Dvl1 is one of three murine Dishevelled genes widely expressed in embryonic development and in the adult central nervous system. Dishevelled proteins are a necessary component of the Wnt and planar cell polarity developmental signaling pathways. We reported previously that mice deficient in Dvl1 exhibited abnormal social interaction and sensorimotor gating. To assess the validity of our earlier findings, we replicated the previous behavioral tests and included several new assays. The behaviors assessed included: social interaction, sensorimotor reflexes, motor activity, nociception, prepulse inhibition of acoustic startle (PPI) and learning and memory. Assessments with an explicit social component included: social dominance test, whisker trimming, nest building, home-cage huddling and ultrasonic vocalization rate analysis in pups. In addition, separate cohorts of wildtype and Dvl1-null mice were assessed for social recognition of a conspecific. Replicating the original report, Dvl1-null mice were impaired in several tasks containing an explicit social component. However, no impairment was observed in the social memory task. A previously observed deficit in PPI did not replicate in two institutions. In conclusion, we provide evidence that the social interaction phenotype of Dvl1-deficient mice has a strong genetic influence, but the sensorimotor gating deficit was subject to environmental influences. The specificity of observed social interaction deficits also suggests that lack of Dvl1 is associated with deficits in the recognition of social hierarchy and dominance.