Our previous studies have revealed a key role of disrupted-in-schizophrenia 1 (DISC1) in the tempo regulation of multiple developmental steps during adult neurogenesis (Duan et al., 2007; Faulkner et al., 2008). Disc1 was originally identified at the breakpoint of a balanced (1;11)(q42;q14) chromosome translocation that co-segregates with schizophrenia, bipolar disorder, and recurrent major depression in a large Scottish family (Blackwood et al., 2001; Millar et al., 2000). Genetic lineage and association studies have further suggested disc1 as a general risk factor for schizophrenia, schizoaffective disorder, bipolar disorder, major depression, autism and Asperger syndrome (Chubb et al., 2008). How DISC1 dysfunction contributes to a wide spectrum of psychiatric and mental disorders remains unknown (Hennah and Porteous, 2009). Certain schizophrenia and/or depression-related phenotypes have been observed in behavioral analysis of mice with DISC1 dysfunction, including mis-sense mutations (Clapcote et al., 2007), over-expression of truncated forms (Hikida et al., 2007; Li et al., 2007; Pletnikov et al., 2008; Shen et al., 2008), deletion of certain isoforms (Ishizuka et al., 2007; Koike et al., 2006; Kvajo et al., 2008) and lentivirus-mediated expression of short-hairpin
