| Budget Amount *help |
¥116,610,000 (Direct Cost: ¥89,700,000、Indirect Cost: ¥26,910,000)
Fiscal Year 2015: ¥20,410,000 (Direct Cost: ¥15,700,000、Indirect Cost: ¥4,710,000)
Fiscal Year 2014: ¥20,410,000 (Direct Cost: ¥15,700,000、Indirect Cost: ¥4,710,000)
Fiscal Year 2013: ¥21,450,000 (Direct Cost: ¥16,500,000、Indirect Cost: ¥4,950,000)
Fiscal Year 2012: ¥21,320,000 (Direct Cost: ¥16,400,000、Indirect Cost: ¥4,920,000)
Fiscal Year 2011: ¥33,020,000 (Direct Cost: ¥25,400,000、Indirect Cost: ¥7,620,000)
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| Outline of Final Research Achievements |
We examined the quality control in neuronal axons through proteolysis and its impairment, and found that p62 and NBR1 was localized only in somatodendrites but not in axons and their terminals of neurons. N-terminal regions of p62 and NBR1 were responsible for this polarized localization. The intraneuronal target components of p62 and NBR1 in CD-deficient neurons were dysfunctional lysosomes whose surface membrane was decorated by p62/NBR1, together with ubiquitin. As for Atg9A-deficient brains, the KO mice did not live beyond four weeks of age. p62 and NBR1, together with ubiquitin, accumulated in neuronal cell bodies at postnatal day (P) 15, but these accumulations were decreased at P28. Severe degenerative changes proceeded only in axons and their terminals at P28. Atg9A-deficiency induced dysgenesis of the corpus callosum and anterior commissures, while the axonal extensions of primary cultured neurons from the mouse embryos were significantly impaired in primary neurons.
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