Cyclic 3′-5′-adenosine Monophosphate: Its Possible Role in Mammalian Cell Mitosis and Radiation-induced Mitotic G<sub>2</sub>-delay

Scaife, J. F.

doi:10.1080/09553007114550251

Cited by 29 publications

(6 citation statements)

References 13 publications

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“…Since microfilament reorganisation seems to be a consequence of MPF kinase activity,it is possiblethat feedback mechanisms exist such that initial disruption of the cytoskeleton by CB or otherwise, prevents the block in the premitotic increase in cyclin level. This would be similar to a mechanism proposed for the action of caffeine, which is known to be able to reduce the length of the G, block (Scaife, 1971). Schlegel et al (1990) have suggested that it may act as a specific protein kinase inhibitor.…”

Section: Introductionsupporting

confidence: 73%

Cycle delay in irradiated cytochalasin‐induced polykaryons. Does cytoskeleton status affect cell cycle checkpoints?

Davies

Court

1995

Cell Biology International

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Following exposure of CHO-K1 cells to 137Cs irradiation at doses up to 20Gy, a delay in G2 was observed to occur in cells permitted to divide normally, while cells induced to become giants by means of cytochalasin B demonstrated a minimal delay in the transition 2C-8C suggesting that the inhibition of cytokinesis results in modification of one or more cell cycle checkpoints. We postulate that this may occur as a consequence of damage tolerance, or by a feedback loop resulting from the reorganisation of the cytoskeleton that precludes cytokinesis.

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Section: Introductionsupporting

confidence: 73%

Cycle delay in irradiated cytochalasin‐induced polykaryons. Does cytoskeleton status affect cell cycle checkpoints?

Davies

Court

1995

Cell Biology International

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“…Exponentially growing cells do not undergo PCC when exposed to caffeine. Caffeine can, however, advance mitosis in G2-phase cells in exponential growth (Scaife, 1971;Rowley, 1985). Cells that are arrested in S phase accumulate within an h the RNA that is needed for mitosis while cycling cells do so only after they have reached G 2 phase (Tobey et al, 1966).…”

Section: Discussionmentioning

confidence: 99%

Exposure to caffeine and suppression of DNA replication combine to stabilize the proteins and RNA required for premature mitotic events

Schlegel

Croy

Pardee

1987

Journal Cellular Physiology

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Caffeine had been shown to induce mitotic events in Syrian hamster fibroblast (BHK) cells that were arrested during DNA replication (Schlegel and Pardee, Science 232:1264-1266, 1986). Inhibition of protein synthesis blocked these caffeine-induced events, while inhibition of RNA synthesis showed little effect. We now report that the protein(s) that are required for inducing mitosis in these cells were synthesized shortly after caffeine addition, the activity was very labile in the absence of caffeine, and the activity was lost through an ATP-dependent mechanism. Caffeine dramatically increased the stability of these putative proteins while having no effect on overall protein degradation. Experiments with an inhibitor of RNA synthesis indicated that mitosis-related RNA had accumulated during the suppression of DNA replication, and this RNA was unstable when replication was allowed to resume. These results suggest that the stability of RNA needed for mitosis is regulated by the DNA replicative state of the cell and that caffeine selectively stabilizes the protein product(s) of this RNA. Conditions can therefore be selected that permit mitotic factors to accumulate in cells at inappropriate times in the cell cycle. Two-dimensional gel electrophoresis has demonstrated several protein changes resulting from caffeine treatment; their relevance to mitosis-inducing activity remains to be determined.

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“…Cells that have been exposed to ionizing radiation respond to the treatment in many ways, for example, by an inhibition of DNA synthesis and a delay of cell proliferation (GROSCH and HOPWOOD 1979). Caffeine reduce4 the inhibitory effect of X-rays on both DNA synthesis PAINTER 1980: BASES et al 1980) and cell cycle progression in G2 (SCAIFE 1971;BOYNTON et al 1974;WALTERS et al 1974;SNYDER et al 1977;TOLMACH et al 1977: TOMASOVIC andBASES et al 1980;KIHLMAN et al 1982a;this paper). On the basis of these findings, Painter suggested that caffeine enhances cell killing and chromosome damage in human cells because it prevents cells from going through delays that would allow them to repair DNA damage before it can be expressed (PAINTER 1980; PAINTER and YOUNG 1980).…”

Section: Discussionmentioning

confidence: 70%

G2 repair and the formation of chromosomal aberrations

Andersson

2008

Hereditas

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The effects of hydroxy urea (HU) and caffeine, alone and in combination, on X‐ray‐induced chromosome damage and mitotic delay were studied in root tips of Viciafaba. In addition, some experiments were carried out in which X‐ray‐irradiated roots were post‐treated with 5‐fluorodeoxyuridine (FdUrd). Post‐treatments with all three agents were given the last few hours before fixation. Both HU and FdUrd strongly increased the frequency of X‐ray‐induced gaps, breaks and isochromatid breaks of the NU‐type, but only when the damage was induced in replicating (S) or replicated (G2) chromosomes. The magnitude of the potentiation was independent of the initial degree of chromosome damage. Potentiation by HU was obtained in cells that were exposed to the inhibitor 2 to 5 hours before they reached metaphase. The potentiating effect of FdUrd on X‐ray‐induced chromosome damage was completely reversed by thymidine. Caffeine was able to potentiate induced chromosome damage only if the cells were X‐ray‐irradiated in the G2 phase and if the post‐treatment with caffeine was given directly after irradiation. The experimental results are compared with results of analogous experiments performed in mammalian cells. Possible molecular mechanisms involved in the action of HU, FdUrd and caffeine on the formation of X‐ray‐induced chromatid aberrations are discussed.

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Cyclic 3′-5′-adenosine Monophosphate: Its Possible Role in Mammalian Cell Mitosis and Radiation-induced Mitotic G₂-delay

Cited by 29 publications

References 13 publications

Cycle delay in irradiated cytochalasin‐induced polykaryons. Does cytoskeleton status affect cell cycle checkpoints?

Cycle delay in irradiated cytochalasin‐induced polykaryons. Does cytoskeleton status affect cell cycle checkpoints?

Exposure to caffeine and suppression of DNA replication combine to stabilize the proteins and RNA required for premature mitotic events

G2 repair and the formation of chromosomal aberrations

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Cyclic 3′-5′-adenosine Monophosphate: Its Possible Role in Mammalian Cell Mitosis and Radiation-induced Mitotic G2-delay

Cited by 29 publications

References 13 publications

Cycle delay in irradiated cytochalasin‐induced polykaryons. Does cytoskeleton status affect cell cycle checkpoints?

Cycle delay in irradiated cytochalasin‐induced polykaryons. Does cytoskeleton status affect cell cycle checkpoints?

Exposure to caffeine and suppression of DNA replication combine to stabilize the proteins and RNA required for premature mitotic events

G2 repair and the formation of chromosomal aberrations

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Product

Resources

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Cyclic 3′-5′-adenosine Monophosphate: Its Possible Role in Mammalian Cell Mitosis and Radiation-induced Mitotic G₂-delay