Figure 2. Caloric restriction (CR) and the ras2Δ mutation under non-CR conditions cause the formation of high-density Q cells by arresting the cell cycle at a checkpoint in early G₁.

In contrast, lithocholic acid (LCA) and the tor1Δ mutation elicit the formation of high-density Q cells under non-CR conditions by arresting the cell cycle at a checkpoint in late G₁. Wild-type (WT) yeast cells were cultured in the nutrient-rich YP medium initially containing 0.2% glucose (CR conditions) or 2% glucose (non-CR conditions) with or without LCA. The tor1Δ and ras2Δ mutant cells were cultured in the nutrient-rich YP medium initially containing 2% glucose (non-CR conditions) without LCA. Culture aliquots were recovered from the logarithmic (L), diauxic (D), post-diauxic (PD) or stationary (ST) growth phase. High-density Q cells were purified from these culture aliquots using centrifugation in Percoll density gradient, as described in Materials and Methods. Differential interference contrast micrographs of high-density Q cells recovered from the ST growth phase on day 7 (A) and mean diameters of high-density Q cells recovered from different growth phases (B) are shown. (C) A model for how CR, LCA (under non-CR conditions), tor1Δ (under non-CR conditions) and ras2Δ (under non-CR conditions) cause the formation of high-density Q cells by arresting the cell cycle at specific checkpoints in early (red) or late (blue) G₁. Data in B are presented as means ± SEM (n = 3; ^* p < 0.05; ns, not significant).