| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
Fpr1/FKBP12 make complex with rapamycin, a medically important immunosuppressive drug. This complex binds to and inhibits the kinase activity of TORC1, a key regulator of cellular responses to nutritional environment, thereby prohibiting a synthesis of ribosomal components. However, function(s) of Fpr1 in the natural cellular-condition without the drug has been unknown. In this study, we identified fpr1 mutation that showed synthetic lethality with the deletion mutant of HMO1 gene, which is involved in a coordinated synthesis of ribosomal components. As the results of genome wide ChIP-seq analysis and the ChIP analysis using variously modified promoters, we demonstrated that Fpr1 bound to the promoter of ribosomal protein genes dependently on Rap1, a master transcriptional regulator of those genes.
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