3 Dec 2010

Dr. Takeda receives Astellas Foundation Metabolic Disorders Research Grant

Dr. Kojiro Takeda, Group Leader of the G0 Cell Unit, has been granted FY2010 research funding from Astellas Foundation for Research on Metabolic Disorders. This grant is awarded for research on the elucidation of disease processes and the development of ground-breaking medical treatments.

The title of Dr. Takeda’s research proposal is: “Cooperative roles of the proteasome and autophagy for mitochondrial maintenance and life span in the quiescent phase of fission yeast. “ Using fission yeast as a model organism, he aims to deepen the understanding of mechanisms for maintaining the function and survivability of cells arrested at G0 phase (cellular quiescence), where cells cease proliferation. Outcomes of this research are expected to contribute to the development of treatment for neurodegenerative diseases including Parkinson’s disease and metabolic syndrome such as diabetes.

Dr. Takeda is one of the grantees selected from a total of 542 applicants. According to the Astellas Foundation for Research on Metabolic Disorders, he is the first scientist conducting research in Okinawa to receive the grant in the more than 40 years of the foundation’s history.

Summary of Dr. Takeda’s research proposal 

We have been investigating the mechanism for maintaining function and survivability of cells arrested at G0 phase (cellular quiescence), where cells cease proliferation. Recently, we found that two major proteolytic machineries, the ubiquitin/proteasome system and autophagy, cooperatively contribute to the survival of G0 cells and the quality control of mitochondria in G0 phase specific manner. This result was published in the Proceedings of the National Academy of Science of the United States of America. In G0 phase, the proteasome is engaged in the maintenance of mitochondrial function and in reducing production of harmful oxidative stress. On the other hand, autophagy contributes to reducing the accumulation of oxidative stress by degrading damaged mitochondria which produce oxidative stress. Therefore, G0 cells are doubly protected from accumulation of lethal oxidative stress by two defense systems, the protesome and autophagy.

To obtain further knowledge of the mechanism of maintaining G0 phase cells, we proposed the following two themes to the Astellas Foundation for Research on Metabolic Disorders.

I. Identification of proteasomal substrates which are important for mitochondrial functions and maintenance.
II. Understanding the mechanism by which the autophagy system recognizes and degrades damaged mitochondria.


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