Increased genome instability is not accompanied by sensitivity to DNA damaging agents in aged yeast cells.

Autor: Novarina D; European Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, 9713 AV Groningen, The Netherlands., Mavrova SN; European Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, 9713 AV Groningen, The Netherlands., Janssens GE; European Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, 9713 AV Groningen, The Netherlands., Rempel IL; European Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, 9713 AV Groningen, The Netherlands., Veenhoff LM; European Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, 9713 AV Groningen, The Netherlands., Chang M; European Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, 9713 AV Groningen, The Netherlands. Electronic address: m.chang@umcg.nl.
Jazyk: angličtina
Zdroj: DNA repair [DNA Repair (Amst)] 2017 Jun; Vol. 54, pp. 1-7. Date of Electronic Publication: 2017 Mar 23.
DOI: 10.1016/j.dnarep.2017.03.005
Abstrakt: 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.
(Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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