of thymidine during S phase until after a period during which new protein is synthesized. Puromycin added during this period prevents both the synthesis of this protein and the subsequent synthesis of DNA.

scholarly journals Cohesin-Mediated Genome Architecture Does Not Define DNA Replication Timing Domains

Genes ◽  
2019 ◽  
Vol 10 (3) ◽  
pp. 196 ◽  
Author(s):  
Phoebe Oldach ◽  
Conrad A. Nieduszynski
Keyword(s):  
Dna Replication ◽  
Genome Organization ◽  
Mammalian Cells ◽  
Replication Timing ◽  
S Phase ◽  
Genome Architecture ◽  
3D Genome ◽  
Synchronized Cells ◽  
Dna Replication Timing ◽  
Phase Entry

3D genome organization is strongly predictive of DNA replication timing in mammalian cells. This work tested the extent to which loop-based genome architecture acts as a regulatory unit of replication timing by using an auxin-inducible system for acute cohesin ablation. Cohesin ablation in a population of cells in asynchronous culture was shown not to disrupt patterns of replication timing as assayed by replication sequencing (RepliSeq) or BrdU-focus microscopy. Furthermore, cohesin ablation prior to S phase entry in synchronized cells was similarly shown to not impact replication timing patterns. These results suggest that cohesin-mediated genome architecture is not required for the execution of replication timing patterns in S phase, nor for the establishment of replication timing domains in G1.

Maximal binding levels of an H1 histone gene-specific factor in S-phase correlate with maximal H1 gene transcription

1988 ◽  
Vol 8 (10) ◽  
pp. 4576-4578
Author(s):  
S Dalton ◽  
J R Wells
Keyword(s):  
Cell Cycle ◽  
Nucleic Acids ◽  
Gene Transcription ◽  
S Phase ◽  
Histone Gene ◽  
Specific Factor ◽  
Synchronized Cells ◽  
Phase Regulation ◽  
G2 Phase ◽  
Binding Component

Levels of trans-acting factor (H1-SF) binding to the histone H1 gene-specific motif (5'-AAACACA-3' [L. S. Coles and J. R. E. Wells, Nucleic Acids Res. 13:585-594, 1985]) increase 12-fold from G1 to S-phase in synchronized cells and decrease again in G2 phase of the cell cycle. Since the H1 element is required for S-phase expression of H1 genes (S. Dalton and J. R. E. Wells, EMBO J. 7:49-56, 1988), it is likely that the increased levels of H1-SF binding component play an important role in S-phase regulation of H1 gene transcription.

Phosphatidylcholine catabolism in the MCF-7 cell cycle

2006 ◽  
Vol 84 (5) ◽  
pp. 737-744 ◽  
Author(s):  
Weiyang Lin ◽  
Gilbert Arthur
Keyword(s):  
Cell Cycle ◽  
S Phase ◽  
Specific Cell ◽  
Synchronized Cells ◽  
M Phase ◽  
G2 Phase ◽  
Cell Cycle Phases ◽  
Kinetics Of ◽  
Mcf 7

The catabolism of phosphatidylcholine (PtdCho) appears to play a key role in regulating the net accumulation of the lipid in the cell cycle. Current protocols for measuring the degradation of PtdCho at specific cell-cycle phases require prolonged periods of incubation with radiolabelled choline. To measure the degradation of PtdCho at the S and G2 phases in the MCF-7 cell cycle, protocols were developed with radiolabelled lysophosphatidylcholine (lysoPtdCho), which reduces the labelling period and minimizes the recycling of labelled components. Although most of the incubated lysoPtdCho was hydrolyzed to glycerophosphocholine (GroPCho) in the medium, the kinetics of the incorporation of label into PtdCho suggests that the labelled GroPCho did not contribute significantly to cellular PtdCho formation. A protocol which involved exposing the cells twice to hydroxyurea, was also developed to produce highly synchronized MCF-7 cells with a profile of G1:S:G2/M of 90:5:5. An analysis of PtdCho catabolism in the synchronized cells following labelling with lysoPtdCho revealed that there was increased degradation of PtdCho in early to mid-S phase, which was attenuated in the G2/M phase. The results suggest that the net accumulation of PtdCho in MCF-7 cells may occur in the G2 phase of the cell cycle.

scholarly journals Polo-Like Kinase Guides Cytokinesis in Trypanosoma brucei through an Indirect Means

2010 ◽  
Vol 9 (5) ◽  
pp. 705-716 ◽  
Author(s):  
Zhi Li ◽  
Takashi Umeyama ◽  
Ziyin Li ◽  
Ching C. Wang
Keyword(s):  
Cell Cycle ◽  
Trypanosoma Brucei ◽  
Critical Role ◽  
S Phase ◽  
Content Type ◽  
Synchronized Cells ◽  
Chromosomal Passenger ◽  
Attachment Zone ◽  
Target Effects ◽  
Rule Out

ABSTRACT Polo-like kinase in Trypanosoma brucei (TbPLK) is confined to the flagellum attachment zone (FAZ) and regulates only cytokinetic initiation. However, it apparently diffuses into the cytoplasm before the trans-localization of chromosomal passenger complex (CPC) from the midzone of central spindle to FAZ, which is known to be required for initiating cytokinesis. Synchronized T. brucei procyclic cells treated with a TbPLK inhibitor, GW843682X (GW), in late S phase were found to go through a full cell cycle at a normal pace before being arrested at cytokinetic initiation in the second cycle. However, synchronized cells treated with GW in G1 phase were arrested at cytokinetic initiation within the first cell cycle, suggesting that inhibition of TbPLK at its emergence blocks cytokinesis within the same cell cycle. To rule out potential off-target effects from GW, TbPLK RNA interference (RNAi) was induced to deplete TbPLK, and the progression of synchronized cells from late S phase was also found to be arrested at cytokinetic initiation within the first cell cycle. Apparently, TbPLK has accomplished its role in guiding cytokinesis before the late S phase, presumably by phosphorylating a certain substrate(s) during S phase, which may play a critical role in initiating the subsequent cytokinesis.

scholarly journals Persistent DNA damage inhibits S-phase and G2 progression, and results in apoptosis.

1997 ◽  
Vol 8 (6) ◽  
pp. 1129-1142 ◽  
Author(s):  
D K Orren ◽  
L N Petersen ◽  
V A Bohr
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Uv Irradiation ◽  
Excision Repair ◽  
Chinese Hamster ◽  
S Phase ◽  
Ovary Cell ◽  
G2 Arrest ◽  
Direct Role ◽  
Synchronized Cells

We used genetically related Chinese hamster ovary cell lines proficient or deficient in DNA repair to determine the direct role of UV-induced DNA photoproducts in inhibition of DNA replication and in induction of G2 arrest and apoptosis. UV irradiation of S-phase-synchronized cells causes delays in completion of the S-phase sometimes followed by an extended G2 arrest and apoptosis. The effects of UV irradiation during the S-phase on subsequent cell cycle progression are magnified in repair-deficient cells, indicating that these effects are initiated by persistent DNA damage and not by direct UV activation of signal transduction pathways. Moreover, among the lesions introduced by UV irradiation, persistence of (6-4) photoproducts inhibits DNA synthesis much more than persistence of cyclobutane pyrimidine dimers (which appear to be efficiently bypassed by the DNA replication apparatus). Apoptosis begins approximately 24 h after UV irradiation of S-phase-synchronized cells, occurs to a greater extent in repair-deficient cells, and correlates well with the inability to escape from an extended late S-phase-G2 arrest. We also find that nucleotide excision repair activity (including its coupling to transcription) is similar in the S-phase to what we have previously measured in G1 and G2.

scholarly journals A UV-responsive G2 checkpoint in rodent cells.

1995 ◽  
Vol 15 (7) ◽  
pp. 3722-3730 ◽  
Author(s):  
D K Orren ◽  
L N Petersen ◽  
V A Bohr
Keyword(s):  
Cell Cycle ◽  
Uv Irradiation ◽  
Mammalian Cells ◽  
Cell Cycle Progression ◽  
Chinese Hamster Ovary Cells ◽  
S Phase ◽  
Serum Starvation ◽  
Cycle Progression ◽  
Synchronized Cells ◽  
G2 Phase

We have studied the effect of UV irradiation on the cell cycle progression of synchronized Chinese hamster ovary cells. Synchronization of cells in S or G2 phase was accomplished by the development of a novel protocol using mimosine, which blocks cell cycle progression at the G1/S boundary. After removal of mimosine, cells proceed synchronously through the S and G2 phases, allowing manipulation of cells at specific points in either phase. Synchronization of cells in G1 was achieved by release of cells after a period of serum starvation. Cells synchronized by these methods were UV irradiated at defined points in G1, S, and G2, and their subsequent progression through the cell cycle was monitored. UV irradiation of G1-synchronized cells caused a dose-dependent delay in entry into S phase. Irradiation of S-phase-synchronized cells inhibited progression through S phase and then resulted in accumulation of cells for a prolonged interval in G2. Apoptosis of a subpopulation of cells during this extended period was noted. UV irradiation of G2-synchronized cells caused a shorter G2 arrest. The arrest itself and its duration were dependent upon the timing (within G2 phase) of the irradiation and the UV dose, respectively. We have thus defined a previously undescribed (in mammalian cells) UV-responsive checkpoint in G2 phase. The implications of these findings with respect to DNA metabolism are discussed.

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