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Annotation

Lee FH, Fadel MP, Preston-Maher K, Cordes SP, Clapcote SJ, Price DJ, Roder JC, Wong AH. Disc1 point mutations in mice affect development of the cerebral cortex. J Neurosci . 2011 Mar 2 ; 31(9):3197-206. PubMed Abstract

Comments on Paper and Primary News
Comment by:  Atsushi Kamiya
Submitted 2 May 2011 Posted 2 May 2011

In this paper, Lee et al. characterized DISC1 mutant mice, animals with ENU-induced mutation of Q31L and L100P, by systematic histological examinations. These animals had been previously reported to show behavioral abnormalities relevant to major mental disorders, such as schizophrenia and major depression, by Roder and Clapcote (Clapcote et al., 2007). The authors found decreased cell proliferation, altered neuronal distribution, as well as impaired dendritic growth and reduction of spine density in pyramidal neurons, all phenotypes observed in the cerebral cortex. As the authors described, these abnormal cellular architectures had been previously reported in the other DISC1 animal models, including studies using RNAi approaches (Kamiya et al., 2005; Li et al., 2007; Kvajo et al., 2008; Pletnikov et al., 2008;   Read more


View all comments by Atsushi Kamiya

Primary News: The DISC1 Switch in Neurodevelopment

Comment by:  Albert H. C. Wong
Submitted 13 May 2011 Posted 13 May 2011

This recent and important paper by Sawa's group adds another layer to the complex story of DISC1 function in neurodevelopment. Their findings clarify and integrate two streams of research implicating DISC1 in both neuron proliferation and migration. The identification of the S170 phosphorylation site also raises the exciting possibility that pharmacological strategies targeted at this phosphorylation-dependent switch might be useful in correcting or preventing mental illness-related problems with brain development. It would be interesting in this context to explore whether disease-associated DISC1 gene variants in humans affect DISC1 phosphorylation, and the subsequent balance between neuron proliferation and migration.

I agree with Atsushi Kamiya that further work is needed to understand which of the many effects of DISC1 perturbation are specific to human psychiatric disease phenotypes. Again, from a treatment perspective, it is vital to know which cellular abnormality underlies the most debilitating symptoms so that new treatments can be screened for effects on these...  Read more


View all comments by Albert H. C. Wong
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