2014 Fiscal Year Final Research Report
The molecular mechanism of asymmetric inheritance of damaged proteins.
Project/Area Number |
25840080
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Cell biology
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Research Institution | The Institute of Physical and Chemical Research |
Principal Investigator |
SUZUKI Genjiro 独立行政法人理化学研究所, 脳科学総合研究センター, 研究員 (60466034)
|
Project Period (FY) |
2013-04-01 – 2015-03-31
|
Keywords | 細胞老化 / プリオン |
Outline of Final Research Achievements |
To elucidate the molecular mechanism of cellular aging, I focused on Mlp proteins and investigated the molecular mechanism of asymmetric inheritance of damaged protein aggregates. I found the mlp mutant strain of budding yeast showed defects in asymmetric inheritance of damaged protein aggregates and prion propagons and shorter life span. I also found Mlp proteins co-localized with damaged protein aggregates. Thus, Mlp proteins must be scaffolds of aggregated proteins in mother cells and retain these aggregates in mother cells to keep the daughter cells fresh.
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Free Research Field |
遺伝学
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