Research Papers:

Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast

Anna Leonov, Rachel Feldman, Amanda Piano, Anthony Arlia-Ciommo, Jennifer Anne Baratang Junio, Emmanuel Orfanos, Tala Tafakori, Vicky Lutchman, Karamat Mohammad, Sarah Elsaser, Sandra Orfali, Harshvardhan Rajen and Vladimir I. Titorenko _

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Oncotarget. 2022; 13:918-943. https://doi.org/10.18632/oncotarget.28256

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Anna Leonov1, Rachel Feldman1, Amanda Piano1, Anthony Arlia-Ciommo1, Jennifer Anne Baratang Junio1, Emmanuel Orfanos1, Tala Tafakori1, Vicky Lutchman1, Karamat Mohammad1, Sarah Elsaser1, Sandra Orfali1, Harshvardhan Rajen1 and Vladimir I. Titorenko1

1 Department of Biology, Concordia University, Montreal, Quebec H4B 1R6, Canada

Correspondence to:

Vladimir I. Titorenko, email: [email protected]

Keywords: cellular aging; cellular quiescence; longevity; gerotargets; geroprotectors

Received: June 01, 2022     Accepted: July 01, 2022     Published: July 28, 2022

Copyright: © 2022 Leonov et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


We propose a hypothesis of a mechanism linking cellular aging to cellular quiescence in chronologically aging budding yeast. Our hypothesis posits that this mechanism integrates four different processes, all of which are initiated after yeast cells cultured in a medium initially containing glucose consume it. Quiescent cells that develop in these cultures can be separated into the high- and low-density sub-populations of different buoyant densities. Process 1 of the proposed mechanism consists of a cell-cycle arrest in the G1 phase and leads to the formation of high-density quiescent cells. Process 2 results in converting high-density quiescent cells into low-density quiescent cells. Processes 3 and 4 cause a fast or slow decline in the quiescence of low- or high-density quiescent cells, respectively. Here, we tested our hypothesis by assessing how four different geroprotectors influence the four processes that could link cellular aging to cellular quiescence. We found that these geroprotectors differently affect processes 1 and 2 and decelerate processes 3 and 4. We also found that a rise in trehalose within quiescent yeast contributes to chronological aging and quiescence maintenance. These data collectively provide conclusive evidence for a mechanistic link between cellular aging and cellular quiescence.

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