Mutations can arise as a consequence of exposure of DNA to damaging agents. DNA damages caused by extrinsic or intrinsic agents are usually repaired by one of the several DNA repair systems of the cell preserving the genetic information. However, a high load of DNA damages can lead to the accumulation of unrepaired ones that block the replication machinery leading to cell death. To ensure survival, cells have evolved mechanisms that can sustain DNA replication on damaged DNA. These so-called DNA damage tolerance or DNA damage bypass processes allow replication to continue on damaged DNA without removing the damaged bases, either in an error-free or an error-prone way. Increased error-prone bypass of DNA lesions causes increased mutagenesis and a rise in the incidence of cancers in humans, whereas error-free replication of damaged DNA contributes to genetic stability.
We investigate the regulation of DNA damage bypass processes in yeast cells, with main focus on the role of ubiquitylation in the regulation of damage bypass.
The yeast Saccharomyces cerevisiae serves as a model organism in our research taking advantage of the high conservation of DNA damage bypass processes from yeasts to humans.
ajánlott nyelvtudás (magyar oldal): angol felvehető hallgatók száma: 1
Jelentkezési határidő: 2014-12-31
2024. IV. 17. ODT ülés Az ODT következő ülésére 2024. június 14-én, pénteken 10.00 órakor kerül sor a Semmelweis Egyetem Szenátusi termében (Bp. Üllői út 26. I. emelet).
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