Response of the Green Alga Chlamydomonas reinhardtii to the DNA Damaging Agent Zeocin
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
31319624
PubMed Central
PMC6678277
DOI
10.3390/cells8070735
PII: cells8070735
Knihovny.cz E-zdroje
- Klíčová slova
- Chlamydomonas reinhardtii, DNA damage, caffeine, cell cycle, cyclin-dependent kinase, double-stranded break, zeocin,
- 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
- Názvy látek
- bleomycin MeSH
- cyklin-dependentní kinasy MeSH
- cytostatické látky MeSH
- DNA rostlinná MeSH
- kofein MeSH
- mutageny MeSH
- Zeocin MeSH Prohlížeč
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.
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