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Updated: Oct 16, 2025

Microscopy of Fission Yeast Sexual Lifecycle
Published on: March 9, 2016
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.
Abstract:
Target of rapamycin (TOR) kinases form two distinct complexes, TORC1 and TORC2, which are evolutionarily conserved among eukaryotes. These complexes control intracellular biochemical processes in response to changes in extracellular nutrient conditions. Previous studies using the fission yeast, Schizosaccharomyces pombe, showed that the TORC2 signaling pathway, which is essential for cell proliferation under glucose-limited conditions, ensures cell-surface localization of a high-affinity hexose transporter, Ght5, by downregulating its endocytosis. The TORC2 signaling pathway retains Ght5 on the cell surface, depending on the presence of nitrogen sources in medium. Ght5 is transported to vacuoles upon nitrogen starvation. In this review, we discuss the molecular mechanisms underlying this regulation to cope with nutritional stress, a response which may be conserved from yeasts to mammals.
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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