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At least 19 recordsLinked to original sources
PubMed1984

S-phase, G2, and nuclear division mutants of Aspergillus nidulans.

Twenty-two temperature-sensitive cell cycle mutants of the fungus Aspergillus nidulans, which block in interphase at restrictive temperature, were analyzed by the reciprocal shift method of Jarvik and Botstein (Proc. Nath Acad. Sci. U.S.A. 70:2046-2050, 1973) and Hereford and Hartwell (J. Mol. Biol. 84:445-461, 1974) to determine whether these mutations were blocked at the G1, S, or G2 phase of the cell cycle. We found five mutants to be blocked in S and nine to be blocked in G2. Two of the G2 mutants were atypical in that they were not able to accomplish the G2 to M transition at restrictive temperature but nevertheless could initiate subsequent cycles of DNA replication. None was blocked in G1. There were nine strains that could not be classified. The block imposed by restrictive temperature was irreversible in three of these strains, and the six other strains were unclassifiable due to their aberrant terminal nuclear phenotypes.

Aspergillus nidulans↗
PubMed1991

The effect of cryopreservation on the development of S- and G2-phase mouse embryos.

The survival rate and development of four-cell-stage mouse embryos frozen and thawed in S phase versus G2 phase was compared. Significantly more G2-phase than S-phase embryos survived freezing and thawing. In both groups, disruption of the zona pellucida, fusion of blastomeres, and dispersion of chromosomes were occasionally observed after thawing. Cryopreservation resulted in a longer delay in cleavage from the four- to the eight-cell stage of S (about 5 hr)- and G2-phase embryos (about 3 hr) compared to unfrozen controls. The number of frozen embryos which developed to the blastocyst stage was reduced compared to controls, and in the case of S-phase embryos, formation of the blastocyst cavity was also delayed. However, the average number of cells in the experimental and control embryos was similar. No increased incidence of chromosome abnormalities was seen. Our results suggest that freezing embryos in G2 is superior to freezing in S phase.

Animals↗
PubMed1981

Nascent replicons are synchronously joined at the end of S phase or during G2 phase in peas.

In synchronized meristematic cells of Pisum sativum replicon-size DNA-fragments ((14--27) . 10(6) daltons) are not joined until the cells achieve a 4C DNA content. The combined use of a pulse-chase labeling protocol, single-cell autoradiography, cytophotometry, and velocity sedimentation in alkaline sucrose gradients showed that, unlike low molecular weight DNA (i.e., Okazaki fragments) which is ligated soon after replication starts, the joining of nascent replicon-size DNA is delayed until G2. In addition, this observation argues for the existence of replicon termini, although the data are insufficient to determine the true nature of these termini, i.e., whether they are coded in the DNA itself or simply arise as a consequence of the convergence of two replicating forks.

Cell Cycle↗
PubMed1988

Effect of caffeine in Fanconi anemia. I. Restoration of a normal duration of G2 phase.

In Fanconi anemia (FA) cells the duration of the G2 phase of the cell cycle prolonged. Such a slowing of the G2 phase can be induced in normal cells by irradiation with gamma rays during S phase, which also further increases the duration of G2 in FA cells. The addition of caffeine during the last 7 h of culture shortens the G2 phase in both nonirradiated and irradiated FA cells. In nonirradiated normal cells it may have no effect or may increase G2 phase duration, but in irradiated normal reduces the slowing of G2 induced by the radiation. This suggests that FA cells recognize and repair preexisting DNA lesions during G2 phase and that caffeine inhibits this process. The principal anomaly in FA may be a deficient repair during S phase, as manifest in the prolonged postreplication repair period during G2 phase required to repair the larger number of lesions passing through S phase.

Anemia, Aplastic↗
PubMed1991

After X-irradiation a transient arrest of L929 cells in G2-phase coincides with a rapid elevation of the level of O6-alkylguanine-DNA alkyltransferase.

Following X-irradiation of exponentially growing L929 cells two major phenomena have been observed. First, there was a delay in cell division which can be ascribed to the arrest of cells in the G2-phase (G2-block), and, second, the cellular content of the O6-alkylguanine-DNA alkyltransferase (AGT) was markedly increased. Flow cytometrical DNA-measurements revealed that cells began to accumulate in the G2-phase 4 h after irradiation (p.r.) irrespective of the X-ray dose, while both the fraction of cells blocked in G2 and the time period the cells persisted in G2 increased with the radiation dose. About 24 h past release from the G2-block the distribution of cells in the cell cycle was similar to that of untreated control cells. In comparison with control cells the AGT content in irradiated cells (4 Gy) was highest at about 48 h p.r. (3.4-fold increase). The highest ratio of increase in AGT was, however, observed to occur between about 4 and 13 h p.r. (2.6-fold increase). As shown by flow cytometrical measurements using a BrdUrd/DNA double labeling technique, this rapid primary increase in AGT coincides very well with the entrance of cells into the G2-phase. This indicates that the cellular AGT content in X-irradiated (parental) cells started to exceed the basal level at the beginning of the G2-phase, but not before or during the S-phase. Once the AGT level was elevated it continued to increase for 2 to 3 cell doubling times.

Animals↗
PubMed1994

Modulation of the spontaneous G2 phase blockage in Fanconi anemia cells by caffeine: differences from cells arrested by X-irradiation.

The effect of caffeine on the endogenous G2 phase cell cycle blockage of Fanconi anemia (FA) cells was compared with the effect of caffeine on the G2 phase blockage induced in control cells by X-irradiation. The G2 phase accumulations in FA cells could be completely resolved by exposure to 1.5 mM caffeine. This was also observed in three brothers with endogenous G2 phase blockage due to unusual BrdU sensitivity. In contrast, G2 phase blockage induced by X-irradiation was only partially resolved by exposure to caffeine. The rescued G2 phase cells from FA patients were arrested within the following G1 phase compartments. This was not seen in X-irradiated cells from control donors. These results point towards a different nature and/or repair mechanism of the endogenous G2 phase lesion in FA cells compared to that induced by X-irradiation in control cells.

Caffeine↗
PubMedDate not supplied

[The nature of the lengthening of the G2 phase in the mitotic cycle of parenchymal cells of the mouse liver].

The phenomenon of G2 phase prolongation was found in the population of mouse hepatocytes. In normal postnatal liver growth, G2 phase prolongation in not pronounced and occurs in a small fraction of proliferating hepatocytes. In case of liver regeneration after removal of 2/3 of the organ, G2 phase prolongation is observed in a population of hepatocytes, which response to the proliferative stimulus first. Estimation of individual variation in expression of prolonged G2 phase along with the detailed analysis of the structure of the process of proliferation in the main population of hepatocytes (cells with normal G2 phase) allows to define the biological meaning of the "G2-population" observed. The prolongation of G2 phase may result from non-specific cell damage in mitotic cycles, caused by destruction of trophic relations in liver during its growth and regeneration.

Aging↗
PubMed1994

Increased expression of cyclin B1 mRNA coincides with diminished G2-phase arrest in irradiated HeLa cells treated with staurosporine or caffeine.

The irradiation of cells results in delayed progression through the G2 phase of the cell cycle. Treatment of irradiated HeLa cells with caffeine greatly reduces the G2-phase delay, while caffeine does not alter progression of cells through the cell cycle in unirradiated cells. In this report we demonstrate that treatment of HeLa cells with the kinase inhibitor staurosporine, but not with the inhibitor H7, also results in a reduction of the G2-phase arrest after irradiation. Cell cycle progression in unirradiated cells is unaffected by 4.4 nM (2 ng/ml) staurosporine, which releases the radiation-induced G2-phase arrest. In HeLa cells, the G2-phase delay after irradiation in S phase is accompanied by decreased expression of cyclin B1 mRNA. Coincident with the reduction in G2-phase delay, we observed an increase in cyclin B1 mRNA accumulation in irradiated, staurosporine-treated cells compared to cells treated with irradiation alone. Caffeine treatment of irradiated HeLa cells also resulted in an elevation in the levels of cyclin B1 message. These results support the hypothesis that diminished cyclin B1 mRNA levels influence G2-phase arrest to some degree. The findings that both staurosporine and caffeine treatments reverse the depression in cyclin B1 expression suggest that these two compounds may act on a common pathway of cell cycle control in response to radiation injury.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

The suppression of the synthesis of a nuclear protein in cells blocked in G2 phase: identification of NP-170 as topoisomerase II.

Previous studies of a nuclear protein of molecular weight 170 kDa (NP-170) have shown it to have two interesting properties. First, NP-170 synthesis began in mid- to late S phase and became maximal in G2 phase. Second, the synthesis of NP-170 was suppressed in cells blocked in G2 phase following irradiation with 6.8 Gy (J. M. Holland et al., Radiat. Res. 122, 197-208, 1990). The molecular weight of NP-170 is the same as that of Topoisomerase II (Topo II), an enzyme involved in the alteration of DNA supercoiling status with a double-strand passing function. This study was undertaken to determine whether NP-170 could be Topo II. The results from the present study show that both the proteins have identical cell cycle synthesis patterns. The synthesis of both these proteins is suppressed following irradiation. NP-170 was found to be recognized by a Topo II antibody in both Western blots and immunoprecipitation. This study characterizes NP-170 as Topo II.

Autoradiography↗
PubMed1993

Staurosporine- and radiation-induced G2-phase cell cycle blocks are equally released by caffeine.

We show here that the arrests of cells in G2 phase of the cell cycle induced by either staurosporine or ionizing radiation are closely related phenomena governed by a common kinase signaling pathway. The protein kinase inhibitor staurosporine induces a complete G2-phase arrest in exponentially growing TK6 human lymphoblastoid and V79 Chinese hamster fibroblast cells. Both cell types are equally sensitive to the kinase inhibitor and the arrest is dependent on its continued presence. Caffeine completely abrogates this arrest at concentrations comparable to those which abrogate radiation-induced G2-phase arrest. The kinetics of caffeine-induced release of both kinds of arrest are essentially identical. The activity of p34cdc2 kinase was also found to increase in a parallel fashion after caffeine-induced release of both kinds of arrest. As opposed to those transformed cell types which arrest only in G2 phase in response to staurosporine, immortalized C3H 10T1/2 fibroblasts and Muntjak skin fibroblasts display both G1- and G2-phase arrests. The results suggest that staurosporine and radiation interact with regulatory pathways in the cell cycle, and specifically with a caffeine-sensitive signal transduction pathway which recognizes DNA damage, regulates the G2/M-phase transition, and attenuates the biological consequences of radiation exposure.

Alkaloids↗
PubMed1991

[The in vivo arrest of Ehrlich ascitic carcinoma cells in the G2 phase of the cell cycle].

Evidence for arrested G2 cell subpopulation in the Ehrlich ascite carcinoma has been provided using flow cytometry stathmokinetic and bromdesoxyuridine--Hoechst 33258 techniques. After exposure in DME--F-12 media G2-arrested cells synchronically enter mitosis and then move trough G1 period. Durations have been measured for G1. G2 phases and G2-G1 transition.

Animals↗
PubMed1988

Serum-dependent regulation of proliferation of cultured rat fibroblasts in G1 and G2 phases.

We reported that: (i) 3Y1tsF121 cells, a temperature-sensitive (ts) mutant of rat 3Y1 fibroblasts, are reversibly arrested either in the G1 or in the G2 phase, at the nonpermissive temperature. (ii) Cells retain the ability to resume proliferation at the permissive temperature after prolonged arrest in the G1 phase (for 5 days), whereas they lose it after prolonged arrest in the G2 phase (over 24 h). (iii) The G1 arrest is overcome at the nonpermissive temperature by the addition of fresh serum (H. Zaitsu and G. Kimura (1984) J. Cell. Physiol. 119, 82; (1985) J. Cell. Physiol. 124, 177). In the present study, the G2 arrest was overcome by exposing the cells to fresh serum, at the nonpermissive temperature. The G2 arrest occurred only at a higher cell density than that of the G1 arrest. The efficiency of the overcome was higher in the case of the G2 arrest than in case of the G1 arrest. When cells synchronized at the G1/S border by aphidicolin at the permissive temperature were released from the block, they divided in the absence of serum, at the permissive temperature. Even if they had passed through the previous G2 phase in a very high concentration of fresh serum at the permissive temperature, mitotic cells did not enter the S phase in the absence of serum, even at the permissive temperature. When the cells arrested in the G1 phase (not in G0) due to the ts defect were incubated in the absence of serum at the permissive temperature, only 34% entered the S phase and only 15% divided. These results suggest that (i) the ts defect in 3Y1tsF121 limiting cellular proliferation in both the G1 and the G2 phases is probably due to a single mutational event, and is a serum-requiring event. (ii) Preparation of the serum-requiring event which is required for the G2 traverse is completed in the G1 phase, under ordinary conditions. (iii) However, cells are able to fulfill the serum-requiring event in the G2 phase as well as in the G1 phase when the preparation is below the required level. (iv) The commitment to DNA synthesis is not necessarily a commitment to cell division. (v) Cells are arrested in the G1 phase more safely and more effectively than in the G2 phase, by the serum-related mechanism.

Animals↗
PubMed1988

Simian virus 40 compensates a cellular mutational defect of a serum-dependent function controlling cell cycle progression in the G2 phase.

Rat 3Y1tsF121 fibroblasts are arrested in the G2 phase at the nonpermissive temperature due to a temperature-sensitive (ts) defect, and the G2 arrest is overcome at the nonpermissive temperature by the addition of a large dose of fresh serum. When the G2-arrested cells which had been exposed to the nonpermissive temperature for 12 hr were shifted down to the permissive temperature, most divided within 12 hr. When the cultures prepared in parallel were infected with simian virus 40 (SV40) at the nonpermissive temperature, the G2-arrested cells divided as early as 6 hr after the expression of T antigen. The G2-arrested cells, which had been exposed to the nonpermissive temperature for 36 hr, lost both the ability to restore the G2 and M traverse at the nonpermissive temperature after the addition of fresh serum and the reversibility of the arrest upon shift down to the permissive temperature. However, SV40 induced these cells to divide at the nonpermissive temperature, as in the case of the reversibly arrested cells. A small t-antigen-deletion mutant (dl-884) also induced both types of the G2-arrested cells to divide at the nonpermissive temperature. These results suggest that (1) SV40 compensates or activates, in the G2 phase, the function regulating G2 and M transition by serum; (2) SV40 induces restoration of the irreversible G2 arrest; and (3) small t antigen is not responsible for these activities of SV40.

Animals↗
PubMed1989

Comparison of gamma-radiation-induced accumulation of ataxia telangiectasia and control cells in G2 phase.

Recent reports from a number of laboratories have linked radiosensitivity in ataxia telangiectasia (A-T) to a large and prolonged block of some cells in G2 phase. Previous results from this laboratory, largely with one Epstein-Barr virus-transformed A-T lymphoblastoid cell line, presented evidence for a dramatic increase in the number of cells in G2 phase over controls during a 24-h period post irradiation. We describe here a study of the effect of gamma-radiation on G2 phase delay in several A-T cell lines. Based on previous results with several cell lines 24 h post irradiation was selected as the optimum time to discriminate between G2 phase delay in control and A-T cells. All A-T homozygotes showed a significantly greater number of cells in G2 phase, 24 h post irradiation, than observed in controls. A more prolonged delay in G2 phase after irradiation was seen in different A-T cell types that included lymphoblastoid cells, fibroblasts and SV40-transformed fibroblasts. At the radiation dose used it was not possible to distinguish A-T heterozygotes from controls.

Ataxia Telangiectasia↗
PubMed1985

An immunological approach to enrich a mitotic stimulator and to reveal G2-phase-specific proteins in Physarum polycephalum.

Purified antibodies from an antiserum against S-phase proteins of the myxomycete Physarum polycephalum were attached to protein-A-Sepharose CL-4B. A late G2-phase extract that contained a mitosis-stimulating protein was applied to this immunoadsorbent, and the mitosis-stimulating protein was enriched by a factor of ten. This protein, which is present in the cell in low amounts, is synthesized in late G2 phase and obviously degraded in a later stage of the cycle. Immunoadsorption of a G2-phase extract with anti-S-antibodies decreased the 700 main proteins to 20 as demonstrated by two-dimensional gel electrophoresis. No difference in protein pattern could be observed on two-dimensional gels between S-phase and G2-phase extracts before and after immunoadsorption with anti-S-antibodies. This indicates that there are no G2-phase-specific proteins among the 700 most abundant proteins of Physarum polycephalum.

Electrophoresis, Polyacrylamide Gel↗
PubMed1993

Induction of chromatid breaks and tetraploidy in Chinese hamster ovary cells by treatment with sodium arsenite during the G2 phase.

Treatment of Chinese hamster ovary (CHO) cells with sodium arsenite during the G2 phase induced poorly condensed chromosomes and chromatid breaks. The induction of chromatid breaks was confirmed by the appearance of micronucleated cells after arsenite-treated G2 cells were allowed to re-enter interphase. When the duration of the G2 phase was artificially divided into 4 periods, more chromatid breaks were induced by treatment with arsenite during the very early G2 phase (or G2/S boundary). In addition to the induction of chromatid breaks, arsenite treatment also remarkably retarded the re-entry of mitotic cells into interphase. By replating and incubating arsenite-treated G2 cells in drug-free medium, we subsequently observed the appearance of a population of cells whose DNA content was between 4C and 8C, and metaphase cells with near-tetraploid chromosome numbers in the next mitotic division.

Animals↗
PubMed1992

Repair of transcriptionally active and inactive genes during S and G2 phases of the cell cycle.

To study the effect of ultraviolet irradiation on S and G2 phases of the cell cycle, BB88 mouse cells synchronized by a double thymidine block were exposed to ultraviolet light, and rates of DNA synthesis and mitotic indexes were determined at regular intervals. It was found that with increasing ultraviolet dose, semiconservative DNA synthesis decreased and the sharp mitotic wave observed in the unirradiated cells gradually degenerated. To study repair, semiconservative DNA replication was inhibited with hydroxyurea at different time intervals after releasing cells from the block and the DNA synthesized as a result of repair of the ultraviolet damage was labeled with 5'-bromodeoxyuridine (BrdU). The newly repaired DNA was separated from bulk DNA by immunoprecipitation with monoclonal anti-BrdU antibody, labeled with 32P and hybridized to nine different gene and oncogene probes dot-blotted in excess on nylon membranes to determine their abundance in the repaired DNA. The results showed that: (a) the most actively repaired segment was a 211-bp sequence adjacent to the promotor region of the beta-actin gene; (b) all transcriptionally active genes were repaired at similar and constant rates throughout S and G2 phases; (c) the nontranscribed genes were repaired at much lower rates in early S phase, but later in S phase and especially in G2 phase, their repair rates increased and approached those of the transcribed genes.

Animals↗