Increased genome instability is not accompanied by sensitivity to DNA damaging agents in aged yeast cellsNovarina, D., Mavrova, S. N., Janssens, G. E., Rempel, I. L., Veenhoff, L. M. & Chang, M., Jun-2017, In : Dna repair. 54, p. 1-7 7 p.
Research output: Contribution to journal › Article › Academic › peer-review
The budding yeast Saccharomyces cerevisiae divides asymmetrically, producing a new daughter cell from the original mother cell. While daughter cells are born with a full lifespan, a mother cell ages with each cell division and can only generate on average 25 daughter cells before dying. Aged yeast cells exhibit genomic instability, which is also a hallmark of human aging. However, it is unclear how this genomic instability contributes to aging. To shed light on this issue, we investigated endogenous DNA damage in S. cerevisiae during replicative aging and tested for age-dependent sensitivity to exogenous DNA damaging agents. Using live-cell imaging in a microfluidic device, we show that aging yeast cells display an increase in spontaneous Rad52 foci, a marker of endogenous DNA damage. Strikingly, this elevated DNA damage is not accompanied by increased sensitivity of aged yeast cells to genotoxic agents nor by global changes in the proteome or transcriptome that would indicate a specific "DNA damage signature". These results indicate that DNA repair proficiency is not compromised in aged yeast cells, suggesting that yeast replicative aging and age-associated genomic instability is likely not a consequence of an inability to repair DNA damage.
|Number of pages||7|
|Early online date||23-Mar-2017|
|Publication status||Published - Jun-2017|
- Rad52, Genome stability, Yeast aging, DNA damage sensitivity, SACCHAROMYCES-CEREVISIAE, PROTEIN LOCALIZATION, AGING YEAST, WIDE SCREEN, REPAIR, GENES, RAD52, MECHANISMS, HALLMARKS, PATHWAYS