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Social interaction and sensorimotor gating abnormalities in mice lacking Dvl1.

Cell | Sep 5, 1997

Mice completely deficient for Dvl1, one of three mouse homologs of the Drosophila segment polarity gene Dishevelled, were created by gene targeting. Dvl1-deficient mice are viable, fertile, and structurally normal. Surprisingly, these mice exhibited reduced social interaction, including differences in whisker trimming, deficits in nest-building, less huddling contact during home cage sleeping, and subordinate responses in a social dominance test. Sensorimotor gating was abnormal, as measured by deficits in prepulse inhibition of acoustic and tactile startle. Thus, Dvl1 mutants may provide a model for aspects of several human psychiatric disorders. These results are consistent with an interpretation that common genetic mechanisms underlie abnormal social behavior and sensorimotor gating deficits and implicate Dvl1 in processes underlying complex behaviors.

Pubmed ID: 9298901 RIS Download

Mesh terms: Adaptor Proteins, Signal Transducing | Animals | Behavior, Animal | Dishevelled Proteins | Drosophila Proteins | Embryo, Mammalian | Female | Gene Expression Regulation, Developmental | Male | Mice | Mice, Knockout | Motor Neurons | Nesting Behavior | Neural Inhibition | Neurons, Afferent | Pain Measurement | Phosphoproteins | Psychomotor Performance | Sleep | Social Behavior | Vibrissae

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Associated grants

  • Agency: NCI NIH HHS, Id: CA63929

Mouse Genome Informatics (Data, Gene Annotation)

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