| Budget Amount *help |
¥18,460,000 (Direct Cost: ¥14,200,000、Indirect Cost: ¥4,260,000)
Fiscal Year 2015: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2013: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
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| Outline of Final Research Achievements |
The gene encoding Ataxin-2 is mutated in the patients with some neurodegenerative diseases, such as spinocerebellar ataxia type 2 and amyotrophic lateral sclerosis. This finding suggests a common pathogenic role of Ataxin-2 in these neurodegenerative diseases. Therefore, a comprehensive understanding of the physiological functions of Ataxin-2 is the first step for elucidating the mechanism underlying Ataxin-2-mediated neurodegeneration. However, although Ataxin-2 has been implicated to be involved in RNA metabolism, the exact biological mechanism and in vivo targets remain unknown. In this study, we identified that Ataxin-2 associates with RNA-induced silencing complex that is required for microRNA-mediated gene silencing. Furthermore, we found that Ataxin-2 binds to distinct elements in the 3’UTRs of target mRNAs. The functional analyses revealed that Ataxin-2 stabilizes target mRNAs, which was attenuated by disease-associated mutations.
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