| Budget Amount *help |
¥20,280,000 (Direct Cost: ¥15,600,000、Indirect Cost: ¥4,680,000)
Fiscal Year 2013: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2012: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥10,660,000 (Direct Cost: ¥8,200,000、Indirect Cost: ¥2,460,000)
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| Research Abstract |
Septins are evolutionarily conserved polymerizing GTPases like the major cytoskeletal nucleotide-binding proteins of tubulins and actins, however, their physiological functions in metazoans are largely unknown. To address this: 1) We have established a line of conditional SEPT7 knockout mice and uncovered that septins promote dendrite and axon development by negatively regulating microtubule stability via HDAC6-mediated deacetylation. 2) We established prion-promoter-driven SEPT4 transgenic mice and uncovered that chronic overload of SEPT4, a parkin substrate that aggregates in Parkinson's disease, causes behavioral alterations but not neurodegeneration in mice. These and other findings, in addition to mouse lines and a set of reagents created in this study, will help understand cellular/molecular mechanisms of septin functions in relation to other cytoskeletal systems in physiologically relevant contexts.
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