| Budget Amount *help |
¥43,810,000 (Direct Cost: ¥33,700,000、Indirect Cost: ¥10,110,000)
Fiscal Year 2021: ¥11,830,000 (Direct Cost: ¥9,100,000、Indirect Cost: ¥2,730,000)
Fiscal Year 2020: ¥13,910,000 (Direct Cost: ¥10,700,000、Indirect Cost: ¥3,210,000)
Fiscal Year 2019: ¥8,580,000 (Direct Cost: ¥6,600,000、Indirect Cost: ¥1,980,000)
Fiscal Year 2018: ¥9,490,000 (Direct Cost: ¥7,300,000、Indirect Cost: ¥2,190,000)
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| Outline of Final Research Achievements |
Due to the stochastic nature of the microtubule interactions at kinetochores, releasing incorrect attachments is crucial for chromosomes to achieve bi-orientation on the mitotic spindle. Vital for this cellular function is the activity of mitotic kinase Aurora B at centromeres. Our previous work showed that a deficiency of this robust control of Aurora B widely affects chromosomal stability in cancer cells. In this mechanism, how mechanistically cells convey the activity of Aurora B enriched at centromeres to kinetochore substrates remains enigmatic. To address this question, we have conducted this project to study structural regulation of the Aurora B complex, or the Chromosomal Passenger Complex (CPC), and found that HP1 association with the CPC trigger a conformational transition of the complex that allows Aurora B to access kinetochore substrates.
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