Detailed Information on Publication Record
2009
DNA repair mechanisms in yeast
KREJČÍ, LumírBasic information
Original name
DNA repair mechanisms in yeast
Name in Czech
DNA opravné mechanismy u kvasinek
Authors
Edition
37th Annual Conference o. Bratislava, Slovakia, 37th Annual Conference on Yeast, 113 pp. 2009
Publisher
Visegrad Strategic Program
Other information
Language
English
Type of outcome
Stať ve sborníku
Field of Study
10600 1.6 Biological sciences
Country of publisher
Slovakia
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Organization unit
Faculty of Medicine
ISSN
Keywords in English
DNA repair; DNA damage; replication; genomic instability
Tags
International impact
Změněno: 23/4/2010 15:30, doc. Mgr. Lumír Krejčí, Ph.D.
V originále
DNA replication is typically highly processive mechanism with astonishing precision, despite the fact that it frequently encounters barriers caused by endogenous and exogenous genotoxic agents. It is not surprising that DNA replication does not act alone, but operates in coordination with homologous recombination (HR), and other DNA repair processes to overcome such replication obstacles to ensure cellular viability, and achieve genomic stability. Numerous mechanisms by which replication forks can be restarted following arrest have been described. Some of the pathways enable the cells to deal with such impediments while keeping the fork in place, including repriming, template switch, and translesion synthesis, others may provoke partial or complete fork collapse followed by fork reversal. This could not only provide time and space for repair but also liberate the new strand to undergo template switch. Alternatively, the fork can be cleaved, creating the DSB break that is repaired by recombination machinery with ability to restart the replication fork. Inability to remove toxic DNA structures often leads to their accumulation, higher mutation frequency and eventually to cancer or other diseases associated with genomic instability.
In Czech
DNA replication is typically highly processive mechanism with astonishing precision, despite the fact that it frequently encounters barriers caused by endogenous and exogenous genotoxic agents. It is not surprising that DNA replication does not act alone, but operates in coordination with homologous recombination (HR), and other DNA repair processes to overcome such replication obstacles to ensure cellular viability, and achieve genomic stability. Numerous mechanisms by which replication forks can be restarted following arrest have been described. Some of the pathways enable the cells to deal with such impediments while keeping the fork in place, including repriming, template switch, and translesion synthesis, others may provoke partial or complete fork collapse followed by fork reversal. This could not only provide time and space for repair but also liberate the new strand to undergo template switch. Alternatively, the fork can be cleaved, creating the DSB break that is repaired by recombination machinery with ability to restart the replication fork. Inability to remove toxic DNA structures often leads to their accumulation, higher mutation frequency and eventually to cancer or other diseases associated with genomic instability.
Links
| GA301/09/1917, research and development project |
| ||
| GD203/09/H046, research and development project |
| ||
| LC06030, research and development project |
| ||
| MSM0021622413, plan (intention) |
|