| Budget Amount *help |
¥18,090,000 (Direct Cost: ¥15,000,000、Indirect Cost: ¥3,090,000)
Fiscal Year 2009: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2008: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2007: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2006: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Research Abstract |
Telomere is an essential chromosomal element that composes of the end of eukaryotic linear chromosome and plays a role in the maintenance of its integrity. Dual functions of the telomere are to discriminate normal chromosomal ends from abnormal damaged ends, and to provide the field to replicate the end through the specific telomerase-mediated system. In this study, we aim to elucidate how the two antagonistic functions of the telomere are coordinated during the cell cycle.
CST (Cdc13-Stn1-Ten1) complex of the budding yeast Saccharomyces cerevisiae has been shown to associate with the telomeric DNA ends and to be involved in the both functions of the telomere. We found that the CST complex was phosphorylated orderly by ATM kinases, that detect shorter telomeres, and by Cdk, that regulates cell cycle events. Moreover, we found that Stn1 was important for modulation of replication restart after replication forks arrested by the addition of hydroxyurea. Finally, we identified a novel alleles of STN1 whose product was defective in its protective role, and showed that coordination of N-terminal protective function with C-terminal replicative function was pivotal for cell viability in this mutant. Together, our results indicated that CST was regulated by a variety of signaling cascades to modify the function of the complex, thereby maintaining the integrity of the telomeres.
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