Inhibition of DNA synthesis and DNA fragmentation in stimulated splenocytes by the concerted action of topoisomerase I and II poisons

1993 ◽  
Vol 45 (2) ◽  
pp. 331-337 ◽  
Author(s):  
Georges Taudou ◽  
Christiane Portemer ◽  
Christine Jaxel ◽  
Michel Duguet
Keyword(s):  
Dna Synthesis ◽  
Dna Fragmentation ◽  
Topoisomerase I ◽  
Concerted Action ◽  
Inhibition Of Dna Synthesis

Effect of inhibitors of DNA replication on early zebrafish embryos: evidence for coordinate activation of multiple intrinsic cell-cycle checkpoints at the mid-blastula transition

Zygote ◽  
1997 ◽  
Vol 5 (2) ◽  
pp. 153-175 ◽  
Author(s):  
Richard Ikegami ◽  
Alma K. Rivera-Bennetts ◽  
Deborah L. Brooker ◽  
Thomas D. Yager
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Dna Synthesis ◽  
Adaptive Response ◽  
Topoisomerase I ◽  
Topoisomerase Ii ◽  
Cell Cycle Checkpoints ◽  
Zebrafish Embryos ◽  
Replication Process ◽  
Inhibition Of Dna Synthesis

SummaryWe address the developmental activation, in the zebrafish embryo, of intrinsic cell-cycle checkpoints which monitor the DNA replication process and progression through the cell cycle. Eukaryotic DNA replication is probably carried out by a multiprotein complex containing numerous enzymes and accessory factors that act in concert to effect processive DNA synthesis (Applegren, N. et al. (1995) J. Cell. Biochem. 59, 91–107). We have exposed early zebrafish embryos to three chemical agents which are predicted to specifically inhibit the DNA polymerase α, topoisomerase I and topoisomerase II components of the DNA replication complex. We present four findings: (1) Before mid-blastula transition (MBT) an inhibition of DNA synthesis does not block cells from attempting to proceed through mitosis, implying the lack of functional checkpoints. (2) After MBT, the embryo displays two distinct modes of intrinsic checkpoint operation. One mode is a rapid and complete stop of cell division, and the other is an ‘adaptive’ response in which the cell cycle continues to operate, perhaps in a ‘repair’ mode, to generate daughter nuclei with few visible defects. (3) The embryo does not display a maximal capability for the ‘adaptive’ response until several hours after MBT, which is consistent with a slow rranscriptional control mechanism for checkpoint activation. (4) The slow activation of checkpoints at MBT provides a window of time during which inhibitors of DNA synthesis will induce cytogenetic lesions without killing the embryo. This could be useful in the design of a deletion-mutagenesis strategy.

scholarly journals Inhibition of DNA synthesis in living cells by microinjection of Gi2 antibodies.

1992 ◽  
Vol 267 (2) ◽  
pp. 691-694 ◽  
Author(s):  
V J LaMorte ◽  
P K Goldsmith ◽  
A M Spiegel ◽  
J L Meinkoth ◽  
J R Feramisco
Keyword(s):  
Dna Synthesis ◽  
Living Cells ◽  
Inhibition Of Dna Synthesis

The effect of ara-C-induced inhibition of DNA synthesis on its cellular pharmacology

1990 ◽  
Vol 25 (6) ◽  
pp. 418-424 ◽  
Author(s):  
Li-Ming Wang ◽  
J. Courtland White ◽  
Robert L. Capizzi
Keyword(s):  
Dna Synthesis ◽  
Cellular Pharmacology ◽  
Inhibition Of Dna Synthesis

Inhibition of DNA synthesis and cell division by a cell surface sialoglycopeptide

1989 ◽  
Vol 139 (2) ◽  
pp. 269-274 ◽  
Author(s):  
Heideh Fattaey ◽  
Terry C. Johnson ◽  
Hsin-Hwei Chou
Keyword(s):  
Cell Division ◽  
Cell Surface ◽  
Dna Synthesis ◽  
A Cell ◽  
Inhibition Of Dna Synthesis
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