Fission Yeast TORC2 Signaling Pathway Ensures Cell Proliferation under Glucose-Limited, Nitrogen-Replete Conditions

Yusuke Toyoda1, Shigeaki Saitoh1

  • 1Institute of Life Science, Kurume University, Asahi-machi 67, Kurume, Fukuoka 830-0011, Japan.

Biomolecules
|October 23, 2021
PubMed

Insights

The TORC2 pathway in yeast controls sugar uptake by keeping the Ght5 transporter on the cell surface. This mechanism helps cells adapt to nutrient scarcity, a process potentially conserved across species.

Area of Science:

  • Cellular biology
  • Molecular mechanisms
  • Nutrient sensing

Background:

  • Target of rapamycin (TOR) kinases, specifically TORC1 and TORC2, are conserved signaling complexes regulating cellular processes in response to nutrient availability.
  • TORC2 signaling is crucial for cell proliferation in fission yeast under glucose limitation.
  • Previous research indicated TORC2 influences hexose transporter localization.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which TORC2 signaling regulates the high-affinity hexose transporter Ght5.
  • To understand how this regulation aids yeast in coping with nutritional stress, particularly nitrogen starvation.
  • To explore the potential conservation of this nutrient-adaptive response in mammals.

Main Methods:

  • Investigated the role of the TORC2 pathway in fission yeast (Schizosaccharomyces pombe).
  • Analyzed the regulation of Ght5 transporter localization and endocytosis.
  • Examined the impact of nutrient availability (glucose and nitrogen) on Ght5 trafficking.

Main Results:

  • The TORC2 pathway downregulates Ght5 endocytosis, maintaining it on the cell surface under nutrient-rich conditions.
  • Ght5 localization is dependent on the presence of nitrogen sources.
  • Nitrogen starvation triggers the transport of Ght5 to the vacuole.

Conclusions:

  • TORC2-mediated regulation of Ght5 is a key mechanism for yeast to adapt to nutritional stress.
  • This pathway ensures efficient sugar uptake when needed and prevents nutrient loss during starvation.
  • The findings suggest a conserved mechanism for nutrient stress adaptation from yeast to mammals.

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