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Giardia intestinalis: aphidicolin influence on the trophozoite cell cycle
K Hofstetrova, M Uzlikova, P Tumova, K Troell, SG Svard, E Nohynkova
Language English Country United States
Document type Research Support, Non-U.S. Gov't
- MeSH
- Aphidicolin pharmacology MeSH
- Bromodeoxyuridine metabolism MeSH
- Cell Cycle drug effects MeSH
- Time Factors MeSH
- Cyclin B analysis MeSH
- DNA-Directed DNA Polymerase MeSH
- Fluorescent Antibody Technique MeSH
- Phosphorylation drug effects MeSH
- Giardia lamblia cytology genetics drug effects MeSH
- Histones metabolism MeSH
- Enzyme Inhibitors pharmacology MeSH
- Nucleic Acid Synthesis Inhibitors MeSH
- Mitotic Index MeSH
- DNA Damage drug effects MeSH
- DNA, Protozoan biosynthesis drug effects MeSH
- Flow Cytometry MeSH
- DNA Replication drug effects MeSH
- Trophozoites cytology drug effects MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
This study is a thorough examination of the effects of the DNA polymerase inhibitor aphidicolin on the nuclear cycle and cell cycle progression characteristics, as well as their reversibility, in Giardia intestinalis. Giardia trophozoites are arrested in the G1/S-junction after aphidicolin treatment according to their DNA content. However, cell growth continues and trophozoites arrested with aphidicolin resemble cells in the G2 phase and trophozoites in ageing cultures. Extensive treatment with aphidicolin causes side effects and we detected positive signals for phosphorylated histone H2A, which, in mammalian cells, is involved in a signalling pathway triggered as a reaction to double stranded DNA breaks. These results suggest that aphidicolin causes dissociation of the nuclear and cytoplasmic cycles, a phenomenon that has also been described for other inhibitors in mammalian cell lines. Thus, if aphidicolin is used for synchronization of Giardia trophozoites, this fact must be accounted for, and treatment with aphidicolin must be minimal. Copyright 2009 Elsevier Inc. All rights reserved.
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- $a This study is a thorough examination of the effects of the DNA polymerase inhibitor aphidicolin on the nuclear cycle and cell cycle progression characteristics, as well as their reversibility, in Giardia intestinalis. Giardia trophozoites are arrested in the G1/S-junction after aphidicolin treatment according to their DNA content. However, cell growth continues and trophozoites arrested with aphidicolin resemble cells in the G2 phase and trophozoites in ageing cultures. Extensive treatment with aphidicolin causes side effects and we detected positive signals for phosphorylated histone H2A, which, in mammalian cells, is involved in a signalling pathway triggered as a reaction to double stranded DNA breaks. These results suggest that aphidicolin causes dissociation of the nuclear and cytoplasmic cycles, a phenomenon that has also been described for other inhibitors in mammalian cell lines. Thus, if aphidicolin is used for synchronization of Giardia trophozoites, this fact must be accounted for, and treatment with aphidicolin must be minimal. Copyright 2009 Elsevier Inc. All rights reserved.
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