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Glutamine Flux Imaging Using Genetically Encoded Sensors
10:23

Glutamine Flux Imaging Using Genetically Encoded Sensors

Published on: July 31, 2014

10.1K

Npr2 inhibits TORC1 to prevent inappropriate utilization of glutamine for biosynthesis of nitrogen-containing

Sunil Laxman1, Benjamin M Sutter1, Lei Shi1

  • 1Department of Biochemistry, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9038, USA.

Science Signaling
|December 18, 2014
PubMed

Insights

The Npr2 protein complex regulates cell growth and autophagy by controlling nutrient utilization. Loss of Npr2 in yeast alters metabolism, enabling proliferation by affecting glutamine and S-adenosyl methionine (SAM) levels.

Area of Science:

  • Cell Biology
  • Metabolic Regulation
  • Molecular Biology

Background:

  • Cells must balance growth and autophagy in response to nutrient availability.
  • The Npr2 protein complex (Iml1, Npr2, Npr3; SEACIT) inhibits target of rapamycin complex 1 (TORC1) signaling, suppressing autophagy in nutrient-rich conditions.
  • Loss of Npr2 allows yeast to bypass autophagy and proliferate under nutrient limitations.

Purpose of the Study:

  • To investigate the distinct metabolic state of Npr2-deficient yeast.
  • To elucidate the role of the Npr2 complex in cellular homeostasis and nutrient utilization.
  • To understand the integration of nutrient cues and metabolic pathways.

Main Methods:

  • Culturing wild-type and Npr2-deficient yeast in minimal media with ammonium and lactate.
  • Metabolomic analysis to compare intracellular metabolite concentrations.
  • Supplementation experiments with methionine to assess its impact on nutrient utilization.

Main Results:

  • Npr2-deficient yeast exhibited a unique metabolic profile compared to wild-type.
  • Npr2-deficient yeast metabolized glutamine into nitrogenous metabolites and maintained high S-adenosyl methionine (SAM) levels.
  • Methionine supplementation in wild-type yeast stimulated glutamine consumption, indicating integrated nutrient signaling.

Conclusions:

  • The Npr2 complex regulates cellular homeostasis through metabolic control, particularly glutamine utilization.
  • TORC1 plays a crucial role in managing glutamine synthesis and consumption as a nitrogen source.
  • This study reveals the metabolic underpinnings of the Npr2 complex's function in nutrient adaptation.

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