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Kvajo M, McKellar H, Arguello PA, Drew LJ, Moore H, Macdermott AB, Karayiorgou M, Gogos JA. A mutation in mouse Disc1 that models a schizophrenia risk allele leads to specific alterations in neuronal architecture and cognition. Proc Natl Acad Sci U S A . 2008 May 13 ; 105(19):7076-81. PubMed Abstract

Comments on Paper and Primary News
Primary News: Human-like DISC1 Mutation Causes Morphological and Cognitive Deficits

Comment by:  David J. Porteous, SRF Advisor
Submitted 16 May 2008 Posted 16 May 2008

This paper is an update on the original report from the Gogos group (Koike et al., 2006) on the phenotype of mice carrying a genetically modified version of the 129 strain derived Disc1 gene and joins an already impressive list of Disc1 mouse models with associated SZ related phenotypes. Koike et al. (2006) attempted to knock out the Disc1 locus by homologous recombination in 129 derived mouse embryonal stem cells. The objective was to mimic as best as possible the effect of the t(1;11) balanced translocation that segregated with SZ and related major mental illness in a large Scottish family (Blackwood et al., 2001) and which led to the identification at the breakpoint of the DISC1 gene (Millar et al., 2000). In the event, this didn’t quite happen as planned, but a fortuitous and positive outcome was the generation of a transgene insertion which introduced two termination codons in exons 7 and 8. Simultaneously,...  Read more

View all comments by David J. Porteous

Primary News: Human-like DISC1 Mutation Causes Morphological and Cognitive Deficits

Comment by:  Akira Sawa, SRF Advisor
Submitted 16 May 2008 Posted 16 May 2008

A leading group studying DISC1, led by Drs. Gogos and Karayiogou, has recently published an intriguing paper on further characterization of mice with genetic mutation/modulation in the Disc1 gene (first described in Koike et al., 2006). I would like to applaud their outstanding and detailed analyses in the manuscript, which obviously provides great benefits to the field. The methodologies that this group employed in this paper would be useful for future studies in modeling mice for psychiatric disorders. However, there are a couple of points in the descriptions in the Discussion section which I would like to comment on for a general audience.

First, isoform disposition of DISC1 is very complex. As Dr. Barbara Lipska has presented in academic conferences from her studies, there seem to be many more DISC1 isoforms than we predicted. Thus, unless one makes knockout mice in which the deleted region of the genome is clearly demonstrated by experimental data, we cannot draw any conclusion on whether or not the mice have no...  Read more

View all comments by Akira Sawa
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