| Budget Amount *help |
¥16,120,000 (Direct Cost: ¥12,400,000、Indirect Cost: ¥3,720,000)
Fiscal Year 2016: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥7,540,000 (Direct Cost: ¥5,800,000、Indirect Cost: ¥1,740,000)
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| Outline of Final Research Achievements |
LIS1 was identified as the gene mutated in individuals with lissencephaly, which is a devastating neurological disorder caused by defective neuronal migration. We previously proposed a model for a mobile tubulin fragments (tMT), in which cytoplasmic dynein is anchored to a short tMT by LIS1 followed by the kinesin-dependent anterograde transport. However, the mechanisms that produce tMTs have not been determined.
Here, we identified α-synuclein by immunoprecipitation method with anti-β III-tubulin antibody, which has been linked to Parkinson’s disease and dementia. Live-cell imaging showed that α-synuclein co-transported with LIS1, dynein and tMT in the anterograde transport. Our in vitro investigations of microtubule dynamics revealed that α-synuclein regulated the polymerization/depolymerization of short microtubule fragment. Our findings indicate that α-synuclein facilitates to form short, mobile tMTs that play an important role in the axonal transport.
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