| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
The target of rapamycin (Tor) plays a pivotal role in cell growth and metabolism. Yeast contains two related proteins, Tor1 and Tor2. In fission yeast, Tor1 is dispensable for normal growth but is involved in amino acid uptake and cell survival under various stress conditions. In contrast, Tor2 is essential for cell proliferation ; however, its physiological function remains unknown. Here we characterize the roles of fission yeast Tor2 by creating temperature sensitive (tor2^<ts>) mutants. Remarkably, we have found that tor2^<ts> mimics nitrogen starvation responses, because the mutant displays a number of phenotypes that are normally induced only upon nitrogen deprivation. These include G1 cell-cycle arrest with a small cell size, induction of autophagy and commitment to sexual differentiation. By contrast, tor1 Δtor2ts double mutant cells show distinct phenotypes, as the cells cease division with normal cell size in the absence of G1 arrest. Tor2 physically interacts with the conserved Rhb1/GTPase. Intriguingly, overexpression of rhb1^+ or deletion of Rhb1-GAP-encoding tsc2^+ is capable of rescuing stress-sensitive phenotypes of the torl mutant, implying that Tor1 and Tor2 also share functions in cell survival under adverse environment. We propose that Tor1 and Tor2 are involved in both corroborative and independent roles in nutrient sensing and stress responses pathways.
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