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At least 289 records · Page 16Linked to original sources

PubMed1982

RNA dependence in the cell cycle of V79 cells.

The cell cycle of V79 Chinese hamster lung cells synchronized by hydroxyurea was investigated by flow cytometry. The metachromatic fluorochrome acridine orange was used to differentially stain DNA and RNA of V79 cells. Green and red fluorescence from individual cells, representing cellular DNA and RNA, respectively, was measured by flow cytometry. Periodic changes of cellular DNA and RNA contents were observed over nine cell cycles. The duration of G1, S, and G2 + M phases of synchronized V79 cells whose RNA content was close to that of the cells in balanced growth was 3, 4.5, and 1.5 hours, respectively. The duration of G1 and S phases of cells containing RNA above a certain threshold was inversely proportional to the RNA content. The RNA content of cells containing RNA above the normal level regressed to normal after a few generations. Coefficients of variation for RNA content were significantly larger than those for DNA. An explanation for the decay of synchrony in a synchronized cell population is proposed.

Animals↗

PubMed2006

Telomere and TRF2/MTBP localization in respect to satellite DNA during the cell cycle of mouse cell line L929.

The mouse Mus musculus chromosomes are all acrocentric; each centromere (CEN) is adjacent to a telomere. The aim of the current work is to find out if at least half of the mouse telomeres (Tel) always follow satellite DNA sequences and if membrane telomere binding protein TRF2/MTBP is always in association with the Tel during the cell cycle. FISH, immunoFISH and confocal microscopy were used. During the cell cycle, Tel undergo extensive movement and rearrangement. Most Tel tend to aggregate into large conglomerates in G0/G1. Aggregates colocalize with major satellite (MaSat) and minor satellite (MiSat) to a lesser extent. Tel aggregates are embedded into the MaSat granules at G0/G1. A number of single Tel signals underline the nuclear envelope. In prometaphase, during the metaphase plate formation, half of the Tel, together with CEN, are arranged in a circle and half of the long arms form four clusters. Most of the Tel hybridization signals are colocalized with TRF2/MTBP throughout all stages of the cell cycle, although it is possible to find some telomeres that are not covered with the protein. A prominent shift of TRF2/MTBP signals in respect to the Tel signals is visible in the prophase. The biochemical features of TRF2/MTBP make it possible for the protein to be responsible for Tel clustering.

Animals↗

PubMed2004

Effect of HIV-1 Vpr on cell cycle regulators.

Cell cycle is one of the most complex processes in the life of a dividing cell. It involves numerous regulatory proteins, which direct the cell through a specific sequence of events for the production of two daughter cells. Cyclin-dependent kinases (cdks), which complex with the cyclin proteins, are the main players in the cell cycle. They can regulate the progression of the cells through different stages regulated by several proteins including p53, p21(WAF1), p19, p16, and cdc25. Downstream targets of cyclin-cdk complexes include pRB and E2F. A cell cycle can be altered to the advantage of many viral agents, most notably polyomaviruses, papillomaviruses, adenoviruses, and retroviruses. In addition, viral protein R (Vpr) is a protein encoded by the human immunodeficiency virus type 1 (HIV-1). HIV-1, the causative agent of acquired immunodeficiency syndrome (AIDS), is a member of the lentivirus class of retroviruses. This accessory protein plays an important role in the regulation of the cell cycle by causing G(2) arrest and affecting cell cycle regulators. Vpr prevents infected cells from proliferating, and collaborates with the matrix protein (MA) to enable HIV-1 to enter the nucleus of nondividing cells. Studies from different labs including ours showed that Vpr affects the functions of cell cycle proteins, including p53 and p21(WAF1). Thus, the replication of HIV-1, and ultimately its pathogenesis, are intrinsically tied to cell-cycle control.

Cell Cycle↗

PubMed1999

The cell cycle and development: redundant roles of cell cycle regulators.

The existence of families of cell cycle regulators reflects the need by a developing organism to precisely control proliferation of its cells and also suggests that family members may play redundant roles. Recent advances have shown redundancy to be a theme in development.

Animals↗

PubMed2005

Influence of double-strand-break repair pathways on radiosensitivity throughout the cell cycle in CHO cells.

Unrepaired DNA double-strand breaks (DSBs) produced by ionizing radiation (IR) are a major determinant of cell killing. To determine the contribution of DNA repair pathways to the well-established cell cycle variation in IR sensitivity, we compared the radiosensitivity of wild-type CHO cells to mutant lines defective in nonhomologous end joining (NHEJ), homologous recombination repair (HRR), and the Fanconi anemia pathway. Cells were irradiated with IR doses that killed approximately 90% of each asynchronous population, separated into synchronous fractions by centrifugal elutriation, and assayed for survival (colony formation). Wild-type cells had lowest resistance in early G1 and highest resistance in S phase, followed by declining resistance as cells move into G2/M. In contrast, HR-defective cells (xrcc3 mutation) were most resistant in early G1 and became progressively less resistant in S and G2/M, indicating that the S-phase resistance in wild-type cells requires HRR. Cells defective in NHEJ (dna-pk(cs) mutation) were exquisitely sensitive in early G1, most resistant in S phase, and then somewhat less resistant in G2/M. Fancg mutant cells had almost normal IR sensitivity and normal cell cycle dependence, suggesting that Fancg contributes modestly to survival and in a manner that is independent of cell cycle position.

Animals↗

PubMed1994

Developmental modification of the Drosophila cell cycle.

The cell cycle is subject to extrinsic regulation that coordinates cell division with developmental events. This important area at the interface of developmental biology and research into the cell cycle has yielded recent exciting advances. Developmental modification of the cell cycle is exemplified during Drosophila embryogenesis. Early in embryogenesis, regulation of the cell cycle becomes progressively more complex as a simple S-M cycle is altered to include gap phases. Later in embryogenesis, the cycle alters again, to include only an S and a gap phase. These developmental alterations are partly effected by regulating the expression of genes that control key transitions in the cell cycle. Certain controls that are unique to the variant cell cycles have also been defined. The field is now poised for the identification of the intervening steps between the developmental signals and their ultimate effects on known cell cycle regulators.

Animals↗

PubMed1996

Cell cycle regulation and cell type-specific localization of the FtsZ division initiation protein in Caulobacter.

Many genes involved in cell division and DNA replication and their protein products have been identified in bacteria; however, little is known about the cell cycle regulation of the intracellular concentration of these proteins. It has been shown that the level of the tubulin-like GTPase FtsZ is critical for the initiation of cell division in bacteria. We show that the concentration of FtsZ varies dramatically during the cell cycle of Caulobacter crescentus. Caulobacter produce two different cell types at each cell division: (i) a sessile stalked cell that can initiate DNA replication immediately after cell division and (ii) a motile swarmer cell in which DNA replication is blocked. After cell division, only the stalked cell contains FtsZ. FtsZ is synthesized slightly before the swarmer cells differentiate into stalked cells and the intracellular concentration of FtsZ is maximal at the beginning of cell division. Late in the cell cycle, after the completion of chromosome replication, the level of FtsZ decreases dramatically. This decrease is probably mostly due to the degradation of FtsZ in the swarmer compartment of the predivisional cell. Thus, the variation of FtsZ concentration parallels the pattern of DNA synthesis. Constitutive expression of FtsZ leads to defects in stalk biosynthesis suggesting a role for FtsZ in this developmental process in addition to its role in cell division.

Amino Acid Sequence↗

PubMedDate not supplied

Lighting the circle of life: fluorescent sensors for covert surveillance of the cell cycle.

The cell cycle is the collective mechanism through which all of us develop, exist and in many cases, when it goes wrong, die. Despite enormous progress in unravelling the complexity of the cell cycle through intensive study over the past 100 years, development of new tools to analyse the process and associated cellular events has not kept pace. All standard cell cycle analysis methods preclude real time dynamic analysis of the cell cycle in live cells at single cell resolution. To address the needs of cell cycle investigations across a range of analysis platforms we are currently developing a range of cell cycle phase markers based on GFP expression controlled by well characterised cell cycle components to allow covert surveillance of the cell cycle in living cells.

Biomarkers↗

PubMed2006

HTLV-1 propels untransformed CD4 lymphocytes into the cell cycle while protecting CD8 cells from death.

Human T cell leukemia virus type 1 (HTLV-1) infects both CD4+ and CD8+ lymphocytes, yet it induces adult T cell leukemia/lymphoma (ATLL) that is regularly of the CD4+ phenotype. Here we show that in vivo infected CD4+ and CD8+ T cells displayed similar patterns of clonal expansion in carriers without malignancy. Cloned infected cells from individuals without malignancy had a dramatic increase in spontaneous proliferation, which predominated in CD8+ lymphocytes and depended on the amount of tax mRNA. In fact, the clonal expansion of HTLV-1-positive CD8+ and CD4+ lymphocytes relied on 2 distinct mechanisms--infection prevented cell death in the former while recruiting the latter into the cell cycle. Cell cycling, but not apoptosis, depended on the level of viral-encoded tax expression. Infected tax-expressing CD4+ lymphocytes accumulated cellular defects characteristic of genetic instability. Therefore, HTLV-1 infection establishes a preleukemic phenotype that is restricted to CD4+ infected clones.

Adult↗

PubMed2002

Cell cycle retardation in monocytoid cells induced by aminopeptidase N (CD13).

Aminopeptidase N (APN, CD13) is highly expressed on human monocytes. Activation of leucocyte subpopulations, such as T-cells, can induce CD13 expression. However, little is known about the physiological role of CD13 expression on human leucocytes. It was suggested that CD13, similar to other peptidases, could be involved in control of cell growth. The hypothesis that CD13 influences proliferation of monocytoid cells by retarding the velocity of the cell cycle was tested. It was shown that CD13 expression was modulated within the cell cycle. Cells entering the S-phase of cell cycle decreased their CD13 surface expression. Occupation of the active center of CD13 with artificial ligands such as monoclonal antibodies (mab) or the low molecular weight inhibitor actinonin induced a prolongation of cell cycle and decreased the rate of cell growth. Additionally, after ligation of CD13 by mab the complex of CD13 and monoclonal antibody was actively internalized into the cell. We suggest that CD13 could have important functions for the proliferation of human monocytoid cells. Here we show for the first time that occupation of the CD13 active center by antibodies or inhibitors influences the cell cycle and thereby diminishes cell growth rate. Occupation of the active center by antibodies or inhibitors might prevent cleavage or binding and internalization of still unknown natural substrate(s) and could evoke a deceleration of the cell cycle and reduced cell growth rate.

Antibodies, Monoclonal↗

PubMed1979

Regulation of the cell cycle of 3T3 cells in culture by a surface membrane-enriched cell fraction.

Addition of a suspension of a surface membrane enriched fraction prepared from confluent 3T3 cells to sparse 3T3 cells in culture results in a concentration dependent and saturable decrease in the rate of DNA synthesis. The inhibition of cell growth by membranes resembles the inhibition of cell growth observed at confluent cell densities by a number of criteria: 1) In both cases the cells are arrested in the G1 portion of the cell cycle; 2) the inhibition by membranes or by high local cell density can to a large extent be compensated for by raising the serum concentration or by addition of fibroblast growth factor plus dexamethasone. Membranes prepared from sparse cultures inhibit less well than membranes from confluent cultures in a manner which suggests that binding of membranes to cells is not by itself sufficient to cause inhibition of cell growth. The inhibitory activity has a subcellular distribution similar to phosphodiesterase (a plasma membrane marker) and appears to reside in one or more intrinsic membrane components. Maximally, membranes can arrest about 40% of the cell population in each cell cycle. Plasma membranes obtained from sparse 3T3 cells are less inhibitory than membranes obtained from confluent cells. This suggests either that the inhibitory component(s) in the plasma membrane responsible for growth inhibition may be in part induced by high cell density, or that this component(s) may be lost from these membranes during purification.

Animals↗

PubMedDate not supplied

Cell size following irradiation in relation to cell cycle.

The cell volume of Ehrlich ascites tumour cells was studied following a radiation dose of 5.0 Gy. The cell volume increased 12 to 30 hours after irradiation by about 20 per cent, was normal at about 50 hours, and increased again at 72 hours. In order to explain these changes the composition of the cells in cell cycle was studied. In addition, the cell volume of irradiated cells from the various parts of the cell cycle, separated by centrifugal elutriation, was measured. The changes in the mean cell volume of unseparated cells could be explained by variations in the cell cycle composition of the cell population. Irradiated cells from the various parts of the cell cycle did not deviate from the volume of non-irradiated cells. The cell volume doubled during the cell cycle. This increase was, however, not linear.

Animals↗

PubMed2005

Dynamics of intracellular metabolites of glycolysis and TCA cycle during cell-cycle-related oscillation in Saccharomyces cerevisiae.

In the present work LC-MS/MS was applied to measure the concentrations of intermediates of glycolysis and TCA cycle during autonomous, cell-cycle synchronized oscillations in aerobic, glucose-limited chemostat cultures of Saccharomyces cerevisiae. This study complements previously reported oscillations in carbon dioxide production rate, intracellular concentrations of trehalose and various free amino acids, and extracellular acetate and pyruvate in the same culture. Of the glycolytic intermediates, fructose 1,6-bisphosphate, 2- and 3-phosphoglycerate, and phosphoenolpyruvate show the most pronounced oscillatory behavior, the latter three compounds oscillating out of phase with the former. This agrees with previously observed metabolic control by phosphofructokinase and pyruvate kinase. Although individually not clearly oscillating, several intermediates of the TCA cycle, i.e., alpha-ketoglutarate, succinate, fumarate, and malate, exhibited increasing concentration during the cell cycle phase with high carbon flux through glycolysis and TCA cycle. The average mass action ratios of beta-phosphoglucomutase and fumarase agreed well with previously determined in vitro equilibrium constants. Minor differences resulted for phosphoglucose isomerase and enolase. Together with the observed close correlation of the pool sizes of the involved metabolites, this might indicate that, in vivo, these reactions are operating close to equilibrium, whereby care must be taken due to possible differences between in vivo and in vitro conditions. Combining the data with previously determined intracellular amino acid levels from the same culture, a few clear correlations between catabolism and anabolism could be identified: phosphoglycerate/serine and alpha-ketoglutarate/lysine exhibited correlated oscillatory behavior, albeit with different phase shifts. Oscillations in intracellular amino acids might therefore be, at least partly, following oscillations of their anabolic precursors.

Cell Cycle↗

PubMed2004

The human histone gene expression regulator HBP/SLBP is required for histone and DNA synthesis, cell cycle progression and cell proliferation in mitotic cells.

Histone proteins are essential for chromatin formation, and histone gene expression is coupled to DNA synthesis. In metazoans, the histone RNA binding protein HBP/SLBP is involved in post-transcriptional control of histone gene expression. In vitro assays have demonstrated that human HBP/SLBP is involved in histone mRNA 3' end formation and translation. We have inhibited human HBP/SLBP expression by RNA interference to determine its function during the mitotic cell cycle. Inhibition of HBP/SLBP expression resulted in the inhibition of histone gene expression and DNA synthesis, the inhibition of cell cycle progression in S phase and the inhibition of cell proliferation. These findings indicate that human HBP/SLBP is essential for the coordinate synthesis of DNA and histone proteins and is required for progression through the cell division cycle.

Base Sequence↗

PubMed2002

[Effects of tea polyphenols and tea pigments on cell cycle of HepG2 cells].

The effects of tea polyphenols and tea pigments on cell cycle of hepatic cancer cells were studied. HepG2 cells were incubated with 50 and 100 mg/L tea polyphenols and tea pigments for 48 h respectively. Flow cytometry, Western blot and RT-PCR analysis were used. Flow cytometry analysis showed that tea polyphenols and tea pigments induced G1 arrest. Western blot analysis showed tea polyphenols and tea pigments significantly inhibited the expression of cyclin D1 protein and induced higher expression of P21WAFI/CIPI protein. The result of RT-PCR analysis demonstrated that Cdk4 was significantly inhibited by tea polyphenols and tea pigments. It is concluded that the induction of cell cycle arrest may be an important mechanism of tea on cancer prevention.

Carcinoma, Hepatocellular↗

PubMed1991

Cell inactivation and cell cycle inhibition as induced by extreme hypoxia: the possible role of cell cycle arrest as a protection against hypoxia-induced lethal damage.

Cycling mammalian cells that are rendered extremely hypoxic (less than 4 ppm O2) tend to accumulate in a pre-DNA-synthesis stage. It is not clear whether or not this is the result of an active regulation by the cells. In the present study we have rendered cells, synchronized by mitotic selection, extremely hypoxic over a relatively long period of time (up to 48 h). We have recorded cell cycle progression during hypoxia as well as cell inactivation depending on where in the cell cycle the cells were located when the hypoxic treatment was started. Three main conclusions are drawn: 1 the cell cycle arrest in late-G1 is complete even during a long-lasting (24 h) hypoxic treatment: 2 while cells in early- and mid-S are completely arrested and quickly inactivated under hypoxic conditions, cells in late-S, G2 and mitosis are able to continue cell cycle progression and divide; 3 whether the cells are located in G2, mitosis or early-G1 at the onset of hypoxia, they were able to survive relatively long-lasting hypoxic treatment. The present results are in favour of the view that the pre-DNA-synthetic arrest induced by extreme hypoxia may function to rescue the cells from severely damaging effects that would appear if the cells were able to initiate DNA synthesis.

Cell Cycle↗

PubMed2003

Murine neonatal lymphocytes show rapid early cell cycle entry and cell division.

Neonatal animals are highly susceptible to infectious agents. At least part of this susceptibility is due to the virtual absence of immunological memory in newborns. One of the hallmarks of memory is the rapidity of the response. We show in this study that neonates may make up for their lack of memory, at least in part, by the rapid entry of large proportions of naive lymphocytes into the cell cycle. Following activation, greater percentages of both CD4(+) and CD8(+) neonatal, as compared with adult, lymph node cells showed early cell cycle entry; this was assessed by propidium iodide staining, CFSE labeling profiles, [(3)H]thymidine uptake, and up-regulation of early activation markers. This rapid cycle entry was observed following polyclonal activation with anti-CD3 or with PMA and ionomycin and in both C57BL/6 and BALB/c mice. Stimulation with specific peptide also elicited more rapid proliferative responses from neonatal vs adult TCR transgenic CD4(+) cells. In addition, more rapid cycle entry was observed in vivo, in lymphopenic RAG2(-/-) hosts. For both CD4(+) and CD8(+) cells, this phenomenon was observed out to 3 wk of life, although the differences between neonatal and adult cells became smaller with increasing time postbirth. These properties of peripheral neonatal T cells appeared to be inherited from their thymic precursors, because CD4(+)8(-) single-positive cells in the neonatal thymus also showed more rapid cycle entry, compared with their counterparts in the adult thymus. Interestingly, rapid early cycling was also observed among activated neonatal B cells, compared with adult B cells. Thus, early cell cycle entry by large proportions of cells may allow the naive lymphocyte population to efficiently mobilize responses against the broad range of pathogens first encountered in neonatal life.

Aging↗

PubMed1992

[The influence of paraquat on cell cycle--analysis of cell kinetics using DNA/BrdU staining].

We examined the in vitro and in vivo effects of paraquat on the cell cycle. After we exposed paraquat to the cultured cell (MDCK), we examined cell kinetics by flow cytometry with BrdU-PI double staining. And we administered paraquat intravenously to the rats, we collected and separated rat's liver and pulmonary cells, and we examined the cell kinetics by same method. Consequently our study found that the cells in the S-phase were noted to be abundant, and we suggested that paraquat apparently arrested the cell cycle at S time, and that DNA damage was importance in the mechanism of paraquat toxicity.

Animals↗