| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Research Abstract |
Macroautpohagy (referred to as autophagy hereafter) accompanies dynamic membrane remodeling such as autophagosome formation and fusion between autophagosome and lysosome. However, the regulation of such membrane remodeling is largely unknown. Since I had identified three Rab-GAPs, inactivators of Rab-type small GTPases, as autophagosome resident proteins, here I addressed the function of these Rab-GAPs (OATL1/TBC1D25, TBC1D2B, TBC1D11) in autophagy. They were localized at autophagosomes and bound with LC3, an autophagosome resident protein used as a marker of autophagosome. TBC1D2B and TBC1D25 required the interaction with LC3 for their localization at autophagosomes, since a point mutation that abolished the interaction impaired their localization. Although I previously revealed that overexpression of TBC1D25 inhibits fusion between autophagosomes and lysosomes, overexpression of TBC1D2B nor TBC1D11 did not inhibit any process of autophagy.
These results so far did not clarify relationship between these Rab-GAPs and autophagy. However, I suppose that it is possible that LC3 acts as a scaffold for Rab-GAPs and has a role in membrane trafficking in addition to in autophagy.
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