DNA damage is a ubiquitous threat endangering DNA integrity in all living organisms. Responses to DNA damage include, among others, induction of DNA repair and blocking of cell cycle progression in order to prevent transmission of damaged DNA to daughter cells. Here, we tested the effect of the antibiotic zeocin, inducing double stranded DNA breaks, on the cell cycle of synchronized cultures of the green alga Chlamydomonas reinhardtii. After zeocin application, DNA replication partially occurred but nuclear and cellular divisions were completely blocked. Application of zeocin combined with caffeine, known to alleviate DNA checkpoints, decreased cell viability significantly. This was probably caused by a partial overcoming of the cell cycle progression block in such cells, leading to aberrant cell divisions. The cell cycle block was accompanied by high steady state levels of mitotic cyclin-dependent kinase activity. The data indicate that DNA damage response in C. reinhardtii is connected to the cell cycle block, accompanied by increased and stabilized mitotic cyclin-dependent kinase activity.
- MeSH
- bleomycin toxicita MeSH
- Chlamydomonas reinhardtii účinky léků genetika MeSH
- cyklin-dependentní kinasy metabolismus MeSH
- cytostatické látky toxicita MeSH
- DNA rostlinná účinky léků MeSH
- dvouřetězcové zlomy DNA MeSH
- kofein farmakologie MeSH
- kontrolní body buněčného cyklu MeSH
- mutageny toxicita MeSH
- replikace DNA MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Telomere homeostasis is regulated at multiple levels, including the local chromatin structure of telomeres and subtelomeres. Recent reports demonstrated that a decrease in repressive chromatin marks, such as levels of cytosine methylation in subtelomeric regions, results in telomere elongation in mouse cells. Here we show that a considerable fraction of cytosines is methylated not only in subtelomeric, but also in telomeric DNA of tobacco BY-2 cells. Drug-induced hypomethylation (demonstrated at subtelomeric, telomeric, and global DNA levels) results in activation of telomerase. However, in contrast to mouse cells, the decrease in 5-methylcytosine levels and upregulation of telomerase do not result in any changes of telomere lengths. These results demonstrate the involvement of epigenetic mechanisms in the multilevel process of regulation of telomerase activity in plant cells and, at the same time, they indicate that changes in telomerase activity can be overridden by other factors governing telomere length stability.
- MeSH
- adenin analogy a deriváty farmakologie MeSH
- aktivace enzymů účinky léků MeSH
- cytidin analogy a deriváty farmakologie MeSH
- DNA rostlinná chemie účinky léků MeSH
- epigeneze genetická MeSH
- genetická transkripce účinky léků MeSH
- kultivované buňky MeSH
- metylace DNA účinky léků MeSH
- nukleozomy účinky léků fyziologie MeSH
- rostlinné proteiny genetika metabolismus MeSH
- tabák cytologie účinky léků genetika metabolismus MeSH
- telomerasa metabolismus MeSH
- telomery chemie účinky léků metabolismus MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
