[en] Using the nearly perfect synchrony of the mitotic stages in Physarum plasmodia, and making use of ³²P as a tracer, studies were made to define the time course of histone phosphorylation during the late G2 and prophase and the alterations in that time course accompanying radiation-induced mitotic delay. Histone H1 was phosphorylated throughout the last 2-3 hours of the mitotic cycle coincident with the early stages of chromosome condensation. H1 phosphorylation appeared to be reduced in irradiated plasmodia. It is postulated that a longer time period, i.e. the mitotic delay, may be required to obtain the same eventual level of H1-phosphate. In normal cultures, nucleosome core histones were phosphorylated late in G2 and prophase, the peak corresponding closely with the γ-transition point. In irradiated plasmodia, phosphorylation of the core histones had an extended time course similar to H1. (U.K.)

[en] The effect of different doses of gamma radiation 5, 10, 30, 50, and 70 kr on mitotic index root tip cells of safflower carthamus tinctorius was studled the percentages of mitotic indicies were scored . the highest number was 268, 99, for the cotrcl and the fwest was 129, 45%, for 10 kr at interval 2 . the hichest number registerad after 22 hours for 5 kr (244%)and after 24 hours at 10 kr (2,3%), the sansitivity to radietion in root tip cells wich was traced as a delay in mitosis seems to be dose dependent caused by loss of some stages, the percentages of anaphase, telophase were low and stickiness phenomenon of the chromosomes was also noticed

[en] Exposure to ionizing radiation temporarily blocks eukaryotic cell cycle progression at the G₂/M boundary (G₂ delay). The delay probably provides time for repair of DNA damage before chromosome segregation and is thus an active response, indicative of a checkpoint control function. Transition from G₂ into mitosis is normally controlled by the activity of a cyclin-dependent kinase, cdc2 in the fission yeast (Schizosaccharomyces pombe). Genetic and cell kinetic evidence suggest that irradiation may impose mitotic delay by inactivation of the cdc2 product, p34^cdc2. The activity of p34^cdc2 in G₂ is regulated by phosphorylation and association with a B-type cyclin, the product of the cdc13 gene, p56^cdc13. Previous work does not support a major role for changes in phosphorylation of p34^cdc2 in the induction of mitotic delay. Alternatively the kinase may be regulated by changes in the activity/availability of p56^cdc13. We have therefore tested the effect of high level, episomal expression of the cdc13 gene on the induction of mitotic delay. No influence of this procedure on the duration of delay was detected, either in a wild-type cell cycle background, or the mutants wee1-50 and cdc2-3w, which show abnormal phosphorylation of p34^cdc2. (Author)

[en] Exposure of mammalian cells to ionizing radiation causes delay in normal progress through the cell cycle at a number of different checkpoints. Abnormalities in these checkpoints have been described for ataxia telangiectasia cells after irradiation. In this report we show that these abnormalities occur at different phases in the cell cycle in several ataxia telangiectasia lymphoblastoid cells. Ataxia telangiectasia cells, synchronized in late G₁ phase with either mimosine or aphidicolin and exposed to radiation, showed a reduced delay in entering S phase compared to irradiated control cells. Failure to exhibit G₁-phase delay in ataxia telangiectasia cells is accompanied by a reduced ability of radiation to activate the product of the tumor suppressor gene p53, a protein involved in G₁/S-phase delay. When the progress of irradiated G₁-phase cells was followed into the subsequent G₂ and G₁ phases ataxia telangiectasia cells showed a more pronounced accumulation in G₂ phase than control cells. When cells were irradiated in S phase and extent of delay was more evident in G₂ phase and ataxia telangiectasia cells were delayed to a greater extent. These results suggest that the lack of initial delay in both G₁ and S phases to the radiosensitivity observed in this syndrome. 26 refs., 3 figs., 2 tabs

[en] The authors previously showed that radiation-sensitive fibroblasts from ataxia-telangiectasia (A-T) patients sustain less G₂ delay after X-irradiation than normal fibroblasts. Caffeine is known to reduce the amount of X-ray-induced delay in various mammalian cell types. It is proposed that A-T cells have an altered chromatin structure, similar to that of caffeine-treated normal cells and that this results in a failure of A-T cells to delay their progression through the cell cycle to allow time for DNA repair. The authors now show that caffeine treatment after X-irradiation reduces G₂ delay in both A-T and normal cells. The authors confirm the results previously obtained on lymphocytes that caffeine potentiates the chromosome-damaging effects of X-rays in both A-T and normal fibroblasts. These and other data suggest that the radiation responses of A-T cells and of caffeine-treated normal cells are caused by different mechanisms. (Auth.)

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No abstract available

[en] Protein synthesis is normally required for G₂-cell progression and for recovery from radiation-induced G₂-arrest. In the presence of 5 mM caffeine this requirement is alleviated, indicating that the mechanism responsible for G₂ cell progression actually remains intact in irradiated or protein synthesis inhibitor-treated cells. It is suggested that both radiation and cylcoheximide-induced G₂-arrest are not, therefore, passive consequences of cellular defects, but are rather, active cellular responses to the state of cellular integrity, implying the existence of G₂ cell progression controls. (author)

[en] Light-dark (L-D) synchronized Chlamydomonas reinhardi were x-irradiated (9108 R) early in the dark period as cells were preparing for or undergoing division. Division delay data were recorded both in terms of the entire population of cells and in terms of cells progressing to form either 4- or 8-celled clones. The lack of division delay exhibited by these cells is striking. The greatest delay among 4's was a 2.2-hr delay in their final division after irradiation at the 14th hour. The greatest delays in 8's were 2.3 and 2.4 hr in their final divisions after irradiation at the 13th and 14th hours. Such delays are small compared to delays induced in other cells by exposures leading to comparable survival levels

[en] The symmetry of radiation-induced chromatid exchanges was studied in relation to the cell cycle in Chinese hamster cells in vivo and in vitro. Both in vivo and in vitro, the ratio between symmetrical and asymmetrical chromatid exchanges was about 1 to 1 during G₂ and S phase of the cell cycle. (Auth.)