Although no finding met genomewide significance, the presence of multiple possible signals in PCLO and the plausibility of a role for PCLO in the etiology of MDD led us to attempt replication in external samples. We assembled a collection of 11,972 independent subjects (6,079 MDD cases and 5,893 controls) from seven different groups and a total of six case-control replication samples (two German samples were combined, see Supplemental Methods). As with NESDA cases, all replication cases were adults of European ancestry on whom a structured clinical interview was used to substantiate the lifetime diagnosis of DSM-IV MDD (1), and all studies excluded common MDD phenocopies (e.g., depressive symptoms due to another psychiatric disorder or a general medical condition). As with NTR controls, all replication controls were adults of European ancestry ascertained from the population, and individuals reporting MDD symptoms were excluded. We estimated statistical power using Quanto (57) (assumptions: log-additive genetic model, MDD lifetime risk 0.15, MAF=0.45 (similar to rs2522833), a genotypic relative risk of 1.14 (“shrunk” down from the observed GRR of 1.26 for rs2522833 to account for the
