Laboratories & Administration Office

Laboratory of Regulation of Neuronal Development

member

Director Kazuaki YOSHIKAWA
助教 Koichi HASEGAWA

連絡先

Tel 81-6-6879-8621
Fax 81-6-6879-8623
E-mail

研究概要

Neurons withdraw from the cell cycle immediately after differentiation from neural stem cells. Thereafter, neurons become terminally differentiated and remain permanently quiescent (postmitotic) to acquire their specific functions. The molecular mechanism of this phenomenon is one of the most important research areas in biology. In 1991, we discovered a novel protein, termed necdin (for neurally differentiated embryonal carcinoma-derived protein), which is expressed predominantly in postmitotic neurons. This protein is capable of suppressing cell proliferation and interacts with cell cycle-related proteins such as E2F and p53, which are known as death-inducing (proapoptotic) proteins in postmitotic neurons. Necdin also interacts with many regulatory proteins such as neurotrophin receptors and transcription factors. Thus, we propose that necdin is a unique adaptor protein that stabilizes terminal differentiation of postmitotic neurons. We are studying the expression and function of necdin and its related MAGE (melanoma antigen) family proteins in neuronal development. We adopt the strategy by which cloned genes with unknown functions are transferred into neurons and neural precursor cells to elucidate their roles in neuronal differentiation and apoptosis. Our goal is to gain a unified view on cell cycle regulation, terminal differentiation, and death of neurons.


<Fig.1>
The neuronal mitotic suppressor necdin (green) and the neural marker protein
MAP2 (red) are co-expressed in nascent neurons generated in vitro from
neural stem cells.


<Fig.2>
Mice with brown eyes and hair are defective in the paternal necdin gene.
They look normal but display various neuronal abnormalities.

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