Trehalose and glycogen accumulation is related to the duration of the G phase of

The Yeast Cyclin-Dependent Kinase Routes Carbon Fluxes to Fuel Cell Cycle Progression

“…While this is consistent with previous observations in fed-batch and chemostat cultures (Kuenzi and Fiechter, 1969, 1972; Muller et al, 2003; Paalman et al, 2003), we now show that this is governed by the cell cycle control network and is downstream of the Start transition at the G1/S boundary. This result contradicts previous hypotheses that the storage switch is upstream of Start and drives entry into the cell cycle (Futcher, 2006; Sillje et al, 1997).…”

“…Moreover, several previous studies support a link between storage carbohydrate metabolism and the cell cycle. It was found that the length of G1 correlates with the amount of carbohydrates stored (Brauer et al, 2008; Paalman et al, 2003; Sillje et al, 1997), budding often correlates with decreases in storage carbohydrates (Kuenzi and Fiechter, 1969, 1972; Muller et al, 2003; Sillje et al, 1997), and the in vitro activities of several storage metabolism enzymes correlate with cell cycle phase (Vandoorn et al, 1988). Furthermore, trehalose utilization accelerates cell cycle entry when recovering from stationary phase (Shi et al, 2010).…”

Growth-limiting Intracellular Metabolites in Yeast Growing under Diverse Nutrient Limitations

“…Of these two metabolites, trehalose concentrations were most tightly correlated to growth rate (Table 2). This observation is consistent with trehalose biosynthesis and utilization being temporally compartmentalized within the cell cycle, with synthesis occurring in G1 and use in S phase (Kuenzi and Fiechter 1969; Paalman et al , 2003; Tu et al , 2005, 2007). As faster growth involves a shortening of G1 but not S phase (Hartwell et al , 1974; Unger and Hartwell 1976), the concentration of trehalose should decrease as the growth rate increases, as we observed.…”

A Novel Radiotracer to Image Glycogen Metabolism in Tumors by Positron Emission Tomography

“…We speculate that the high 18 F-FDG/glucose uptake attributed to the Warburg effect aims to provide the building blocks for cellular proliferation through, for example, the pentose phosphate shunt, whereas in quiescent tumor cells the excess glucose is instead diverted to glycogen. This could then be potentially mobilized when the cell re-enters cell cycle for both energy and as a carbon source for the synthesis of proteins, nucleotides and other building blocks; analogous to nutrient stress-induced quiescence, and synthesis of glycogen and trehalose by budding yeast (13, 14). …”

“…In addition, when cancer cells enter the stationary growth phase (quiescence), like budding yeast (13, 14), they synthesize glycogen (or trehalose), with the switch to growth being associated with diminished glycogenesis (6, 7, 15). While the molecular mechanisms responsible for enhanced glycogenesis in mammalian cells are not well understood, it can be appreciated that non-invasive assessment of this metabolic switch could have important applications in cancer.…”