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Susceptibility to complex disease appears to be partly mediated by heritable differences in gene expression. Where  cis -acting effects on a gene's expression influence disease susceptibility, other genes containing polymorphism with a  trans -acting effect on expression of that gene may also be expected to modulate risk. Use of the expression of an identified disease gene as an endophenotype for quantitative linkage analysis may therefore provide a powerful method for mapping loci that modulate disease susceptibility. We performed genome-wide linkage analysis on expression of  dystrobrevin binding protein 1  ( DTNBP1 ), a well-supported susceptibility gene for schizophrenia, in large CEPH pedigrees. We observed genome-wide significant evidence for linkage at the  DTNBP1  locus on chromosome 6p22, and demonstrated that this reflects variable  cis -acting effects on  DTNBP1  expression. In addition, we observed genome-wide suggestive evidence for linkage of  DTNBP1  expression to chromosome 8p, suggesting a locus that exerts a  trans -acting effect on  DTNBP1  expression. The region of linkage to  DTNBP1  expression on chromosome 8 is contiguous with linkage findings based upon the clinical schizophrenia phenotype, and contains another well-supported schizophrenia susceptibility gene,  neuregulin-1  ( NRG1 ). Our data provide complementary evidence for chromosome 8p as a susceptibility locus for schizophrenia, and suggest that genetic variation within this region may influence risk, at least in part, through effects on  DTNBP1  expression.

Cis - and trans - loci influence expression of the schizophrenia susceptibility gene DTNBP1