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Recent meta-analyses of schizophrenia genome-wide association studies (GWASs) have identified the  CUB and SUSHI multiple domains 1  ( CSMD1 ) gene as a statistically strong risk factor. CSMD1 is a complement control-related protein suggested to inhibit the classical complement pathway, being expressed in developing neurons. However, expression of  CSMD1  is largely uncharacterized and relevance for behavioral phenotypes is not previously demonstrated. Here, we assess neuropsychological behaviors of a  Csmd1  knockout (KO) mouse in a selection of standard behavioral tests. Deregulation of neuropsychological responses were observed in both the open field and the elevated plus maze tests, in which KO mice spent 55% and 33% less time than WT littermate mice in open areas, respectively. Altered behaviors were also observed in tail suspension and to higher acoustic stimuli, for which  Csmd1  KO mice showed helplessness and moderate increase in startle amplitude, respectively. Furthermore,  Csmd1  KO mice also displayed increased weight-gain and glucose tolerance, similar to a major phenotype of the metabolic syndrome that also has been associated to the human  CSMD1  locus. Consistent with a role in the control of behaviors,  Csmd1  was found highly expressed in the central nervous system (CNS), and with some expression in visceral fat and ovary, under tissue-specific control by a novel promoter-associated lncRNA. In summary, disruption of  Csmd1  induces behaviors reminiscent of blunted emotional responses, anxiety and depression. These observations suggest an influence of the  CSMD1  schizophrenia susceptibility gene on psychopathology and endophenotypes of the negative symptom spectra.

Neuropsychological Deficits in Mice Depleted of the Schizophrenia Susceptibility Gene CSMD1