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Response of the Green Alga Chlamydomonas reinhardtii to the DNA Damaging Agent Zeocin
M. Čížková, M. Slavková, M. Vítová, V. Zachleder, K. Bišová,
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 2012
Free Medical Journals
od 2012
PubMed Central
od 2012
Europe PubMed Central
od 2012
ProQuest Central
od 2012-03-01
Open Access Digital Library
od 2012-01-01
Open Access Digital Library
od 2012-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2012
PubMed
31319624
DOI
10.3390/cells8070735
Knihovny.cz E-zdroje
- 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
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.
Citace poskytuje Crossref.org
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