Abstract
The growth rate of a yeast cell is controlled by the target of rapamycin kinase complex I (TORC1) and cAMP-dependent protein kinase (PKA) pathways. To determine how TORC1 and PKA cooperate to regulate cell growth, we performed temporal analysis of gene expression in yeast switched from a non-fermentable substrate, to glucose, in the presence and absence of TORC1 and PKA inhibitors. Quantitative analysis of these data reveals that PKA drives the expression of key cell growth genes during transitions into, and out of, the rapid growth state in glucose, while TORC1 is important for the steady-state expression of the same genes. This circuit design may enable yeast to set an exact growth rate based on the abundance of internal metabolites such as amino acids, via TORC1, but also adapt rapidly to changes in external nutrients, such as glucose, via PKA.
Highlights
The growth rate of a yeast cell is controlled by the target of rapamycin kinase complex I (TORC1) and cAMP-dependent protein kinase (PKA) pathways
Most of the genes upregulated in glucose are involved in ribosome and protein synthesis (Ribi genes, Fig. 1b), while those downregulated in glucose tend to be involved in aerobic respiration (Fig. 1b)
Our expression data show that the genes involved ribosome biogenesis and protein synthesis are highly expressed 20 min after glucose repletion, but the expression levels drop once cells enter log phase growth at 120 and 180 min (Figs. 1b and 2a and Supplementary Fig. 2)
Summary
The growth rate of a yeast cell is controlled by the target of rapamycin kinase complex I (TORC1) and cAMP-dependent protein kinase (PKA) pathways. Experiments in the model organism, Saccharomyces cerevisiae, have led to the identification of a interesting signaling circuit that includes the highly conserved target of rapamycin kinase complex I (TORC1) and cAMP-dependent protein kinase (PKA) pathways. In this circuit, the TORC1 and PKA pathways work together to regulate expression of the ribosome and protein synthesis genes[1,2,3,4,5,6,7] and, as a consequence, set the growth rate of the cell[1,2,8,9,10]. This model does not explain how signals transmitted through the TORC1 and PKA pathways are integrated to set overall gene expression levels
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