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. 2022 Jul 28;13:918–943. doi: 10.18632/oncotarget.28256

Figure 1. A hypothetical model for the four processes linking cellular aging to cellular quiescence.

Figure 1

We hypothesized that these processes converge into a mechanism that links cellular aging to cellular quiescence in chronologically aging budding yeast. To test our hypothesis, we had the following two objectives. The first objective of this study was to investigate how geroprotective interventions other than caloric restriction (CR) affect each of these processes. The second objective of this study was to test how some CR-specific biochemical traits of quiescent (Q) cells contribute to the abilities of CR and LCA to slow down a decline in the cellular quiescence of chronologically aging budding yeast. Process 1: CR creates a sub-population of high-density Q cells by arresting the cell-division cycle of some cells and eliciting their entry into the G0 state in early G1; yet, the development of such a cell sub-population under non-CR conditions happens by a cell-cycle arrest in late G1. Process 2: CR accelerates the conversion of high-density Q cells into low-density Q cells. CR postpones a fast transformation of low-density Q cells into low-density NQ cells (process 3) and a slow conversion of high-density Q cells into high-density NQ cells (process 4). See the text for more details. The metabolic traits of Q cells that can contribute to the different effects of CR and LCA on processes 1 and 2 (A) and their similar effects on processes 3 and 4 (B) are shown. Other Abbreviations: HD: high-density cells; LD: low-density cells. ↑an increase ↓a decrease →→ activation arrows ˧˧inhibition bars.