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Keywords:

  • carbon metabolism;
  • nitrogen metabolism;
  • nutrient sensing;
  • Snf1;
  • TORC1

Nutrient sensing and coordination of metabolic pathways are crucial functions for all living cells, but details of the coordination under different environmental conditions remain elusive. We therefore undertook a systems biology approach to investigate the interactions between the Snf1 and the target of rapamycin complex 1 (TORC1) in Saccharomyces cerevisiae. We show that Snf1 regulates a much broader range of biological processes compared with TORC1 under both glucose- and ammonium-limited conditions. We also find that Snf1 has a role in upregulating the NADP+-dependent glutamate dehydrogenase (encoded by GDH3) under derepressing condition, and therefore may also have a role in ammonium assimilation and amino-acid biosynthesis, which can be considered as a convergence of Snf1 and TORC1 pathways. In addition to the accepted role of Snf1 in regulating fatty acid (FA) metabolism, we show that TORC1 also regulates FA metabolism, likely through modulating the peroxisome and β-oxidation. Finally, we conclude that direct interactions between Snf1 and TORC1 pathways are unlikely under nutrient-limited conditions and propose that TORC1 is repressed in a manner that is independent of Snf1.

Synopsis

Nutrient sensing and coordination of metabolic pathways are crucial functions for living cells. A combined analysis of the yeast transcriptome, phosphoproteome and metabolome is used to investigate the interactions between the Snf1 and TORC1 pathways under nutrient-limited conditions.

  • Snf1 regulates a broad range of biological processes, while target of rapamycin complex 1 (TORC1) seems to be repressed under both glucose- and ammonium-limited conditions.
  • Snf1 has a role in regulating amino acids by upregulating the NADP+-dependent glutamate dehydrogenase (encoded by GDH3) under glucose-limited condition.
  • In addition to the accepted role of Snf1 in regulating fatty acid (FA) metabolism, TORC1 may also regulate FA metabolism.
  • Direct interactions between Snf1 and TORC1 pathways are unlikely under nutrient-limited conditions and TORC1 might be repressed in a manner that is independent of Snf1.