Mice completely deficient for Dvl1, one of three mouse homologs of the
Drosophila segment polarity gene Dishevelled, were created by gene ta
rgeting. Dv1-deficient mice are viable, fertile, and structurally norm
al. Surprisingly, these mice exhibited reduced social interaction, inc
luding differences in whisker trimming, deficits in nest-building, les
s huddling contact during home cage sleeping, and subordinate response
s in a social dominance test. Sensorimotor gating was abnormal, as mea
sured by deficits in prepulse inhibition of acoustic and tactile start
le. Thus, Dv1 mutants may provide a model for aspects of several human
psychiatric disorders. These results are consistent with an interpret
ation that common genetic mechanisms underlie abnormal social behavior
and sensorimotor gating deficits and implicate Dvl1 in processes unde
rlying complex behaviors.