IMR Press / FBL / Volume 17 / Issue 3 / DOI: 10.2741/3974

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review
Mitochondrial and nuclear genomic integrity after oxidative damage in Saccharomyces cerevisiae
Show Less
1 University of Alaska Anchorage, Alaska 99508, USA
Academic Editor:Min-Hao Kuo
Front. Biosci. (Landmark Ed) 2012, 17(3), 1079–1093;
Published: 1 January 2012
(This article belongs to the Special Issue Chromatin and cell cycle)

All cells have the ability to adjust their metabolism to their changing environment to be able to survive. This adaptation is coordinated by various systems in the cell and mitochondria seem to play a unique and important role. Most endogenous oxidative damage to cells is actually generated as a byproduct of the mitochondrial function, which in turn damages mitochondrial structures more extensively due to their proximity to the source. Excessive damage to mitochondria leads to loss of parts or all of mtDNA, but unlike other organisms, S. cerevisiae cells are able to survive without mtDNA or respiration when grown on fermentative carbon sources. This allows studies of the role of mitochondria in the maintenance of cellular integrity, since lack of mitochondrial DNA frequently leads to genomic instability. Mitochondria are known for their role in respiration, ATP production and apoptosis, but it is now becoming clear that their function is intimately connected to diverse processes such as calcium and iron homeostasis and amino acid metabolism, and thus their dysfunction is not well tolerated. In this review, we discuss the mechanisms by which mitochondrial dysfunction can lead to genomic instability and the effect of the carbon source on this process.

Oxidative stress
DNA repair
Saccharomyces cerevisiae
Iron-Sulfur Cluster Proteins
DNA Lesions
Glucose Repression
Damage Sensing
Back to top