News Release

A molecular genetic mechanism for schizophrenia

Peer-Reviewed Publication

Molecular Psychiatry

Disrupted-In-Schizophrenia 1 (DISC1) was identified as a novel gene disrupted by a (1;11)(q42.1;q14.3) translocation that segregated with schizophrenia in a Scottish family. Predicted DISC1 product has no significant homology to other known proteins. Here, Dr. Katayama and colleagues in Osaka, Japan, demonstrated the existence of DISC1 protein and identified fasciculation and elongation protein zeta-1 (FEZ1) as an interacting partner of DISC1 by a yeast two-hybrid study. FEZ1 and its nematode homolog are reported to represent a new protein family involved in axonal outgrowth and fasciculation. In cultured hippocampal neurons, DISC1 and FEZ1 colocalized in growth cones. Interactions of these proteins were associated with F-actin. In the course of neuronal differentiation of PC12 cells, upregulation of DISC1/FEZ1 interaction was observed as along with enhanced extension of neurites by overexpression of DISC1. The present study shows that DISC1 participates in neurite outgrowth through its interaction with FEZ1. Recent studies have provided reliable evidence that schizophrenia is a neurodevelopmental disorder. As there is a high level of DISC1 expression in developing rat brain, dysfunction of DISC1 may confer susceptibility to psychiatric illnesses through abnormal development of the nervous system.

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Authors: K Miyoshi, A Honda, K Baba, M Taniguchi, K Oono, T Fujita, S Kuroda, T Katayama, M Tohyama

Citation source: Molecular Psychiatry 2003 Volume 8, number 7, pages 685-694.

Department of Anatomy and Neuroscience, Graduate School of Medicine, Osaka University, Suita, Japan; Discovery Research Laboratory, Tanabe Seiyaku Company Limited, Osaka, Japan; CREST of Japan Science and Technology Corporation (JST), Kawaguchi, Japan; Department of Structural Molecular Biology, Institute of Scientific and Industrial Research, Osaka University, Ibaraki, Japan

For further information on this work, please contact Dr. Dr. Taiichi Katayama, Osaka University Graduate School of Medicine Anatomy and Neuroscience; 2-2 Yamada-oka; Suita, Osaka 565-0871; Japan; phone: 81-6-6879-3221; FAX: 81-6-6879-3229; e-mail: katayama@anat2.med.osaka-u.ac.jp

Molecular Psychiatry is published by the Nature Publishing Group. http://www.nature.com/mp

Editor: Julio Licinio, M.D.; phone: 1-310-825-7113; FAX: 1-310206-6715; e-mail: licinio@ucla.edu

For a copy of this article, please contact Aimee Midei, editorial assistant, e-mail: molecularpsychiatry@mednet.ucla.edu.

Please cite Molecular Psychiatry as the source of this material.


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