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At least 433 records · Page 24Linked to original sources
PubMed1998

Cell cycle control protein p34cdc2 homologue and its phase specific accumulation in synchronized onion (Allium cepa L.) root meristem cells.

A key regulator of the cell cycle is a highly conserved protein kinase whose catalytic subunit, p34cdc2, is encoded by cdc2 gene. Immunoblotting with a polyclonal antibody raised against PSTAIRE sequence (found in the N-terminal region of all cdc2 and cdc2 related proteins throughout the phylogenetic scale including higher plants), was used to study the presence of p34cdc2 in onion scale leaves and root tip cells. p34cdc2 homologues are beyond the detection level in scale leaves. PSTAIRE antibody was used to estimate p34cdc2 kinase protein levels during cell cycle in highly synchronous population of Allium cepa L. root meristem cells. p34cdc2 kinase protein showed gradual increase in their levels from S phase to G2 phase boundary. Immunoprecipitation followed by in vitro histone H1 kinase assays also depicted that its kinase activity increased parallel to the increase in p34cdc2 level.

Amino Acid Sequence↗
PubMed1994

Radiosensitivity of polyamine-depleted HeLa cells and modulation by the aminothiol WR-1065.

The radiosensitivity of cultured HeLa cells was increased upon depletion of the natural cellular polyamines putrescine, spermidine and spermine through treatment of cultures with inhibitors of polyamine biosynthesis. This increased radiosensitivity was manifested as a decrease in the D0 and by the absence of a shoulder in the survival curves. However, our previous studies have shown that the initial yield of X-ray-induced DNA damage did not appear to be elevated in polyamine-depleted cells. In addition, polyamine-depleted cells exhibited markedly altered X-ray-induced changes in the distribution of cells in the phases of the cell cycle characterized by increased time of onset and lengthened duration of G2-phase delay. Addition of polyamines to cultures for short periods prior to irradiation restored normal radioresistance and reversed the anomalous features of the G2-phase delay profile. Polyamine supplementation experiments as well as studies in which combinations of inhibitors were employed to modulate specific polyamine levels suggest that spermidine may play a primary role in governing cellular radioresponsiveness. The radioprotective aminothiol WR-1065 protected normal and polyamine-depleted cells to a proportionately similar extent (protection factor of 2.4 and 2.8, respectively) but had no apparent ability to restore the shoulder or alter the G2-phase delay markedly in polyamine-depleted cells. The findings reported here extend our previous observations that polyamine depletion results in a compromised ability to respond to X irradiation and suggest that a defect in repair and/or the G2-phase delay response may be the determining factors.

Cell Survival↗
PubMed2005

Protein kinase A regulates cell cycle progression of mouse fertilized eggs by means of MPF.

Cell cycle of one-cell stage mouse fertilized eggs was accompanied by fluctuation in the concentration of adenosine 3'5'-monophosphate (cAMP) and in the activity of free catalytic subunit of cAMP-dependent protein kinase (PKA). The concentration of cAMP and the activity of free catalytic subunit of PKA decreased at the onset of mitosis and increased at the transition between mitosis and G1 phase. Stimulation of PKA by microinjection of cAMP into one-cell stage mouse embryos at G2 phase induced interphase arrest and prevented the activation of M-phase promoting factor (MPF). Upon blockage of the activation of PKA by microinjecting a thermostable PKA inhibitor (PKI) into one-cell stage mouse embryos at G2 phase, the increase in the MPF activity occurred 30 min earlier than in control group. When a high dose of PKI was microinjected, a transition into interphase was prevented, and the activity of MPF remained high. Western blot analysis showed that Cdc2 remained phosphorylated in cAMP microinjected embryos by the time when control embryos were at metaphase and showed dephosphorylated Cdc2; conversely, Cdc2 dephosphorylation was accelerated in PKI-microinjected embryos. At the same time, Cdc2 was phosphorylated at Tyr15 at G2 phase and even at M phase when cAMP was microinjected but was dephosphorylated when PKI was microinjected. PKI microinjection also prevented cyclin B degradation and sustained MPF activity, thus delaying the transition from metaphase to anaphase. Our results show that PKA, by inhibiting MPF, regulates cell cycle progression of fertilized eggs.

Anaphase↗
PubMed1987

Distinct replication-independent and -dependent phases of histone gene expression during the Physarum cell cycle.

During the S phase of the cell cycle, histone gene expression and DNA replication are tightly coupled. In mitotically synchronous plasmodia of the myxomycete Physarum polycephalum, which has no G1 phase, histone mRNA synthesis begins in mid-G2 phase. Although histone gene transcription is activated in the absence of significant DNA synthesis, our data demonstrate that histone gene expression became tightly coupled to DNA replication once the S phase began. There was a transition from the replication-independent phase to the replication-dependent phase of histone gene expression. During the first phase, histone mRNA synthesis appears to be under direct cell cycle control; it was not coupled to DNA replication. This allowed a pool of histone mRNA to accumulate in late G2 phase, in anticipation of future demand. The second phase began at the end of mitosis, when the S phase began, and expression became homeostatically coupled to DNA replication. This homeostatic control required continuing protein synthesis, since cycloheximide uncoupled transcription from DNA synthesis. Nuclear run-on assays suggest that in P. polycephalum this coupling occurs at the level of transcription. While histone gene transcription appears to be directly switched on in mid-G2 phase and off at the end of the S phase by cell cycle regulators, only during the S phase was the level of transcription balanced with the rate of DNA synthesis.

Actins↗
PubMed1994

[Effect of cisplatin on cell cycle regulators].

An anticancer agent, cisplatin (CDDP), induced G2-phase arrest in PC-9 human cancer cells. To elucidate how CDDP acts on cell-cycle regulation, we analyzed the effect of CDDP on cell-cycle regulators such as P34cdc2 protein kinase. P34cdc2 kinase activity was maximum in G2 phase and decreased after G2/M transition in synchronized PC-9 cells. Evidence for a phosphorylated p34cdc2 complexed with cyclin B was obtained from cells in G2 phase and the p34cdc2 appeared to be dephosphorylated at M phase. After exposure to CDDP in G1 phase, PC-9 cells were arrested at G2 phase. The activation of p34cdc2 was inhibited by CDDP. Cyclin A, B and wee-1 kinase were not affected by the exposure to CDDP. Our data suggested that the effect of CDDP on cell-cycle phase might be regulated by the dephosphorylation of p34cdc2. We hypothesize that inhibition of p34cdc2 dephosphorylation by CDDP is important for its growth-inhibiting properties.

CDC2 Protein Kinase↗
PubMed2005

Downregulation of protein phosphatase 2A activity in HeLa cells at the G2-mitosis transition and unscheduled reactivation induced by 12-O-tetradecanoyl phorbol-13-acetate (TPA).

In the cell cycle the transition from G2 phase to cell division (M) is strictly controlled by protein phosphorylation-dephosphorylation reactions effected by several protein kinases and phosphatases. Although much indirect and direct evidence point to a key role of protein phosphatase 2A (PP2A) at the G2/M transition, the control of the enzyme activity prior to and after the transition are not fully clarified. Using synchronized HeLa cells we determined the PP2A activity (i.e. the increment sensitive to inhibition by 2nM okadaic acid) in immunoprecipitates obtained with antibodies raised against a conserved peptide sequence (residues 169-182, Ab(169/182)) of the PP2A catalytic subunit (PP2A C). Two different substrates were offered: the phospho-peptide KR(p)TIRR and histone H1 phosphorylated by means of the cyclin-dependent protein kinase p34(cdc2). The results indicate that in HeLa cells the specific activity of PP2A towards both substrates goes through a minimum in late G2 phase and stays low until metaphase. Treatment of G2 cells with TPA (10(-7) M) caused a reactivation of the downregulated PP2A activity within 20 min, i.e. the same time frame within which TPA was shown earlier to block HeLa cells at the transition from G2 to mitosis [Kinzel et al., 1988. Cancer Res. 48, 1759-1762]. Activation of PP2A was also induced by TPA in mitotic cells. The low activity of PP2A in mitotic cells was accompanied by a strong reaction of mitotic PP2A C with anti-P-Tyr antibodies in Western blots, which was reversed by treatment of mitotic cells with TPA. The results suggest that the activity of cellular PP2A requires downregulation for the transition from G2 phase to mitosis. Unscheduled reactivation of PP2A induced by TPA in late G2 phase appears to inhibit the progress into mitosis.

Antibodies↗
PubMed1991

Oxygen enhancement ratio as a function of dose and cell cycle phase for radiation-resistant and sensitive CHO cells.

There is still controversy over whether the oxygen enhancement ratio (OER) varies as a function of dose and cell cycle phase. In the present study, the OER has been measured as a function of survival level and cell cycle phase using volume flow cell sorting. This method allows both the separation of cells in different stages of the cycle from an asynchronously growing population, and the precise plating of cells for accurate measurements at high survival levels. We have developed a cell suspension gassing and sampling system which maintained an oxygen tension less than 20 ppm throughout a series of sequential radiation doses. For both radiation-resistant cells (CHO-K1) and a radiation-sensitive clone (CHO-xrs6), we could separate relatively pure populations of G1-phase, G1/S-boundary, S-, and G2-phase cells. Each cell line showed a typical age response, with cells at the G1/S-phase boundary being 4 (CHO-K1) to 12 (CHO-xrs6) times more sensitive than cells in the late S phase. For both cell lines, G1-phase cells had an OER of 2.3-2.4, compared to an OER of 2.8-2.9 for S-phase and 2.6-2.7 for G2-phase cells. None of these age fractions showed a dependence of OER on survival level. Asynchronously growing cells or cells at the G1/S-phase boundary had an OER similar to that of G1-phase cells at high survival levels, but the OER increased with decreasing survival level to a value near that of S-phase cells. These results suggest that the decrease in OER at high survival levels for asynchronous cells may be due to differences in the OERs of the inherent cell age subpopulations. For cells in one cell cycle stage, oxygen appears to have a purely dose-modifying effect.

Animals↗
PubMedDate not supplied

Photomodulation of the melanocyte cell cycle by indoleamines.

Melanocytes are photoresponsive cells which respond to varying doses of UV exposure in the G2 phase of the cell cycle by prominent dendricity. This photoresponse is related to indoleamine light sensitivity. The present study highlights the role of indoleamines in the photomodulation of the melanocyte cell cycle. The study was conducted on 40 whole-skin organ cultures taken from the marginal zone of vitiligo. Twenty organ cultures were subjected to G2-phase arrest, while 20 were incubated in tryptamine. The organ cultures were incubated in the dark, exposed to a pulse of 120 s UV at 2 h of incubation and harvested 3 and 6 h after UV exposure. It has been reported that the photosensitive enzymes N-acetyl transferase (NAT) and hydroxyindole-o-methyl transferase (HIOMT) are activated during the G2 phase. The conversion of serotonin to melatonin is inhibited by UV exposure as seen at 3 h. This activity recovers on continued dark incubation 6 h after UV exposure. On incubation with tryptamine, UV exposure results in utilisation of tryptamine as seen by prominent indoleamine positivity. Three hours after UV exposure, there is 75% dendricity indicating G2 phase traverse. There is a corresponding high serotonin positivity with a low melatonin positivity. This is reversed following 6 h of dark incubation with high melatonin positivity indicating reactivation of NAT and HIOMT. This is accompanied by a doubling of the melanocyte number due to mitotic traverse and an arrest in G1 phase with low utilisation of tryptamine. Thus tryptamine is utilised by melanocytes on UV exposure to be synchronised and traversed into G2 phase activating the photosensitive enzymes NAT and HIOMT. When followed by a dark phase, melatonin accumulates to traverse the melanocytes through M-phase of the cell cycle with doubling of the cell number. Thus the uptake and metabolisation of indoleamine precursors photomodulate the melanocyte cell cycle on UV exposure.

Acetylserotonin O-Methyltransferase↗
PubMed2006

Cell cycle synchronization at the G2/M phase border by reversible inhibition of CDK1.

Chemical agents for cell cycle synchronization have greatly facilitated the study of biochemical events driving cell cycle progression. G1, S and M phase inhibitors have been developed and used widely in cell cycle research. However, currently there are no effective G2 phase inhibitors and synchronization of cultured cells in G2 phase has been challenging. Recently, a selective CDK1 inhibitor, RO-3306, has been identified that reversibly arrests proliferating human cells at the G2/M phase border and provides a novel means for cell cycle synchronization. A single-step protocol using RO-3306 permits the synchronization of >95% of cycling cancer cells in G2 phase. RO-3306 arrested cells enter mitosis rapidly after release from the G2 block thus allowing for isolation of mitotic cells without microtubule poisons. RO-3306 represents a new molecular tool for studying CDK1 function in human cells.

Animals↗
PubMed1988

Staining with pyronin Y detects changes in conformation of RNA during mitosis and hyperthermia of CHO cells.

Cellular RNA in Chinese hamster ovary (CHO) cells synchronized in mitosis (M) or G2 phase, as well as in interphase cells subjected to hyperthermia (42 degrees C, 10 min), was stained with acridine orange (AO), ethidium bromide (EB), or pyronin Y (PY) and the resultant fluorescence was measured by flow cytometry. Total RNA content detected after staining with AO increased in M as compared to G2-phase cells, consistent with continued RNA synthesis during G2 phase. The content of double-stranded RNA, stained with EB (after DNase treatment), was also somewhat higher in M cells. In contrast, the stainability of RNA with PY decreased by 27% in M- compared to G2-phase cells. Furthermore, a decrease in stainability of RNA with PY was observed in G2 cells compared to cells in G1 phase. In separate experiments, RNA stainability with AO or EB was generally unaffected when interphase CHO cells were exposed to 42 degrees C for 10 min, though this same treatment resulted in a 26% decrease in RNA stainability with PY. The decreased PY stainability of cellular RNA in M or heat-treated cells was observed at a relatively narrow range of dye concentration (1.0-2.0 micrograms/ml). The observed hypochromicity of RNA coincides with dissociation of polyribosomes into single ribosomes known to occur during mitosis and following exposure to hyperthermia. It is presumed that the phenomenon involves selective denaturation and condensation of ribosomal (r) RNA by PY in single ribosomes which does not occur in polyribosomes. While the molecular mechanisms responsible for stabilization of rRNA in polyribosomes preventing its denaturation and condensation by PY are unknown, PY appears to be a sensitive probe that can be used to detect and study these changes in rRNA confirmation in situ.

Animals↗
PubMedDate not supplied

Effects of PKC zeta on early genome transcription activation in mouse 1-cell stage fertilized eggs.

Effects of PKC zeta on the activation of embryonic transcription in 1-cell stage fertilized mouse eggs were explored. The effects of PKC antagonist calphostin C and PKC zeta specific inhibitor on the activation of embryonic early transcription were observed by Western blotting and cell immunofluorescence. PKC activity increased gradually from G1 phase to late G2 phase in mouse 1-cell stage fertilized eggs, and reached a maximum in G2 stage. Calphostin C inhibited PKC activity by about 47% in 1-cell stage fertilized eggs. Calphostin C inhibited early transcription in 1-cell stage fertilized eggs (p < 0.01). PKC zeta-Thr410 in G2 were about 27% and 110% higher than those in G1 phase of 1-cell stage fertilized eggs and MII oocytes, respectively. PKC zeta specific inhibitor can also inhibit early transcription in 1-cell stage fertilized eggs (p < 0.05). The results suggest that PKC zeta participates in early transcription activation in mouse 1-cell stage fertilized eggs.

Animals↗
PubMed2004

Copper may interact with selenite extracellularly in cultured HT-29 cells.

Previous studies have demonstrated that copper (15.7 micromol/L) can inhibit selenite (12.6 micromol/L)-induced cytotoxicity and apoptosis in HT-29 cells. However, the exact nature of the interactions between selenium and copper is not fully understood. In this study, the effect of copper on the cell cycle arrest induced by selenite or selenocystine was examined. Both selenite and selenocystine were effective in inhibition of cell growth and cell cycle progression. Cell cycle analysis revealed that selenite (3-5 micromol/L) caused a decrease in G1 phase cells that corresponded with an increase in S and G2 phase cells, and that 0.625 or 1.25 micromol/L copper sufficiently inhibited selenite-induced cell cycle arrest. In contrast, selenocystine caused an increase in G1 phase cells that corresponded with a decrease in S and G2 phase cells. Interestingly, 0.625 or 1.25 micromol/L copper did not inhibit selenocystine-induced cell cycle arrest. In addition, cell free gel shift assay demonstrated that selenite suppressed the inhibitory effect of copper on SP-1 DNA binding. Furthermore, although 5 micromol/L selenite in culture media significantly increased the intracellular selenium content, 1.25 micromol/L copper sulfate blocked this increase of the intracellular selenium content. Collectively, these data demonstrate that selenite and selenocystine cause cell cycle arrest via distinct mechanisms, and suggest that copper may interact with selenite extracellularly, which represents the basis of antagonism between copper sulfate and selenite.

Cell Cycle↗
PubMed1988

The RAD9 gene controls the cell cycle response to DNA damage in Saccharomyces cerevisiae.

Cell division is arrested in many organisms in response to DNA damage. Examinations of the genetic basis for this response in the yeast Saccharomyces cerevisiae indicate that the RAD9 gene product is essential for arrest of cell division induced by DNA damage. Wild-type haploid cells irradiated with x-rays either arrest or delay cell division in the G2 phase of the cell cycle. Irradiated G1 and M phase haploid cells arrest irreversibly in G2 and die, whereas irradiated G2 phase haploid cells delay in G2 for a time proportional to the extent of damage before resuming cell division. In contrast, irradiated rad9 cells in any phase of the cycle do not delay cell division in G2, but continue to divide for several generations and die. However, efficient DNA repair can occur in irradiated rad9 cells if irradiated cells are blocked for several hours in G2 by treatment with a microtubule poison. The RAD9-dependent response detects potentially lethal DNA damage and causes arrest of cells in G2 until such damage is repaired.

Cell Cycle↗
PubMed1996

Cell cycle defect in connection with oxygen and iron sensitivity in Fanconi anemia lymphoblastoid cells.

Fanconi anemia (FA) is an autosomal recessive disorder involving progressive pancytopenia, skeletal malformations, and a predisposition to leukemia. The in vitro growth of FA fibroblasts is impaired, due to a defective G2 phase traverse of the cell cycle. Analyzing the cell cycle of lymphoid cell lines (LCLs) obtained from peripheral blood of FA patients by transformation with Epstein-Barr virus, we found a similar G2 phase defect, which was dependent upon the oxygen concentration. In addition, FA cells exhibited hypersensitivity toward cis-dichlorodiammineplatinum and mitomycin C, and moderate sensitivity toward trans-dichlorodiammineplatinum. FA cells, however, showed no elevated sensitivity toward paraquat, an intracellular generator of superoxide radicals, or cumene hydroperoxide, a model organic peroxide. Chelating iron with low concentrations of o-phenanthrolin improved cell proliferation and G2 phase transit of FA cells at 20% oxygen, but little at 5% oxygen. LCL cultures from healthy subjects were inhibited in their proliferation rate at all concentrations of o-phenanthrolin. Exposure to excess iron, on the other hand, was very toxic to FA cells at 20%, but less toxic at 5% oxygen. In conclusion, the FA mutation leads to a cell cycle defect, which is expressed in cultures of lymphoid cells from FA patients, and involves hypersensitivity toward bifunctional alkylating agents, oxygen, and iron.

Alkylating Agents↗
PubMed2004

Cell cycle alteration, apoptosis and response of leukemic cell lines to gamma radiation with high- and low-dose rate.

The aim of this work was to compare the effect of gamma radiation with sub-low dose-rate 1.8 mGy/min (SLDR), low dose-rate 3.9 mGy/min (LDR) and high dose-rate 0.6 Gy/min (HDR) on human leukemic cell lines with differing p53 status (HL-60, p53 deficient and MOLT-4, p53 wild) and to elucidate the importance of G2/M phase cell cycle arrest during irradiation. Radiosensitivity of HL-60 and MOLT-4 cells was determined by test of clonogenity. Decrease of dose-rate had no effect on radiosensitivity of MOLT-4 cells (D(0) for HDR 0.87 Gy, for LDR 0.78 Gy and for SLDR 0.70 Gy). In contrast, a significant increase of radioresistance after LDR irradiation was observed for p53 negative HL-60 cells (D(0) for HDR 2.20 Gy and for LDR 3.74 Gy). After an additional decrease of dose-rate (SLDR) D(0) value (2.92 Gy) was not significantly different from HDR irradiation. Considering the fact that during HDR the cells are irradiated in all phases of the cell cycle and during LDR mainly in the G2 phase, we have been unable to prove that the G2 phase is the most radiosensitive phase of the cell cycle of HL-60 cells. On the contrary, irradiation of cells in this phase induced damage reparation and increased radioresistance. When the dose-rate was lowered, approximately to 1.8 mGy/min, an opposite effect was detected, i.e. D(0) value decreased to 2.9 Gy. We have proved that during SLDR at first (dose up to 2.5 Gy) the cells accumulated in G2 phase, but then they entered mitosis or, if the cell damage was not sufficiently repaired, the cells entered apoptosis. The entry into mitosis has a radiosensibilizing effect.

Apoptosis↗
PubMed2006

Regulation of Polo-like kinase 1 by DNA damage in mitosis. Inhibition of mitotic PLK-1 by protein phosphatase 2A.

DNA damage triggers multiple checkpoint pathways to arrest cell cycle progression. Polo-like kinase 1 (Plk1) is an important regulator of several events during mitosis. In addition to Plk1 functions in cell cycle, Plk1 is involved in DNA damage check-point in G2 phase. Normally, ataxia telangiectasia-mutated kinase (ATM) is a key enzyme involved in G2 phase cell cycle arrest following DNA damage, and inhibition of Plk1 by DNA damage during G2 occurs in a ATM/ATR-dependent manner. However, it is still unclear how Plk1 is regulated in response to DNA damage in mitosis in which Plk1 is already activated. Here, we show that treatment of mitotic cells with doxorubicin and gamma-irradiation inhibits Plk1 activity through dephosphorylation of Plk1, and cells were arrested in G2 phase. Treatments of the phosphatase inhibitors and siRNA experiments suggested that PP2A pathway might be involved in regulating mitotic Plk1 activity in mitotic DNA damage. Finally, we propose a novel pathway, which is connected between ATM/ATR/Chk and protein phosphatase-Plk1 in DNA damage response in mitosis.

Ataxia Telangiectasia Mutated Proteins↗
PubMed2001

[Influence of cell cycle in human trabecular cells induced by dexamethsone].

PURPOSE: To investigate the influence of dexamethesone (Dex) on cell cycle in human trabecular cells(HTC). METHODS: The trabecular specimens from human eyes were cultured in vitro. Then the cultured cells were immersed in DMEM solution containing 10(-7) M dexamethesone for three, five and seven days. The cell cycle was detected by Flow Cycometry. RESULTS: The G2 phase of cell cycle in HTC increased when HTC were treated by Dex. The G2 phase was 2% in control group. For three, five and seven days treated by Dex, the G2 phase were 8%, 16.3 and 19.4%. CONCLUSION: The influence of cell cycle might be induced by Dex, it may be related with the pathogenesis of glucocorticoid induced glaucoma.

Cell Cycle↗
PubMed1987

The effect of 9-beta-D-arabinofuranosyladenine on the formation of X-ray induced chromatid aberrations in X-irradiated G2 human cells.

The effects of the nucleoside analogue 9-beta-D-arabinofuranosyladenine (are A) alone or in combination with X-rays on the induction of G2-phase chromosomal damage were studied in immortalized human fibroblasts of lung origin (MRC5-SV1). Ara A is known to be an S-phase specific clastogen, a powerful inhibitor of DNA synthesis and an inhibitor of DNA double-strand break (dsb) repair. The length of the G2-phase of this cell line could be defined as approximately 4 h from data for treatment of cells with ara A alone in which a sharp rise in number of chromatid aberrations was found to occur when ara A treatment times exceeded 4 h; i.e. when cells were in late S-phase at the time of treatment. The frequency of chromatid deletions in X-irradiated G2-phase cells was found to decrease as the time between irradiation and fixation increased. This was interpreted as reflecting the underlying repair of dsb. When X-irradiated cells were treated with ara A between irradiation and fixation, the decrease in deletions found after X-rays alone was not observed. This was interpreted as reflecting the inhibition of dsb repair. Unlike deletions, the yield of exchanges increased during incubation of G2-phase cells after X-ray exposure and the rate of this increase was found to be trebled by the addition of ara A to the medium. We postulate that the increased rate of exchange aberration formation in the absence of dsb repair indicates the existence of a second 'error-prone' misjoining mechanism which is independent of DNA synthesis.

Cell Line↗