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Cell Rep. 2013 Dec 26;5(6):1589-99. doi: 10.1016/j.celrep.2013.11.013. Epub 2013 Dec 12.

Aging yeast cells undergo a sharp entry into senescence unrelated to the loss of mitochondrial membrane potential.

Author information

1
Institut de Génétique et de Biologie Moléculaire et Cellulaire, 1 Rue Laurent Fries, 67400 Illkirch Cedex, France.
2
LJC, ENS Lyon, 46 Allée d'Italie, 69364 Lyon Cedex 07, France.
3
LBMC, ENS Lyon, 46 Allée d'Italie, 69364 Lyon Cedex 07, France.
4
Institut de Génétique et de Biologie Moléculaire et Cellulaire, 1 Rue Laurent Fries, 67400 Illkirch Cedex, France. Electronic address: charvin@igbmc.fr.

Abstract

In budding yeast, a mother cell can produce a finite number of daughter cells before it stops dividing and dies. Such entry into senescence is thought to result from a progressive decline in physiological function, including a loss of mitochondrial membrane potential (ΔΨ). Here, we developed a microfluidic device to monitor the dynamics of cell division and ΔΨ in real time at single-cell resolution. We show that cells do not enter senescence gradually but rather undergo an abrupt transition to a slowly dividing state. Moreover, we demonstrate that the decline in ΔΨ, which is observed only in a fraction of cells, is not responsible for entry into senescence. Rather, the loss of ΔΨ is an age-independent and heritable process that leads to clonal senescence and is therefore incompatible with daughter cell rejuvenation. These results emphasize the importance of quantitative single-cell measurements to decipher the causes of cellular aging.

PMID:
24332850
DOI:
10.1016/j.celrep.2013.11.013
[Indexed for MEDLINE]
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